If CLA increases lipid peroxidation (and presumably you mean at the
mitochonrial level) then this may increase the mitochondrial proton
leak. This in turn would dissipate redox gradient and decrease mt FR
production, whilst at the same time increasing metabolic rate - proton leak
accounts for about 25% of SMR in an animal such as the rat.
Of course, less CO2 per O2 inhaled could also be interpreted as more O2
utilisation per CO2, i.e. a greater turnover of cytochrome oxidase for a
given rate of TCA cycle - something proton leak would be very good at
implementing.
I suppose the only way to tell if this stuff really increases oxidative
load would be to run tests for common ROS/RNS adducts (protein carbonyls,
plasma nitrite/nitrate, nitrotyrosine, MDA) in patients taking the stuff.
On another tack, any idea what CLA does to atherosclerosis, invoking the
excercise paradox/mild LDL oxidation hypothesis?
PSB
_________________________________________
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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