I'm sure there was supposed to be a link, probably a google reader link
by the look of the App in use.
Yet another reason to sigh at Mobile-App mediated communication, if you
ask me.
--
http://www.physorg.com/news/2011-12-oxidative-stress.html
Gmail is being wonky recently.
http://www.cell.com/cell-metabolism/abstract/S1550-4131%2811%2900419-0
Highlights
- Genetically encoded redox probes visualize redox differences and
changes in vivo
- A chemical trapping strategy enables robust redox imaging in
dissected animals
- Physiological redox changes are redox couple, compartment, and
tissue specific
- Increased life span coincided with increased rather than decreased
tissue oxidation
Summary
The glutathione redox couple (GSH/GSSG) and hydrogen peroxide (H2O2)
are central to redox homeostasis and redox signaling, yet their
distribution within an organism is difficult to measure. Using
genetically encoded redox probes in Drosophila, we establish
quantitative in vivo mapping of the glutathione redox potential (EGSH)
and H2O2 in defined subcellular compartments (cytosol and
mitochondria) across the whole animal during development and aging. A
chemical strategy to trap the in vivo redox state of the transgenic
biosensor during specimen dissection and fixation expands the scope of
fluorescence redox imaging to include the deep tissues of the adult
fly. We find that development and aging are associated with redox
changes that are distinctly redox couple-, subcellular compartment-,
and tissue-specific. Midgut enterocytes are identified as prominent
sites of age-dependent cytosolic H2O2 accumulation. A longer life span
correlated with increased formation of oxidants in the gut, rather
than a decrease.
On Dec 6, 8:02 am, Jeswin <phillyj...@gmail.com> wrote:
> and tissue-specific. Midgut enterocytes are identified as prominent
> sites of age-dependent cytosolic H2O2 accumulation. A longer life span
> correlated with increased formation of oxidants in the gut, rather
> than a decrease.
Thanks for the redox redux. I don't think anyone had any
strong expectations about correlation between lifespan and
oxidants in the gut. ROS production within mitochondria
is the contentious issue. For decades, it was believed
by an increasing number of people that increased ROS in
mitochondria decreases lifespan. IIRC some recent studies refute
this.
Also, elimination of ROS in all mitochondria is fatal,
though this hasn't been published AFAIK.
Signalling via ROS may be essential to mitochondrial functioning.
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And yes, the difference is profound: with oxygen, each Glucose
molecule provides (IIRC) 32 units of ATP, whereas without oxygen you
only get.. 2? 4?