The timing of the shrew: continuous melatonin treatment maintains youthful rhythmic activity in aging
Tim
The timing of the shrew: continuous melatonin treatment maintains
youthful rhythmic activity in aging Crocidura russula.Magnanou E,
Attia J, Fons R, Boeuf G, Falcon J.
UPMC University of Paris 06, UMR 7628, Banyuls/Mer, France.
elodie....@obs-banyuls.fr
BACKGROUND: Laboratory conditions nullify the extrinsic factors that
determine the wild expected lifespan and release the intrinsic or
potential lifespan. Thus, wild animals reared in a laboratory often
show an increased lifespan, and consequently an increased senescence
phase. Senescence is associated with a broad suite of physiological
changes, including a decreased responsiveness of the circadian system.
The time-keeping hormone melatonin, an important chemical player in
this system, is suspected to have an anti-aging role. The Greater
White-toothed shrew Crocidura russula is an ideal study model to
address questions related to aging and associated changes in
biological functions: its lifespan is short and is substantially
increased in captivity; daily and seasonal rhythms, while very marked
the first year of life, are dramatically altered during the senescence
process which starts during the second year. Here we report on an
investigation of the effects of melatonin administration on locomotor
activity of aging shrews. METHODOLOGY/PRINCIPAL FINDINGS: 1) The diel
fluctuations of melatonin levels in young, adult and aging shrews were
quantified in the pineal gland and plasma. In both, a marked diel
rhythm (low diurnal concentration; high nocturnal concentration) was
present in young animals but then decreased in adults, and, as a
result of a loss in the nocturnal production, was absent in old
animals. 2) Daily locomotor activity rhythm was monitored in pre-
senescent animals that had received either a subcutaneous melatonin
implant, an empty implant or no implant at all. In non-implanted and
sham-implanted shrews, the rhythm was well marked in adults. A marked
degradation in both period and amplitude, however, started after the
age of 14-16 months. This pattern was considerably delayed in
melatonin-implanted shrews who maintained the daily rhythm for
significantly longer. CONCLUSIONS: This is the first long term study
(>500 days observation of the same individuals) that investigates the
effects of continuous melatonin delivery. As such, it sheds new light
on the putative anti-aging role of melatonin by demonstrating that
continuous melatonin administration delays the onset of senescence. In
addition, the shrew appears to be a promising mammalian model for
elucidating the precise relationships between melatonin and aging.
PMID: 19526053 [PubMed - in process]
PMCID: PMC2690841
Tim
Taka
> PLoS One. 2009 Jun 15;4(6):e5904. Links
> The timing of the shrew: continuous melatonin treatment maintains
> youthful rhythmic activity in aging Crocidura russula.Magnanou E,
> Attia J, Fons R, Boeuf G, Falcon J.
> UPMC University of Paris 06, UMR 7628, Banyuls/Mer, France.
What the mechanism behind this could be ..... Taka
Curr Mol Med. 2007 Nov;7(7):638-49.
The ability of melatonin to counteract lipid peroxidation in
biological membranes.
Catalá A.
Instituto de Investigaciones Fisicoquímicas Teóricas y Aplicadas
(INIFTA), Facultad de Ciencias Exactas, Universidad Nacional de La
Plata, CONICET, La Plata, Argentina.
This paper reviews recent data relevant to the antioxidant effects of
melatonin with special emphasis on the changes produced in
polyunsaturated fatty acids located in the phospholipids of biological
membranes. The onset of lipid peroxidation within cellular membranes
is associated with changes in their physicochemical properties and
with the impairment of protein functions located in the membrane
environment. All cellular membranes are especially vulnerable to
oxidation due to their high concentration of polyunsaturated fatty
acids. These processes combine to produce changes in the biophysical
properties of membranes that can have profound effects on the activity
of membrane-bound proteins. This review deals with aspects for lipid
peroxidation of biological membranes in general, but with some
emphasis on changes of polyunsaturated fatty acids, which arise most
prominently in membranes and have been studied extensively in our
laboratory. The article provides current information on the effect of
melatonin on biological membranes, changes in fluidity, fatty acid
composition and lipid-protein modifications during the lipid
peroxidation process of photoreceptor membranes and modulation of gene
expression by the hormone and its preventive effects on adriamycin-
induced lipid peroxidation in rat liver. Simple model systems have
often been employed to measure the activity of antioxidants. Although
such studies are important and essential to understand the mechanisms
and kinetics of antioxidant action, it should be noted that the
results of simple in vitro model experiments cannot be directly
extrapolated to in vivo systems. For example, the antioxidant capacity
of melatonin, one of the important physiological lipophilic
antioxidants, in solution of pure triglycerides enriched in omega-3
polyunsaturated fatty acids is considerably different from that in
subcellular membranes.
PMID: 18045142
Taka
The protection of long chain polyunsaturated fatty acids by melatonin
during nonenzymatic lipid peroxidation of rat liver microsomes.
Leaden P, Barrionuevo J, Catalá A.
Cátedra de Bioquímica, Facultad de Ciencias Veterinarias, Universidad
Nacional de La Plata, Argentina.
The in vivo and in vitro effects of melatonin (N-acetyl-5-
methoxytryptamine) on lipid peroxidation of long chain polyunsaturated
fatty acids (PUFA) located in rat liver microsomes were determined.
The effect of intraperitoneal administration of melatonin (10 mg/kg
weight/24 hr) on ascorbate-Fe++ induced lipid peroxidation of isolated
rat liver microsomes was first examined. The ascorbate induced light
emission in hepatic microsomes was inhibited by melatonin treatment
[control group: 10.714 +/- 0.894; melatonin group: 3.162 +/- 0.515,
counts per minute (cpm) x 10(-5)]. Significant differences in the
content of arachidonic C20:4 n-6 and docosahexaenoic acid C22:6 n-3
were observed when control microsomes were lipid peroxidized in the
presence of ascorbic acid. These changes were less pronounced in liver
microsomes isolated from melatonin treated rats. In vitro assays
showed that after incubation of rat liver microsomes in an ascorbate-Fe
++ system, at 37 degrees C for 210 min, the total cpm originated from
light emission (chemiluminescence) was found to be lower in those
membranes incubated in the presence of melatonin. The fatty acid
composition of total lipids isolated from rat liver microsomes was
substantially modified when subjected to nonenzymatic lipid
peroxidation with a considerable decrease of docosahexaenoic acid 22:6
n-3 and arachidonic acid 20:4 n-6. The inhibition of the lipid
peroxidation process evaluated as chemiluminescence (total cpm at
selected times) was melatonin concentration dependent. Melatonin, at a
concentration 1.2 mm, inhibited almost completely the lipid
peroxidation process. Arachidonic and docosahexaenoic acids were more
affected than docosapentaenoic acid during the lipid peroxidation
process. Not all fatty acids were equally protected after the addition
of melatonin to the incubation medium. Our results indicate that
melatonin may act in vivo and in vitro as an antioxidant protecting
long chain PUFA present in rat liver microsomes from the deleterious
effect by a selective mechanism that reduces the loss of
docosahexaenoic and arachidonic acids.
PMID: 12074095
J Pineal Res. 2005 Sep;39(2):164-9.
Protective effect of melatonin on ascorbate-Fe2+ lipid peroxidation of
polyunsaturated fatty acids in rat liver, kidney and brain microsomes:
a chemiluminescence study.
Leaden PJ, Catalá A.
Cátedra de Bioquímica, Facultad de Ciencias Veterinarias, Universidad
Nacional de La Plata, Argentina.
Melatonin (N-acetyl-5-methoxytryptamine), the main secretory product
of the pineal gland, is a free radical scavenger that has been found
to protect against lipid peroxidation in many experimental models. In
the present study the effect of melatonin on lipid peroxidation of
long chain polyunsaturated fatty acids located in rat liver, kidney
and brain microsomes was determined using gas chromatography and a
chemiluminescence assay. In vitro assays showed that after incubation
of rat liver, kidney or brain microsomes in an ascorbate-Fe++ system,
at 37 degrees C for 180 min, the total cpm originated from light
emission (chemiluminescence) was found to be lower in those membranes
incubated in the presence of melatonin. The incubation of rat liver,
kidney or brain microsomes in the presence of ascorbate-Fe2+ resulted
in lipid-peroxidation of membranes as evidenced by light emission and
decrease of docosahexaenoic acid 22:6 n-3 and arachidonic acid 20:4
n-6. In the presence of melatonin (0.5, 1.0, 1.5 mm), light emission
percent inhibition of microsomes was: (liver - 3.33, 9.98, 39.40)
(kidney - 46.79, 61.88, 68.36) and (brain - 33.36, 28.89, 43.32). Not
all fatty acids were equally protected after the addition of melatonin
to the incubation medium. Our results indicate a selective protection
of C20:4 n6 and C22:6 n3 by melatonin during non-enzymatic lipid
peroxidation of rat liver, kidney and brain microsomes.
PMID: 16098094
Int J Biochem Cell Biol. 2003 Mar;35(3):359-66.
Melatonin preserves arachidonic and docosapentaenoic acids during
ascorbate-Fe2+ peroxidation of rat testis microsomes and mitochondria.
Gavazza M, Catalá A.
Facultad de Ciencias Veterinarias, Cátedra de Bioqui;mica, Universidad
Nacional de La Plata CC 296, B1900 AVW La Plata, Argentina.
The pineal hormone melatonin (N-acetyl, 5-methoxytryptamine) was
recently accepted to act as an antioxidant under both in vivo and in
vitro conditions. In this study, we examined the possible preventive
effect of melatonin on ascorbate-Fe(2+) lipid peroxidation of rat
testis microsomes and mitochondria. Special attention was paid to the
changes produced on the highly polyunsaturated fatty acids C20:4 n6
and C22:5 n6. The lipid peroxidation of testis microsomes or
mitochondria produced a significant decrease of C20:4 n6 and C22:5 n6.
The light emission (chemiluminescence) used as a marker of lipid
peroxidation was similar in both kinds of organelles when the control
and peroxidized groups were compared. Both long chain polyunsaturated
fatty acids were protected when melatonin was incorporated either in
microsomes or mitochondria. The melatonin concentration required to
inhibit by 100% the lipid peroxidation process was 5.0 and 1.0mM in
rat testis microsomes and mitochondria, respectively. IC 50 values
calculated from the inhibition curve of melatonin on the
chemiluminescence rates were higher in microsomes (4.98 mM) than in
mitochondria (0.67 mM). The protective effect observed by melatonin in
rat testis mitochondria was higher than that observed in microsomes
which could be explained if we consider that the sum of C20:4 n6+C22:5
n6 in testis microsomes is two-fold greater than present in
mitochondria.
PMID: 12531249
Prostaglandins Leukot Essent Fatty Acids. 2006 Apr;74(4):247-54. Epub
2006 Mar 23.
The effect of alpha-tocopherol on lipid peroxidation of microsomes and
mitochondria from rat testis.
Gavazza MB, Catalá A.
Cátedra de Bioquímica, Facultad de Ciencias Veterinarias, Argentina.
The testis is a remarkably active metabolic organ; hence it is
suitable not only for studies of lipid metabolism in the organ itself
but also for the study of lipid peroxidation processes in general. The
content of fatty acids in testis is high with a prevalence of
polyunsaturated fatty acids (PUFA) which renders this tissue very
susceptible to lipid peroxidation. Studies were carried out to
evaluate the effect of alpha-tocopherol in vitro on ascorbate-Fe(++)
lipid peroxidation of rat testis microsomes and mitochondria.
Chemiluminescence and fatty acid composition were used as an index of
the oxidative destruction of lipids. Special attention was paid to the
changes produced on the highly PUFA [C20:4 n6] and [C22:5 n6]. Lipid
peroxidation of testis microsomes or mitochondria induced a
significant decrease of both fatty acids. Total chemiluminescence was
similar in both kinds of organelles when the peroxidized without
(control) and with ascorbate-Fe(++) (peroxidized) groups were
compared. Arachidonic acid was protected more efficiently than
docosapentaenoic acid at all alpha-tocopherol concentrations tested
when rat testis microsomes or mitochondria were incubated with
ascorbate-Fe(++). The maximal percentage of inhibition in both
organelles was approximately 70%; corresponding to an alpha-tocopherol
concentration between 1 and 0.25 mM. IC50 values from the inhibition
of alpha-tocopherol on the chemiluminescence were higher in microsomes
(0.144 mM) than mitochondria (0.078 mM). The protective effect
observed by alpha-tocopherol in rat testis mitochondria was higher
compared with microsomes, associated with the higher amount of [C20:4
n6]+[C22:5 n6] in microsomes that in mitochondria. It is proposed that
the vulnerability to lipid peroxidation of rat testis microsomes and
mitochondria is different because of the different proportion of PUFA
in these organelles The peroxidizability index (PI) was positively
correlated with the level of long chain fatty acids. The results
demonstrated the protective effect of alpha-tocopherol on lipid
peroxidation in microsomes and mitochondria from rat testis.
PMID: 16549341
Prostaglandins Leukot Essent Fatty Acids. 2007 Jul;77(1):29-35. Epub
2007 Jul 27.
Melatonin and N-acetyl serotonin inhibit selectively enzymatic and non-
enzymatic lipid peroxidation of rat liver microsomes.
Leaden PJ, Catalá A.
Cátedra de Bioquímica, Facultad de Ciencias Veterinarias, Argentina.
Melatonin (N-acetyl-5-methoxytryptamine) and its immediate precursor N-
acetyl serotonin in the metabolism of tryptophan are free radical
scavengers that have been found to protect against non-enzymatic lipid
peroxidation in many experimental models. By contrast, little is known
about the antioxidant ability of these indoleamines against NADPH
enzymatic lipid peroxidation. The light emission produced by rat-liver
microsomes, expressed as total cpm during 180 min of incubation at 37
degrees C, was two-fold greater in the presence of ascorbate (0.4mM)
when compared with NADPH (0.2 mM). Maximal peaks of light emission
produced by microsomes lipid peroxidized with ascorbic-Fe(2+) or NADPH
and expressed as cpm were 354,208 (at 60 min) and 135,800 (at 15 min),
respectively. During non-enzymatic lipid peroxidation a decrease of
total chemiluminescence (inhibition of lipid peroxidation) was
observed when increasing concentrations of melatonin were added to
liver microsomes. The protective effect was concentration-dependent.
The inhibition observed in light emission was coincident with the
protection of the most PUFAs. Preincubation of microsomes with N-
acetyl serotonin reduced these changes very dramatically. Thus, in the
presence of both antioxidants (0.36, 0.75, 1.5 mM), light emission
percent inhibition during non-enzymatic (ascorbate-Fe(2+)) lipid
peroxidation of rat liver microsomes was for melatonin: 6.12, 16.20,
34.88 and for N-acetyl serotonin: 85.10, 88.48, 84.4 respectively. The
incubation of rat liver microsomes in the presence of NADPH (0.36,
0.75, 1.5 mM) produce a sudden increase of chemiluminescence that
gradually increased and reached a maximal value at about 15 min;
however, N-acetyl serotonin reduced these changes very efficiently.
PMID: 17681744
Taka
Polyunsaturated fatty acids, melatonin, and cancer prevention.
Sauer LA, Dauchy RT, Blask DE.
Bassett Research Institute, The Mary Imogene Bassett Hospital,
Cooperstown, NY 13326, USA.
Many nutritional, hormonal, and environmental factors affect
carcinogenesis and growth of established tumors in rodents. In some
cases, these factors may either enhance or attenuate the neoplastic
process. Recent experiments performed in our laboratory using tissue-
isolated rat hepatoma 7288CTC in vivo or during perfusion in situ have
demonstrated new interactions among four of these factors. Two agents,
dietary linoleic acid (C18:2n6) and "light at night," enhanced tumor
growth, and two others, melatonin and n3 fatty acids, attenuated
growth. Linoleic acid stimulated tumor growth because it is converted
by hepatoma 7288CTC to the mitogen, 13-hydroxyoctadecadienoic acid (13-
HODE). Melatonin, the neurohormone synthesized and secreted at night
by the pineal gland, and dietary n3 fatty acids are potent antitumor
agents. Both inhibited tumor linoleic acid uptake and 13-HODE
formation. Artificial light, specifically "light at night," increased
tumor growth because it suppressed melatonin synthesis and enhanced 13-
HODE formation. Melatonin and n3 fatty acids acted via similar or
identical G(i) protein-coupled signal transduction pathways, except
that melatonin receptors and putative n3 fatty acid receptors were
used. The results link the four factors in a common mechanism and
provide new insights into the roles of dietary n6 and n3
polyunsaturated fatty acid intake, "light at night," and melatonin in
cancer prevention in humans.
PMID: 11377374
--------------------
Note that the n3 fatty acids will halt and kill the cancerous cells
but will also shorten the lifespan (MLSP). Melatonin is far better
choice given the molecular mechanisms behind its protective
effects :-)
Taka
Taka
ScienceDaily (Apr. 24, 2007) — A study carried out by researchers from
the University of Granada’s Institute of Biotechnology shows that
consuming melatonin neutralizes oxidative damage and delays the
neurodegenerative process of aging. In this study researchers used
normal and genetically-modified mice which were subjected to
accelerated cell aging. Researchers believe their results can also be
applied to humans.
The Spanish aging Research Network (Red Nacional de Investigación del
Envejecimiento), funded by Carlos III Health Institute and headed by
professor Darío Acuña Castroviejo, from the University of Granada
(Universidad de Granada), is very near to achieving one of science's
greatest goals: allowing humans to age in the best possible health
conditions.
As well as from the UGR, researchers from the Spanish universities of
Seville, Oviedo, Saragossa, Barcelona and Reus also took part in this
study, concluding that the consumption of melatonin – a natural
substance produced in small amounts by human beings and present in
many types of food – delays the oxidative damage and inflammatory
processes typical of the old age. Melatonin can be found in small
amounts in some fruits and vegetables, like onions, cherries and
bananas, and in cereals like corn, oats and rice, as well as in some
aromatic plants, such as mint, lemon verbena, sage or thyme, and in
red wine.
UGR participation in this study was leaded by professor Darío Acuña
Castroviejo, member of the Institute of Biotechnology and lecturer at
this University’s department of Physiology. Professor Acuña
Castroviejo also coordinates the Spanish aging Research Network. Both
normal and genetically-modified mice, with an accelerated cell aging,
were analysed. "We proved", says professor Acuña Castroviejo, “that
the first signs of aging in animal tissues start at the age of five
months [in mice] – equivalent to 30 human years of age – due to an
increase in free radicals (oxygen and nitrogen), which cause an
inflammatory reaction.”
The UGR researcher points out that such oxidative stress also has
effects in animals’ blood, as blood cells have been proven to be “more
fragile with the years and, therefore, their cell membranes become
easier to break".
Use in mice
The authors administered small amounts of melatonin to mice and
observed that not only did this substance neutralize the oxidative
stress and the inflammatory process caused by aging, but it also
delayed its effects, thus increasing longevity. In particular, the
University of Granada’s goal was to analyse the mitochondrial function
in mice and check their mitochondrial capacity to produce ATP –
adenosine triphosphate – a molecule whose mission is to store the
energy every cell needs to carry out its functions.
Professor Acuña Castroviejo highlights that chronic administration of
melatonin in animals from the moment they stop producing this
substance – five months of age in mice – helps counteract all age-
related processes. Therefore, the researcher asserts, daily melatonin
intake in humans from the age of 30 or 40 could prevent – or, at
least, delay – illnesses related to aging, free radicals and
inflammatory processes, such as many neurodegenerative disorders (e.g.
Parkinson's disease) and complications linked to other illnesses, like
diabetes.
The researcher is confident that the Spanish Ministry of Health will
soon legalise the use of melatonin since, being a substance naturally
produced by the body, it cannot be patented and the drug industry
would not make much profit out of its artificial production. However,
“while the substance becomes legalised, humans should try to increase
melatonin consumption through food", recommends professor Acuña
Castroviejo.
The results of this study have been published in several medical
journals, including Free Radical Research, Experimental Gerontology,
Journal of Pineal Research and Frontiers in Bioscience.
SOURCE: http://www.sciencedaily.com/releases/2007/04/070424062819.htm
Taka
ScienceDaily (Apr. 7, 2009) — In China, the incidence of liver
cirrhosis is still high. Liver cirrhosis results from fibrosis. If
treated properly at fibrosis stage, cirrhosis can be prevented.
However, no effective antifibrosis drugs are available at present.
Several lines of evidences suggest that oxidative stress plays an
important role in the etiopathogenesis of hepatic fibrosis.
Melatonin can protect cells, tissues, and organs against oxidative
damage induced by a variety of free-radical-generating agents and
processes.
A research team led by Professor Jian-Ming Xu from the First
Affiliated Hospital of Anhui Medical University, China evaluated the
possible fibrosuppressant effect of melatonin in rat.
In this study, hepatic fibrosis in rats was successfully induced by
subcutaneous injection of sterile CCl4 twice weekly for a total of 12
wk. At the beginning of injection of CCl4, melatonin (2.5, 5, 10 mg/kg
body weight) was intraperitoneally administered to the rats daily for
12 wk. Hepatic fibrotic changes were evaluated biochemically by
measuring tissue hydroxyproline levels and histopathogical
examination. The serum activities of alanine aminotransferase (ALT),
aspartate aminotransferase (AST) were used to evaluate the hepatic
injury. Hepatic oxidative stress markers were evaluated by changes in
the amount of lipid peroxides, measured as malondialdehyde (MDA) and
glutathione peroxidase (GPx) in liver homogenates. Serum hyaluronic
acid (HA), laminin (LN), and procollagen 3 N-terminal peptide (P3NP)
were determined as serum markers of hepatic fibrogenesis.
Their results suggested that treatment with melatonin (10 mg/kg) could
decrease the scores of hepatic fibrosis grading, reduced the contents
of HA, LN in serum and Hydroxyproline (HYP) in liver, treatment with
melatonin (5,10 mg/kg ) could decrease serum levels of ALT, AST and
blocked the increase in MDA in rats with hepatic injury caused by
CCl4.
Their result indicated melatonin could ameliorate CCl4-induced hepatic
fibrosis in rats. The protective effect of melatonin on hepatic
fibrosis may be related to its antioxidant activities. This may
provide a basis for further studies on the potentially protective
effect of melatonin on liver function in cirrhotic patients
Journal reference:
1.Hong et al. Melatonin ameliorates experimental hepatic fibrosis
induced by carbon tetrachloride in rats. World Journal of
Gastroenterology, 2009; 15 (12): 1452 DOI: 10.3748/wjg.15.1452
SOURCE: http://www.sciencedaily.com/releases/2009/03/090330123210.htm
Taka
ScienceDaily (June 16, 2006) — Scientists in Italy say they have
discovered that the grapes used to make some of the most popular red
wines contain high levels of the sleep hormone melatonin. (Journal of
the Science of Food and Agriculture DOI 10.1002/jsfa2537). Melatonin
is naturally secreted by the pineal gland in the brain, especially at
night. It tells the body when it is time to sleep.
The discovery of melatonin in grape skin could explain why so many of
us hit the bottle in the evening to wind down after a day's hard slog.
'The melatonin content in wine could help regulate the circadian
rhythm [sleep-wake patterns], just like the melatonin produced by the
pineal gland in mammals,' says researcher Iriti Marcello at the
University of Milan.
Until recently, melatonin was thought to be exclusively produced by
mammals but has recently been discovered in plants. It is thought to
have antioxidant properties. Iriti's study discovered high levels of
melatonin in Nebbolo, Merlot, Cabernet Savignon, Sangiovesse and
Croatina grape varieties.
Iriti's team have also shown that melatonin content can be enhanced in
grapes by treating vines with a plant vaccine Benzothiadiazole.
Richard Wurtman of the brain and cognitive science department at MIT
is unconvinced, however, and believes further research is needed to
determine whether the compounds discovered are melatonin, or something
very similar.
SOURCE: http://www.sciencedaily.com/releases/2006/06/060616135307.htm
montygraham
support their notions, don't realize (or refuse to acknowledge, for
one reason or another) that all roads lead to the same underlying
cause, when you examine the totality of the evidence. Often, a report
appears, it says this or that mineral or vitamin is so important, but
then when you look at the evidence, you find the same reason for there
to be deficiency in the first place.
Taka
Melatonin can slow down the effects of aging. Scientists have found
that a treatment based on melatonin can delay the first signs of aging
in a small mammal.
ScienceDaily (June 22, 2009) — Melatonin can slow down the effects of
aging. A team at laboratoire Arago in Banyuls sur Mer (CNRS /
Université Pierre et Marie Curie) has found that a treatment based on
melatonin can delay the first signs of aging in a small mammal.
Better known as the ‘time-keeping' hormone, melatonin is naturally
secreted by the body during the night. It is therefore a kind of
biological signal for nightfall, allowing an organism to synchronize
itself with the day/night rhythm.
At Laboratoire Arago, Elodie Magnanou and her co-workers studied the
long-term effects of melatonin on the Greater White-toothed shrew, a
small nocturnal insectivorous mammal. Under normal conditions, this
animal shows the first signs of aging after reaching 12 months, mainly
through the loss of circadian rhythm in its activities. By
continuously administering melatonin, starting a little before 12
months, the appearance of these first signs was delayed by at least 3
months, which is a considerable period in relation to the lifespan of
this shrew*.
Melatonin is now known to play several beneficial roles. These include
being an antioxidant, an anti-depressant, and helping to remediate
sleep problems. The next step will be to understand the mode of action
of the hormone on aging, so we can perhaps envisage its use on humans.
These results appeared in the journal PLoS One on 15 June 2009.
*The Greater White-toothed shrew has a lifespan of 12 to 18 months in
the wild and up to 30 months in captivity. Captivity does not change
the time at which signs of aging appear, it simply lengthens life.
SOURCE: http://www.sciencedaily.com/releases/2009/06/090622064807.htm
Taka
have already heard something from "MikeV" and here follows what I came
across on the net:
"I'm a 62 year old male and have been using malatonin for 20 years
now.
I still have all my hair.
My hair is it's natural color.
My sex drive is what it was when I was twenty, and I need no pill to
help me stand at attention.
I am white, northern European, but my skin has not gone thin on me
like so many other 62 year olds.
I have few wrinkles, just a few below my eyes that I had back when I
was forty, too. When I am out in the sun, my skin turns a golden
brown, and people tell me I look many years younger than my age.
MY wife who is three years younger than me looks like she is 70, with
white hair, and wrinkles and faded skin. all these years she has not
used melatonin.
Believe me, there is a Big difference."
"I concur. I'm a fifty eight year old female. I appear to be in my
late thirties to early forties. I've taken melatonin for about ten
years, but have taken many more vitamins and supplements for 30 years.
I'm currently taking high grade tryptophan as well as melatonin. I
don't have wrinkles, my skin is very supple and I just look really
young for my "age"."
"I've been takig melatonin for nearly 15 years now. I mentioned to a
coworker a few months ago that I was 50 years old. She didn't believe
me and I showed her my ID. You should've seen the stunned look on her
face while she was searching my face for even one wrinkle. Couldn't
find one.
And the "Fountain of Youth" upside of taking melatonin is but just one
boon. What it does for one's third eye functioning is another. It's
also an antioxidant."
-------------------------
Please any negative experience or downside of taking melatonin too!
Taka
trigonometry1972@gmail.com |
I'll suggest a dose of 6 milligrams or more is worth looking at.
Taking a number of betaine HCl with pepsin capsules at
larger meals and also taking 6 milligrams of melatonin keeps
all my GERD symptoms away. Or at least there is one study
that indicates melatonin at a 6 milligram dose helps in GERD
and a 3 milligrams dose doesn't.
The PA told me I'd have to take PPI meds for the rest of my
life not so it seems as I've been good for 5 years now.
"His" prescription just made me sicker in new ways over time and it
drained
the wallet as well.
To regulate my sleep to a normal pattern it takes at least 9
milligrams
taken an hour or so prior to bedtime.
I've been taking 6 milligrams for the last 5 years and recently I've
increased the dose. I've taking some dose (lower) of melatonin for
over 10 years and off and on for even longer. A third of a milligram
only worked for a night or two as I recall.
The best alarm clock is a full light of the morning sun..........Trig
rs1...@yahoo.com
sleep. However, larger doses, even below 1 mg will quite noticeably
have a negative effect on my mood and cognition the next day,
especially if I take it for a number of consecutive days. For that
reason, I don't take it as an antioxidant. The shrew study focused
attention on circadian rhythm and aging. Only minute doses of this
are needed to aid circadian rhythm responses.
Taka
The Pineal Gland is the Least Known of All the Endocrine Glands
The pineal gland, no larger than a grain of wheat, is the most
mysterious endocrine gland of all. In 1628 the famous French
philosopher Descartes called the pineal gland, "The seat of the soul."
Because of its inaccessible location, deep within the center of the
skull and attached by a stalk to the posterior wall of the third
ventricle of the brain, the pineal gland hasn't been studied as
exhaustively as the other glands.
The gland will sometimes shrink and then fill up with specific types
of mineral salts that are referred to as "brain sand." The condition
has been traced directly to poor nutrition. When this condition exists
in the pineal gland, thinking and sexual processes are affected. The
pineal gland will respond quickly to proper nutrition even after being
"starved" and degeneration has begun. The pineal contains more
lecithin than any other body part.
The pineal isn't an actual gland; it's a neuroendocrine transducer:
meaning it converts incoming nerve impulses into outgoing hormones.
Most glands are triggered by changes in the body or hormones secreted
by other glands. The pineal gland releases hormones in response to
bioelectrical messages from the outside environment received through
the eyes. The optic nerve sends information to the visual portion of
the brain through nerve fibers. The impulses from the brain are
carried to the superior cervical ganglia (a cluster of nerve cells) in
the upper part of the neck by smaller nerve fibers. From there the
autonomic nervous system relays the information to the pineal.
In low light, or darkness, the pineal gland secretes the hormone
melatonin. Melatonin has been connected to many body functions. If one
references back to medical information written before the early 90's
they may find no information on melatonin, even in medical
dictionaries. Excesses of melatonin have been connected with
alcoholism. Aging accelerates calcification of the pineal and
calcification is connected with higher cancer rates. People who eat
less sugar, less highly processed foods and spend more time outdoors,
exhibit a lower incidence of calcification.
Melatonin production increases after dark. In the morning when
sunlight hits the retina, production of the hormone slows. Light meals
in the evening help improve sleep and maximize melatonin's anti-aging
effects. Keeping a regular schedule and eating at set times increases
hormone production. If we exercise or participate in any strenuous
activity at night, we delay melatonin output. Stimulants and caffeine
at any time of the day, but especially at night, slow or stop
melatonin production.
Human growth hormone (HGH), dehydroepiandrosterone (DHEA) and
melatonin are all free radical scavenging, antioxidant and anti-aging
hormones. Melatonin may be the most efficient of the free radical
scavengers, especially for anti-aging, since it has the ability to
permeate any cell in any part of the body. Within the cells, melatonin
provides protection for the nucleus, the central structure containing
the DNA. Protection of the central structure allows a damaged cell to
repair itself. If a cell can't repair itself, it can mutate and turn
into a cancer cell. The enzyme glutathione is stimulated by melatonin.
Glutathione is a tripeptide containing the amino acids glutamic acid,
cysteine and glycine. Glutothione functions in several oxidation-
reducing capacities, meaning it's an antioxidant. Research during the
30's and 40's showed it to be necessary for delivery of calcium to the
brain cells. Research studies on 44 mentally retarded children using
supplemental glutamic acid, raised their test scores from an average
of 69 to 87 (almost normal). One of the test subjects, a 17-year-old
boy, scored 107 (average/normal) on his first test and after 6 months
of treatment with glutamic acid scored 120 (superior intelligence,
just below genius).
Organs and other body parts take their share of glutamic acid before
the brain receives any. A nutritionally deficient diet has low or
nonexistent amounts of this necessary amino acid. When added to the
diets of hyperactive children, and others with behavior problems,
glutamic acid was able to obtain the same calming effects as the
chemicals so often prescribed and without side effects.
Glutothione has shown to be highly beneficial in removing lead from
the body. Lack of glutothione contributes to chronic fatigue.
Glutamic acid can be found in almost all protein rich foods, natural
cheddar cheese, (not cheese substitutes or highly refined and
processed cheeses), eggs, lean meats, peanuts, whole grains, soybeans,
legumes, peas and beans.
Balance out your mental powers, get some sleep and slow the aging
processes by "naturally" caring for your pineal gland.
SOURCE: http://hubpages.com/hub/Human_Growth_Hormone__Melatonin_And_The_Pineal_Gland
RFR
John Hasenkam
increase the risk for ocular pathology. Raises interesting questions about
the suppression of melatonin by blue light.
--
http://healthycuriousity.blogspot.com/
<rs1...@yahoo.com> wrote in message
news:015c18d9-4ba2-4cb9...@z34g2000vbl.googlegroups.com...
trigonometry1972@gmail.com |
> Be careful with melatonin supplements. There is some suggestion these can
> increase the risk for ocular pathology. Raises interesting questions about
> the suppression of melatonin by blue light.
>
>
> news:015c18d9-4ba2-4cb9...@z34g2000vbl.googlegroups.com...
>
> > It doesn't take more than 125 - 150 mcg of melatonin to help me
> > sleep. However, larger doses, even below 1 mg will quite noticeably
> > have a negative effect on my mood and cognition the next day,
> > especially if I take it for a number of consecutive days. For that
> > reason, I don't take it as an antioxidant. The shrew study focused
> > attention on circadian rhythm and aging. Only minute doses of this
> > are needed to aid circadian rhythm responses.
One needs to be careful not to get overly concerned by voices
possessed with hand wringing concerns. And the blog site referred to
above
is a classic example of such hand wringing.
As to bright morning light, speaking from personal experience it
clearly tends to suppress tendency sleep. Shift workers often
black there windows out in order to get there sleep. And some
people used bright morning light exposure to help reset extended
wake sleep cycles such that its syndrome victims tend to have
longer days than normal going 24 1/2, 25, 26 hours in a "day."
And I'll note some also use melatonin in this context to get
to sleep earlier. And I'll add one needs to take the doses
sometime before (perhaps an hours or so) bedtime in order to increase
the opportunity chances of timely sleep.
there is always a suggestion of something/
anything..................Trig
John Hasenkam
--
http://healthycuriousity.blogspot.com/
<trigonom...@gmail.com> wrote in message
news:2e123c6c-2fea-4c77...@f10g2000vbf.googlegroups.com...
John Hasenkam
photoreceptor susceptibility to light-induced damage.
--It is believed that disturbances in melatonin metabolism can be one of
causes leading to development of retinal dystrophy.
?
--The retinas of animals exposed during the middle of the dark period or
during the first 5 hr of the light period were significantly more damaged
than the retinas of animals exposed during the last 9 hr of the light
period.
?
--There is a question whether or not regular doses of melatonin may damage
the eye over time. Melatonin could affect the timing of hormone peaks in the
eye. High retinal melatonin levels combined with exposure to bright light
might cause retinal damage. This is speculation (a caution) at this time.
?
--Gastrointestinal: Mild gastrointestinal distress commonly occurs,
including nausea, vomiting, or cramping. Melatonin has been linked to a case
of autoimmune hepatitis and with triggering of Crohn's disease symptoms.
?
--Gynecomastia (increased breast size) has been reported in men, as well as
decreased sperm count (both which resolved with cessation of melatonin).
Decreased sperm motility has been reported in rats and humans.
?
--
"Melatonin treatment increases the susceptibility of retinal photoreceptors
to light-induced cell death... Chronic exposure to natural or artificial
light and simultaneous intake of melatonin may potentially contribute to a
significant loss of photoreceptor cells in the aging retina. ...The
illuminances and exposure times were chosen to mimic the conditions of the
human eye in the presence of high and low dosages of melatonin and exposed
to intermittent bright sunlight. The low concentrations of melatonin were
used to mimic normal dosages for taken as a sleep aid.
In light of the evidence presented in this study, we suggest that it would
be prudent for individuals to avoid chronic self-administration of melatonin
in the presence of high levels of environmental illumination." Influence of
dietary melatonin on photoreceptor survival in the rat retina: An ocular
toxicity study. Exp Eye Res. 2008 Feb;86(2):241-50 Wiechmann AF, Chignell
CF, Roberts JE.
--Taking a typical dose (1 to 3 mg) may elevate your blood melatonin levels
to 1 to 20 times normal. Side effects do not have to be listed on the
product's packaging. Yet, fatigue and depression have occasionally been
reported with use of melatonin.
----
And, there is a general warning that those with autoimmune diseases should
not take Mt, and those with retinal degeneration should not take Mt. Thus
some suspect it may play a role in R. arthritis.
Mt also inhibits axoplasmic transport processes, a cardinal feature of
neurodegeneration in PD and ALZ is disruption of transport processes.
And there are a few articles arguing for a linkage between Mt. and PD.
---
I don't have a real problem with Mt supplements but I do advise "wash out""
periods because any hormone that can be elevated beyond normal physiological
levels is going to be problematic.
"Taka" <taka...@gmail.com> wrote in message
news:48a4deca-92e3-4cdb...@r33g2000yqn.googlegroups.com...
Taka
> Invest Ophthalmol Vis Sci 1992 May;33(6):1894-902.Melatoninincreases
> photoreceptor susceptibility to light-induced damage.
Ah, those DHA rich retinas ... UV-A induced lipid peroxidation ...
Looks like the timing is everything. Melatonin probably triggers
tissue maintenance mode during which cells are more vulnerable due to
ongoing DNA replication. It also stimulates the immune system
(prolactin release?) so the "autoimmunity". And of course we want to
reproduce during the full moon nights or during the summer when the
days are long. Bright sunlight in the morning stimulates testosterone
release. It all fits nicely together. Anyhow I think melatonin
should be safe when administered on empty stomach just before the bed
while sleeping in the dark.
Taka
> --It is believed that disturbances inmelatoninmetabolism can be one of
> causes leading to development of retinal dystrophy.
>
> ?
>
> --The retinas of animals exposed during the middle of the dark period or
> during the first 5 hr of the light period were significantly more damaged
> than the retinas of animals exposed during the last 9 hr of the light
> period.
>
> ?
>
> --There is a question whether or not regular doses ofmelatoninmay damage
> the eye over time.Melatonincould affect the timing of hormone peaks in the
> eye. High retinalmelatoninlevels combined with exposure to bright light
> might cause retinal damage. This is speculation (a caution) at this time.
>
> ?
>
> --Gastrointestinal: Mild gastrointestinal distress commonly occurs,
> including nausea, vomiting, or cramping.Melatoninhas been linked to a case
> of autoimmune hepatitis and with triggering of Crohn's disease symptoms.
>
> ?
>
> --Gynecomastia (increased breast size) has been reported in men, as well as
> decreased sperm count (both which resolved with cessation ofmelatonin).
> Decreased sperm motility has been reported in rats and humans.
>
> ?
>
> --
>
> "Melatonintreatment increases the susceptibility of retinal photoreceptors
> to light-induced cell death... Chronic exposure to natural or artificial
> light and simultaneous intake ofmelatoninmay potentially contribute to a
> significant loss of photoreceptor cells in the aging retina. ...The
> illuminances and exposure times were chosen to mimic the conditions of the
> human eye in the presence of high and low dosages ofmelatoninand exposed
> to intermittent bright sunlight. The low concentrations ofmelatoninwere
> used to mimic normal dosages for taken as a sleep aid.
>
> In light of the evidence presented in this study, we suggest that it would
> be prudent for individuals to avoid chronic self-administration ofmelatonin
> in the presence of high levels of environmental illumination." Influence of
> dietarymelatoninon photoreceptor survival in the rat retina: An ocular
> toxicity study. Exp Eye Res. 2008 Feb;86(2):241-50 Wiechmann AF, Chignell
> CF, Roberts JE.
>
> --Taking a typical dose (1 to 3 mg) may elevate your bloodmelatoninlevels
> to 1 to 20 times normal. Side effects do not have to be listed on the
> product's packaging. Yet, fatigue and depression have occasionally been
> reported with use ofmelatonin.
>
> ----
>
> And, there is a general warning that those with autoimmune diseases should
> not take Mt, and those with retinal degeneration should not take Mt. Thus
> some suspect it may play a role in R. arthritis.
> Mt also inhibits axoplasmic transport processes, a cardinal feature of
> neurodegeneration in PD and ALZ is disruption of transport processes.
> And there are a few articles arguing for a linkage between Mt. and PD.
>
> ---
>
> I don't have a real problem with Mt supplements but I do advise "wash out""
> periods because any hormone that can be elevated beyond normal physiological
> levels is going to be problematic.
>
> "Taka" <taka0...@gmail.com> wrote in message
>
> news:48a4deca-92e3-4cdb...@r33g2000yqn.googlegroups.com...
>
> > Any anecdotalexperiencewithmelatoninsupplementation anyone? We
> > have already heard something from "MikeV" and here follows what I came
> > across on the net:
>
> > "I'm a 62 year old male and have been using malatonin for 20 years
> > now.
> > I still have all my hair.
> > My hair is it's natural color.
> > My sex drive is what it was when I was twenty, and I need no pill to
> > help me stand at attention.
> > I am white, northern European, but my skin has not gone thin on me
> > like so many other 62 year olds.
> > I have few wrinkles, just a few below my eyes that I had back when I
> > was forty, too. When I am out in the sun, my skin turns a golden
> > brown, and people tell me I look many years younger than my age.
>
> > MY wife who is three years younger than me looks like she is 70, with
> > white hair, and wrinkles and faded skin. all these years she has not
> > usedmelatonin.
>
> > Believe me, there is a Big difference."
>
> > "I concur. I'm a fifty eight year old female. I appear to be in my
> > late thirties to early forties. I've takenmelatoninfor about ten
> > years, but have taken many more vitamins and supplements for 30 years.
> > I'm currently taking high grade tryptophan as well asmelatonin. I
> > don't have wrinkles, my skin is very supple and I just look really
> > young for my "age"."
>
> > "I've been takigmelatoninfor nearly 15 years now. I mentioned to a
> > coworker a few months ago that I was 50 years old. She didn't believe
> > me and I showed her my ID. You should've seen the stunned look on her
> > face while she was searching my face for even one wrinkle. Couldn't
> > find one.
>
> > And the "Fountain of Youth" upside of takingmelatoninis but just one
John Hasenkam
retina. Too much ... Don't think in such absolutist terms, biological
processes will crucify that logic time and again.
--
http://healthycuriousity.blogspot.com/
"Taka" <taka...@gmail.com> wrote in message
news:08f313fe-3a6d-46cf...@d10g2000vbm.googlegroups.com...
Taka
> But Taka it is a balancing act. Too little DHA will quickly destroy the
> retina. Too much ... Don't think in such absolutist terms, biological
> processes will crucify that logic time and again.
You can either play the balancing act with Omega-6 and Omega-3 at the
expense of increased lipid peroxidation or let the body use the less
oxidizable Omega-9 substitute. It's still questionable whether the
n-9 fatty acids can 100% substitute for the Omega-6+3s functions but
the "side effects" reported so far are not fatal and mostly related to
reproduction and growth suppression the benefits of which for life
extension are being discussed here day and night (e.g. TOR
signaling). Humans have never been consuming the Omega-6es in such
concentrated forms as in this century so their retinas are overloaded
with them and need increased maintenance by the Omega-3 driven
apoptosis ... I think the 22:4n9 derivative of Mead acid would be a
safer substitute for the 22:6n3 DHA but this is like saying that the
Earth is not flat several hundred years ago.
"N-9 FATTY ACIDS
Among that series, the best known compound is the trienoic 20:3(n-9)
with the double bonds in positions 5,8 and 11. It was discovered first
by Klenk E. (Z Physiol Chem 1952, 291, 104 and 1955, 299, 74) in brain
phospholipids. It was later shown to be present in relatively high
amounts in all tissues of animals subjected to long-term deprivation
of nutritionally essential (n-6) fatty acids (Holman RT, J Nutr 1960,
70, 405). This author had proposed the ratio of 20:3(n-9) to 20:4(n-6)
as a measure of essential fatty acid requirement. Recently, it was
reported the presence of unusually high levels of this fatty acid in
the cartilage of several animal species (birds, mammals, human). Its
concentration in phospholipids was about 5% in the growth plate
cartilage and 16% in the hyaline cartilage in chicken (Adkisson HD et
al., FASEB J 1991, 5, 344). As 20:3(n-9) is markedly concentrated in
human fetal cartilage, it has been hypothesized that it can decrease
osteoblastic activity and thus may be important for the prevention of
calcification in the cartilage (Hamazaki T et al., Lipids 2009, 44,
97).
An unusual geometrical isomer of 22:4 n-9 with a trans double bond
(cis-4,7,10,trans-13-docosatetraenoic acid) has been identified in the
scallop Pecten maximus and may be of endogenous origin and specific to
the pectinid family (Marty Y et al., J Chromatogr A 1999, 839, 119). "
SOURCE: http://www.cyberlipid.org/fa/acid0003.htm
Taka
John Hasenkam
forms as in this century so their retinas are overloaded
with them and need increased maintenance by the Omega-3 driven
apoptosis
...
Now show me how omega 9 can create NPD1 and I will listen. Not a
speculation, but empirical evidence. Go and go away.
--
http://healthycuriousity.blogspot.com/
"Taka" <taka...@gmail.com> wrote in message
news:2d5affdd-2df4-4f33...@g1g2000pra.googlegroups.com...
Taka
> Now show me how omega 9 can create NPD1 and I will listen. Not a
> speculation, but empirical evidence. Go and go away.
NPD1 protects cells from the arachidonic metabolites such as those
created by the action of COX-2. For what on the Earth would you need
it in the absence of arachidonic acid? There is no COX-2 if Omega-9
substitutes for Omega-6 ...
Photoreceptor survival depends on the integrity of retinal pigment
epithelial (RPE) cells. The pathophysiology of several retinal
degenerations involves oxidative stress-mediated injury and RPE cell
death; in some instances it has been shown that this event is mediated
by A2E and its epoxides. Photoreceptor outer segments display the
highest DHA content of any cell type. RPE cells are active in DHA
uptake, conservation, and delivery. Delivery of DHA to photoreceptor
inner segments is mediated by the interphotoreceptor matrix. DHA is
necessary for photoreceptor function and at the same time is a target
of oxidative stress-mediated lipid peroxidation. It has not been clear
whether specific mediators generated from DHA contribute to its
biological properties. Using ARPE-19 cells, we demonstrated the
synthesis of 10,17S-docosatriene [neuroprotectin D1 (NPD1)]. This
synthesis was enhanced by the calcium ionophore A-23187, by IL-1β, or
by supplying DHA. Added NPD1 (50nM) potently counteracted H2O2/tumor
necrosis factor-α oxidative stress-triggered apoptotic DNA damage in
RPE. NPD1 also up-regulated the anti-apoptotic proteins Bcl-2 and Bcl-
xL and decreased pro-apoptotic Bax and Bad expression. Moreover, NPD1
(50nM) inhibited oxidative stress-induced caspase-3 activation. NPD1
also inhibited IL-1β-stimulated expression of COX-2. Furthermore, A2E-
triggered oxidative stress induction of RPE cell apoptosis was also
attenuated by NPD1. Overall, NPD1 protected RPE cells from oxidative
stress-induced apoptosis. In conclusion, we have demonstrated an
additional function of the RPE: its capacity to synthesize NPD1. This
new survival signaling is potentially of interest in the understanding
of the pathophysiology of retinal degenerations and in exploration of
new therapeutic modalities.
SOURCE: http://www.springerlink.com/content/w5080g0l80784758/
"The biosynthesis of oxygenated arachidonic acid messengers triggered
by cerebral ischemia-reperfusion is preceded by an early and rapid
phospholipase A2 activation reflected in free arachidonic and
docosahexaenoic acid (DHA) accumulation. These fatty acids are
released from membrane phospholipids. Both fatty acids are derived
from dietary essential fatty acids; however, only DHA, the omega-3
polyunsaturated fatty acyl chain, is concentrated in phospholipids of
various cells of brain and retina. Synaptic membranes and
photoreceptors share the highest content of DHA of all cell
membranes."
SOURCE: http://www.fabresearch.org/view_item.aspx?item_id=838&list_id=list1-1348&list_index=2
John Hasenkam
--
http://healthycuriousity.blogspot.com/
"Taka" <taka...@gmail.com> wrote in message
news:a618ea80-107a-4896...@k8g2000yqn.googlegroups.com...
On Jul 3, 3:30 pm, "John Hasenkam" <jo...@goawayplease.com> wrote:
> Now show me how omega 9 can create NPD1 and I will listen. Not a
> speculation, but empirical evidence. Go and go away.
NPD1 protects cells from the arachidonic metabolites such as those
created by the action of COX-2. For what on the Earth would you need
it in the absence of arachidonic acid? There is no COX-2 if Omega-9
substitutes for Omega-6 ...
Taka,
This is an opinion and you deliberately avoided the question: show me how an
omega 9 can produce NPD1. That was the challenge and you still have not met
it. As to NPD1 being *solely* about protection from cox 2 issues, another
huge assumption. Cox 2 is necessary for NMDA transmission, it is involved in
a great many reactions. Eliminating cox 2 function is silly. Now go again.
John.
Photoreceptor survival depends on the integrity of retinal pigment
epithelial (RPE) cells. The pathophysiology of several retinal
degenerations involves oxidative stress-mediated injury and RPE cell
death; in some instances it has been shown that this event is mediated
by A2E and its epoxides. Photoreceptor outer segments display the
highest DHA content of any cell type. RPE cells are active in DHA
uptake, conservation, and delivery. Delivery of DHA to photoreceptor
inner segments is mediated by the interphotoreceptor matrix. DHA is
necessary for photoreceptor function and at the same time is a target
of oxidative stress-mediated lipid peroxidation. It has not been clear
whether specific mediators generated from DHA contribute to its
biological properties. Using ARPE-19 cells, we demonstrated the
synthesis of 10,17S-docosatriene [neuroprotectin D1 (NPD1)]. This
synthesis was enhanced by the calcium ionophore A-23187, by IL-1�, or
by supplying DHA. Added NPD1 (50nM) potently counteracted H2O2/tumor
necrosis factor-� oxidative stress-triggered apoptotic DNA damage in
RPE. NPD1 also up-regulated the anti-apoptotic proteins Bcl-2 and Bcl-
xL and decreased pro-apoptotic Bax and Bad expression. Moreover, NPD1
(50nM) inhibited oxidative stress-induced caspase-3 activation. NPD1
also inhibited IL-1�-stimulated expression of COX-2. Furthermore, A2E-
Agible
undergo a change to exclusive Omega-9 in their diet? --the n-6 and
n-3s are ubiquitous throughout all sources of n-9.
Taka
> --http://healthycuriousity.blogspot.com/"Taka" <taka0...@gmail.com> wrote in message
>
> news:a618ea80-107a-4896...@k8g2000yqn.googlegroups.com...
> On Jul 3, 3:30 pm, "John Hasenkam" <jo...@goawayplease.com> wrote:
>
> > Now show me how omega 9 can create NPD1 and I will listen. Not a
> > speculation, but empirical evidence. Go and go away.
>
> NPD1 protects cells from the arachidonic metabolites such as those
> created by the action of COX-2. For what on the Earth would you need
> it in the absence of arachidonic acid? There is no COX-2 if Omega-9
> substitutes for Omega-6 ...
>
> Taka,
>
> This is an opinion and you deliberately avoided the question: show me how an
> omega 9 can produce NPD1.
If you did not get it - Omega-9 cannot be converted into NPD1 of
course like it cannot be converted into prostaglandins (yet COX will
metabolize it into different biologically active molecules!). I
think it could be converted into structurally different metabolites
which you can call e.g. NPD3 if you need a name for it (by the NPD1-
making machinery like LOX-15 etc.).
> That was the challenge and you still have not met
> it. As to NPD1 being *solely* about protection from cox 2 issues, another
> huge assumption. Cox 2 is necessary for NMDA transmission, it is involved in
> a great many reactions. Eliminating cox 2 function is silly. Now go again.
Will you become blind without Omega-6/arachidonic acid (AA)? Think
quantitatively, not qualitatively. If your retina is overloaded with
AA NPD1 may be useful, but with less AA and more Mead acid you don't
need suppressing the natural damaged cell cleaning mechanisms.
Now back to the blue light topic. Given that blue light is causing
damage to the retina in the presence of melatonin, does it mean that
melatonin may inhibit the synthesis of your neuroprotectin NPD1 ??
Taka