Carnitine protects mitochondria and removes toxic acyls from xenobiotics.

The carnitine system is altered by several xenobiotics (drugs and chemicals). These alterations are responsible for most toxic effects, which can be reverted or minimized by L-carnitine administration. Formation of nonmetabolizable acyl coenzyme A (CoA) is a typical step in the biotransformation of pivaloyl antibiotics, valproate and ifosfamide.

Regulation by carnitine of myocardial fatty acid and carbohydrate metabolism under normal and pathological conditions.

This review focuses on the regulation of myocardial fatty acids and glucose metabolism in physiological and pathological conditions, and the role of L-carnitine and of its derivative, propionyl-L-carnitine. Fatty acids are the major oxidation fuel for the heart, while glucose and lactate provide the remaining need. Fatty acids in cytoplasm are transformed to long-chain acyl-CoA and transferred into the mitochondrial matrix by the action of three carnitine dependent enzymes to produce acetyl-CoA through the beta-oxidation pathway.

Attenuation by acetyl-L-carnitine of neurological damage and biochemical derangement following brain ischemia and reperfusion.

Alterations in brain metabolism after ischemia and reperfusion are described herein. Several roles played by carnitine and acetylcarnitine can be of particular relevance in counteracting these brain metabolism alterations. The effects of acetylcarnitine in several experimental models of brain ischemia in rats are described.

[The repair of the membrane lipid bilayer in oxidative stress: phosphatidylethanolamine reacylation in synaptosome, photoreceptor and erythrocyte membranes].

The participation of unsaturated (linoleic and arachidonic) and saturated (palmitic) fatty acids in reacylation of phosphatidylethanolamine (PE) in synaptosomes, photoreceptor membranes and erythrocytes at oxidative stress was studied. Induction of lipid peroxidation (LPO) was found to result in a significant decrease in the content of PE polyenoic fatty acids due to their oxidative destruction. It might be related to both an activation of phospholipase A2 and a decrease in PE reacylation rate.