Kidneys are primarily sensitive to lead (Pb) poisoning due to their cardinal role in lead excretion. Then, we studied the effect of glutamine (Gln) on lead nephrotoxicity in rats by assessing the histopathological and biochemical parameters (the renal NF-kβ expression, metabolic pro le, oxidative stress, in ammatory markers, methylglyoxal (MGO), and glyoxalase-I activity).
Materials and MethodsForty rats were allotted into four groups (ten rats in each): normal (N), Gln treated N, Pb intoxication (Pbi), and Gln treated Pbi. The treated groups took 0.1% Gln in drinking water for one month. To motivate lead poisoning, rats gained 50 mg/l lead acetate in drinking water for one month. Oxidative stress indices (total glutathione, its reduced and oxidized forms, and their ratios as well as advanced protein oxidation products, malondialdehyde, and ferric ion reducing power) and in ammatory markers (renal nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) were measured. Further, metabolic pro le (fasting blood sugar, insulin, insulin sensitivity, lipid pro le, and atherogenic index) and renal dysfunction parameters were also determined. Pb-induced renal damage and dysfunction were assessed with Histopathological examination.
ResultsIn the kidney of Pbi rats, the glomerulus was damaged. Gln prevented kidney damage and reduced kidney dysfunction parameters. In addition, Gln decreased oxidative stress and in ammation in sera and kidney homogenates as well as improved insulin resistance, dyslipidemia, and carbonyl stress (p < 0.001).