گلوتامین با افزایش آنتی اکسیدان های داخلی و کاهش التهاب و کاهش استرس کربونیل از کلیه در برابر سمیت سرب حفاظت می کند و از مقاومت انسولینی و دیس لیپیدمی را بهبود می بخشد

عنوان انگليسی

Glutamine Defended the Kidneys Versus Lead Intoxication Via Elevating Endogenous Antioxidants, Reducing Inflammation and Carbonyl Stress, as well as Improving Insulin Resistance and Dyslipidemia

خلاصه انگلیسی

Kidneys are primarily sensitive to lead (Pb) poisoning due to their cardinal role in lead excretion. Then, we studied the efect of glutamine (Gln) on lead nephrotoxicity in rats by assessing the histopathological and biochemical parameters (the renal NF-kβ expression, metabolic profle, oxidative stress, infammatory markers, methylglyoxal (MGO), and glyoxalase-I activity). Forty 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 1 month. To motivate lead poisoning, rats gained 50 mg/l lead acetate in drinking water for 1 month. Oxidative stress indices (total glutathione, its reduced and oxidized forms, their ratios, advanced protein oxidation products, malondialdehyde, and ferric ion reducing power) and infammatory markers (renal nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) were measured. Furthermore, metabolic profle (fasting blood sugar, insulin, insulin resistance, lipid profle, and atherogenic index) and renal dysfunction parameters were determined. Pb-induced renal histopathological alterations were investigated by a pathologist. In 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 infammation in sera and kidney homogenates. In addition, it improved insulin resistance, dyslipidemia, and carbonyl stress (p < 0.001). Gln guarded the kidneys versus lead intoxication by improving insulin resistance and dyslipidemia, elevating antioxidant markers, and diminishing infammation and carbonyl stress.

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