Studying the Potential Palliative Activity of Selenium and Sulfur Against Aluminum-Induced Toxicity in Adult Male Albino Rats

Abstract

Aluminum (Al3+) toxicity results from the accumulation of Al3+ in the body without excretion. Most studies focused on the neurotoxic effects of aluminum and only a handful of studies investigated its deleterious effect on liver and kidneys. The present study aimed to investigate the hepatotoxic and nephrotoxic effects of aluminum by assessing the changes caused in many biochemical parameters, enzyme activities and oxidative stress in addition to the histopathology of liver by light and electron microscopic studies. The therapeutic and the prophylactic effects of N-acetylcysteine (NAC) and sodium selenite (SS) in counteracting or preventing the damage caused by aluminium were also investigated. Al3+-intoxication resulted in significant reductions in serum alanine aminotransferase (ALT) activity, albumin level, A/G, triacylglycerols (TAGs), high density lipoprotein cholesterol (HDL-chol.), very low density lipoprotein cholesterol (VLDL-chol.), and reduced glutathione (GSH) levels, and catalase, glutathione peroxidase (GPx), superoxide dismutase (SOD), and glutathione S-transferase (GST) activities in liver, and vitamin E level in serum. It also resulted in significant elevations in serum levels of globulins, creatinine, gamma- glutamyl transpeptidase (γ-GT) activity, total cholesterol (T.chol.), low density lipoprotein (LDL-chol.) levels, atherogenic indices, and malondialdehyde (MDA) level in liver as compared to control. The photo and electron micrographs of liver in aluminu