Biochemistry of Reactive Oxygen and Nitrogen Species

Reactive species or free radicals include reactive oxygen and nitrogen species that are called reactive oxygen nitrogen species. Reactive oxygen species are formed as a natural by-product of the normal metabolism of oxygen and have significant roles in cell signaling and homeostasis. The reactive oxygen species are generated as a by-product of biochemical reactions, in mitochondria, peroxisomes, cytochrome P450, and other cellular components. When oxygen homeostasis is not maintained, oxidative stress is increased in the cellular environment. Superoxide, hydrogen peroxide and hydroxyl radicals are normal metabolic by-products which are generated continuously by the mitochondria in growing cells. Microsomal cytochrome P450 enzymes, flavoprotein oxidases and peroxisomal enzymes are other significant intracellular sources of reactive oxygen species

Effect of L-carnitine on oxidative damage to liver, kidney and spleen induced by phenylhydrazine in mice

To investigate the ameliorative effect of L-carnitine on phenylhydrazine induced oxidative damage to liver, kidney and spleen, twenty-eight Swiss albino mice were divided into four groups and injected 0.9% NaCl (control), 40 mg/kg/day phenylhydrazine, phenylhydrazine+L-carnitine or 1000 mg/kg/day L-carnitine. Malondialdehyde (MDA) level was found to be significantly (P<0.001) lower in phenylhydrazine+L-carnitine group compared to the phenylhydrazine group in all tissues. Reduced kidney glutathione (GSH) level in phenylhydrazine given group was restored to normal by L-carnitine. However, increased uric acid level by phenylhydrazine was not decreased by L-carnitine administration. It appears that L-carnitine may prevent tissue damage and lipid peroxidation induced by phenylhydrazine

Protective effect of L-carnitine against oxidative damage caused by experimental chronic aflatoxicosis in quail (Coturnix coturnix)

This study was designed to evaluate the effect of L-carnitine supplementation on the plasma malondialdehyde (MDA) and whole blood reduced glutathione (GSH) concentrations in experimentally-induced chronic aflatoxicosis in quails. For this purpose, a total of 80 quails up to 8 weeks old were divided into four equal groups. Group I served as control, Group II was given L-carnitine at the dose of 200 mg/litre in the drinking water for 60 days, Group III was given 60 µg total aflatoxin/kg diet for 60 days, and Group IV was given both 60 µg total aflatoxin/kg diet and 200 mg L-carnitine/litre in the drinking water for 60 days. Aflatoxin treatment caused a significant increase in plasma MDA and a significant decrease in blood GSH concentrations. On the other hand, there was a significant decrease in plasma MDA and a significant increase in whole blood GSH in the L-carnitine-supplemented group. The present study demonstrated that L-carnitine brought about the inhibition of lipid peroxidation by enhancing antioxidant capacity in quails with chronic aflatoxicosis