Regarding my comment that less CO2 per O2 inhaled could also be translated
as more O2 utilisation per CO2.
Aubrey commented that cyt-c-oxidase turnover is very closely linked to TCA
activity, and therefore it's unlikely that one could accelerate COX without
also accelerating TCA.
This raises another possibility....
If we assume that TCA runs a full pelt, and that the turnover of oxidase
(i.e. the amount of oxygen consumed) is always less than 100% efficient,
due to leakage of electrons sideways, or due to proton pump slip, or just
that NADH gets used for things other than electron transport. Then a
greater rate of O2 utilisation per CO2 could arise from a decrease in these
"alternative pathways of TCA product utilisation".
Although this would make ox-phos more efficient, and wouldn't account for
the weight loss properties of CLA's, a cut in mito' superoxide production
might have an anti-ageing effect?
WRT athersclerosis, I would have expected the opposite result, i.e. CLA's
would intervene and activate signalling pathways involving beneficial low
levels of oxidised LDL, to inhibit fatty streak formation. There's
certainly a lot of evidence that excercise works in this way, by
stimulating endothelial antioxidant production (such as glutathione).
Paul
_________________________________________
Dr. Paul S. Brookes. (brookes at uab.edu)
UAB Department of Pathology, G004 Volker Hall
1670 University Blvd., Birmingham AL 35294 USA
Tel (001) 205 934 1915 Fax (001) 205 934 1775
http://peir.path.uab.edu/brookes
The quality of e-mails can go down as well as up
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