Aluminium-induced changes in hemato-biochemical parameters, lipid peroxidation and enzyme activities of male rabbits: protective role of ascorbic acid.
For a long time, aluminium (Al) has been considered an indifferent element from a toxicological point of view. In recent years, however, Al has been implicated in the pathogenesis of several clinical disorders, such as dialysis dementia, the fulminant neurological disorder that can develop in patients on renal dialysis. Therefore, the present experiment was carried out to determine the effectiveness of l-ascorbic acid (AA) in alleviating the toxicity of aluminium chloride (AlCl3) on certain hemato-biochemical parameters, lipid peroxidation and enzyme activities of male New Zealand white rabbits. Six rabbits per group were assigned to 1 of 4 treatment groups: 0mg AA and 0mg AlCl3/kg body weight (BW) (control); 40 mg AA/kg BW; 34 mg AlCl3/kg BW (1/25 LD50); 34 mg AlCl3 plus 40 mg AA/kg BW. Rabbits were orally administered their respective doses every other day for 16 weeks. Evaluations were made for lipid peroxidation, enzyme activities and hemato-biochemical parameters. Results obtained showed that AlCl3 significantly (P<0.05) induced free radicals and decreased the activity of glutathione S-transferase (GST) and the levels of sulfhydryl groups (SH groups) in rabbit plasma, liver, brain, testes and kidney. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP), and phosphorylase activities were significantly decreased in liver and testes due to AlCl3 administration. While, plasma, liver, testes and brain lactate dehydrogenase (LDH) activities were significantly increased. Contrariwise, the activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma. Aluminium treatment caused a significant decrease in plasma total lipids (TL), blood haemoglobin (Hb), total erythrocytic count (TEC) and packed cell volume (PCV), and increased total leukocyte count (TLC) and the concentrations of glucose, urea, creatinine, bilirubin and cholesterol. Ascorbic acid alone significantly decreased the levels of free radicals, TL, cholesterol, glucose and creatinine, and increased the activity of GST, SH groups, Hb, TEC and PCV. While, the rest of the tested parameters were not affected. Also, the present study showed that ascorbic acid can be effective in the protection of aluminium-induced toxicity.
Yousef
Mokhtar I
MI
Department of Environmental Studies, Institute of Graduate Studies and Research, University of Alexandria, 163 Horreya Avenue, P.O. Box 832, Alexandria 21526, Egypt. mokhtar_yousef@yahoo.com
D000284:Administration, Oral; D000535:Aluminum / Q000008:administration & dosage / Q000633:toxicity*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D019963:Clinical Chemistry Tests; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D005982:Glutathione Transferase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects*; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D011817:Rabbits; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013737:Testis / Q000187:drug effects / Q000201:enzymology; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
D000975:Antioxidants; D013438:Sulfhydryl Compounds; D017392:Thiobarbituric Acid Reactive Substances; D000535:Aluminum; D005982:Glutathione Transferase; D001205:Ascorbic Acid