Antioxidant effect of vitamin E and selenium on lipid peroxidation, enzyme activities and biochemical parameters in rats exposed to aluminium.
Aluminium has the potential to be neurotoxic in humans and animals, and is present in many manufactured foods and medicines and is also added to drinking water for purification purposes. Therefore, the present study was carried out to investigate (1) the alterations in biochemical parameters, free radicals and enzyme activities induced by aluminium chloride (AlCl3) in plasma and different tissues of male rats, and (2) the role of vitamin E (VE) and selenium in alleviating the negative effects of aluminium. VE plays an important role as an antioxidant and is consequently expected to protect tissues from damage caused by reactive oxygen metabolites. Selenium is also generally recognized to be a trace mineral of great importance for human health, protecting the cells from the harmful effects of free radicals. Seven rats per group were assigned to one of six treatment groups: 0 mg VE, 0 mg Se and 0 mg AlCl3/kg body weight (BW) (control); 100 mg VE/kg BW; 200 microg Se kg BW; 34 mg AlCl3/kg BW (1/25 LD50); 34 mg AlCl3 plus 100 mg VE/kg BW; 34 mg AlCl3 plus 200 microg Se/kg BW. Rats were orally administered their respective doses every other day for 30 days. Evaluations were made for lipid peroxidation, enzyme activities and biochemical parameters. Results obtained showed that AlCl3 significantly (p<0.05) induced free radicals (thiobarbituric acid-reactive substances) and decreased the activity of glutathione S-transferase (GST) and the levels of sulphydryl groups (SH groups) in rat plasma, liver, brain, testes and kidney. Aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, acid phosphatase, and phosphorylase activities were significantly decreased in liver and testes due to AlCl3 administration, while the activities of these enzymes were significantly increased in plasma. In addition, plasma, liver, testes and brain lactate dehydrogenase activities were significantly increased. On the contrary, the activity of acetylcholinesterase was significantly decreased in brain and plasma. Al treatment caused a significant decrease in plasma total protein (TP), albumin and total lipids (TL), and increased the concentrations of glucose, urea, creatinine, bilirubin and cholesterol. VE or Se alone significantly decreased the levels of free radicals, TL, cholesterol, urea and bilirubin, and increased the activity of GST, and SH groups, TP and albumin, while the rest of the tested parameters were not affected. VE or Se in combination with Al partially or totally alleviated its toxic effects on the studied parameters. In conclusion, VE and Se have beneficial effects and could be able to antagonize Al toxicity.
Department of Environmental Studies, Institute of Graduate Studies and Research, Alexandria University, 163 Horreya Avenue, P.O. Box. 832, Alexandria 21526, Egypt. feldemerdash@yahoo.com
Fatma M
FM
El-Demerdash
D000077410:Aluminum Chloride; D017607:Aluminum Compounds / Q000008:administration & dosage / Q000378:metabolism / Q000633:toxicity; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001921:Brain / Q000378:metabolism; D002712:Chlorides / Q000008:administration & dosage / Q000378:metabolism / Q000633:toxicity; D005982:Glutathione Transferase / Q000378:metabolism; D006801:Humans; D007668:Kidney / Q000378:metabolism; D015227:Lipid Peroxidation; D008099:Liver / Q000378:metabolism; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012643:Selenium / Q000378:metabolism*; D013737:Testis / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism*
D017607:Aluminum Compounds; D000975:Antioxidants; D002712:Chlorides; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D000077410:Aluminum Chloride; D005982:Glutathione Transferase; D012643:Selenium