The influence of L-carnitine suplementation on the antioxidative abilities of serum and the central nervous system of ethanol-induced rats.
The brain is exceptionally susceptible to oxidative stress that may be caused by xenobiotics such as ethanol. Alcohol metabolism is accompanied by enhanced free radical formation and a decrease in antioxidant abilities. However, L-carnitine appears to have antioxidant properties and the ability to regulate ethanol metabolism. The present study was designed to estimate the effect of L-carnitine on the antioxidant capacity of the rat brain and blood serum. For 5 weeks during the study, L-carnitine was given to rats in the amount of 1.5 g/1 l of drinking water, and from the second week the rats were intragastrically treated with ethanol. A significant decrease in the activity of antioxidant enzymes (Cu,Zn-SOD, GSH-Px, GSSG-R and CAT) and in the level of non-enzymatic antioxidants (vitamin C, E, A, GSH and GSH-t) as well as a significant increase in the level of GSSG in the brain and blood serum of ethanol intoxicated rats have been demonstrated. It has also been shown that alcohol caused a significant increase in the level of lipid peroxidation products-lipid hydroperoxides, malondialdehyde and 4-hydroxynonenal-and an increase in dityrosine, as well as a decrease in tryptophan-markers of protein oxidative modifications. The administration of L-carnitine to ethanol intoxicated rats partially normalized the activity of the examined enzymes and the level of the above non-enzymatic antioxidants. Moreover, L-carnitine significantly protects lipids and proteins against oxidative modifications. In conclusion, it has been proved that L-carnitine protects rat brain and blood serum against oxidative stress formation and it is possible that this small molecular amine has a similar beneficial effect on the human CNS.
Department of Analytical Chemistry, Medical University of Białystok, Mickiewicza 2a, 15-230, Białystok 8, P. O. Box 14, Poland.
Agnieszka
A
Augustyniak
Elżbieta
E
Skrzydlewska
D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000097:blood / Q000378:metabolism; D015415:Biomarkers; D001923:Brain Chemistry / Q000187:drug effects; D002331:Carnitine / Q000494:pharmacology*; D002374:Catalase / Q000097:blood / Q000378:metabolism; D002490:Central Nervous System / Q000187:drug effects / Q000378:metabolism*; D002492:Central Nervous System Depressants / Q000494:pharmacology*; D000431:Ethanol / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000097:blood / Q000378:metabolism; D005980:Glutathione Reductase / Q000097:blood / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000097:blood / Q000378:metabolism; D014801:Vitamin A / Q000097:blood / Q000378:metabolism; D014810:Vitamin E / Q000097:blood / Q000378:metabolism
D000447:Aldehydes; D000975:Antioxidants; D015415:Biomarkers; D002492:Central Nervous System Depressants; D008054:Lipid Peroxides; D014801:Vitamin A; D014810:Vitamin E; D000431:Ethanol; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione; C027576:4-hydroxy-2-nonenal; D001205:Ascorbic Acid; D002331:Carnitine