Periplasmic SOD vs pathogenicity

[Kevin Bown]

Does anyone have any experience with periplasmic SODs in pathogens
(human or animal) Arguably the product of dismutation (H2O2) is more
damaging than the superoxide anion, is there a catalase in the
periplasm? As these SODs are not extracellular, the superoxide anion
must have to cross the outer membrane, what limits chain
initiation/propagation in lipid peroxidation? (ie are there massive
amounts of glutathione peroxidase, tocopherols, quinones etc, either
in the membrane or periplasm). What levels of iron or iron
chelators/sequestrants are in the periplasm, if Fenton chemistries
are involved then again, the products would be more damaging than the
progenitor species. There is obviously a correlation between
periplasmic SOD and pathogenicity (eg in Salmonella, Legionella,
Neisseria &c), but SOD alone cannot protect against the battery of
carbon and/or oxygen centred free-radicals, and non-radical species
elicited by host responses ('respiratory burst') Any comments
welcome!

Regards

Kevin Bown

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Kevin Bown,
Centre for Applied Microbiology & Research,
Porton,
Wilts, SP4 OJG. UK.
Tel: +44(0)1980 612666
Fax: +44(0)1980 612731
e-mail: kevin...@camr.org.uk
pager: 01426 157893
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