The protecting effect of L-carnitine in septic damage in rat mitochondria

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The purpose of this study was to evaluate the possible involvement of oxidative stress derived from xanthine-xanthine oxidase and LPS system in rat liver mitochondria and the possible protective effect of carnitine. Mitochondria exposed to free radicals exhibited a significant degree in O^2 consumption supported by NAD^1 linked substrates, but showed almost no change in O^2 consumption in the presence of succinate and ascorbate. The presence of carnitine in oxidative stress caused the recovery of mitochondrial respiration to retern the degree of control values. Oxidative stress caused the loss of intramitochondrial nicotinamide nucleotides, and addition of NAD^1 fully prevented any fail in O^2 consumption with NAD^1 linked substrates. the activity of electron-transfer complex 1 and the energy dependent reduction of NAD^1 by succinate were unaltered by oxidative stress. The degree of mitochondrial swelling was closely correlated with the inhibition of State-3 oxidation and with the increase in the State-4 oxidation of succinate. The carnitine prevented the mitochondrial damage (swelling, Ca^2 release, sucrose trapping uncoupling) induced by oxygen free radicals. These findings suggest that the deleterious effect of free radicals on mitochondria in the present experimental system was triggered by Ca^2 dependent membrane transition and carnitine to protect in isolated mitochondria is a consequence of the ability to prevent the mitochondrial permeability transition.