Mahdavifard Sina, Nowruz Najafzadeh
Department of Clinical Biochemistry, Ardabil University of Medical Sciences, Ardabil, Iran.
Research Laboratory for Embryology and Stem Cells, Department of Anatomical Sciences, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran.
Biol Trace Elem Res. 2024 Jul;202(7):3141-3148. doi: 10.1007/s12011-023-03887-7. Epub 2023 Sep 30.
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 profile, oxidative stress, inflammatory 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 inflammatory markers (renal nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) were measured. Furthermore, metabolic profile (fasting blood sugar, insulin, insulin resistance, lipid profile, 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 inflammation 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 inflammation and carbonyl stress.
由于肾脏在铅排泄中起主要作用，所以它们对铅（Pb）中毒尤为敏感。接下来，我们通过评估组织病理学和生化参数（肾脏NF-kβ表达、代谢谱、氧化应激、炎症标志物、甲基乙二醛（MGO）和乙二醛酶-I活性），研究了谷氨酰胺（Gln）对大鼠铅肾毒性的影响。将40只大鼠分为四组（每组10只）：正常组（N）、Gln处理的正常组、铅中毒组（Pbi）和Gln处理的Pbi组。处理组在饮用水中摄入0.1%的Gln，持续1个月。为诱导铅中毒，大鼠在饮用水中摄入50 mg/l醋酸铅，持续1个月。测量氧化应激指标（总谷胱甘肽及其还原和氧化形式、它们的比率、晚期蛋白质氧化产物、丙二醛和铁离子还原能力）和炎症标志物（肾脏核因子-kβ表达、白细胞介素1β水平和髓过氧化物酶活性）。此外，还测定了代谢谱（空腹血糖、胰岛素、胰岛素抵抗、血脂谱和动脉粥样硬化指数）和肾功能障碍参数。由病理学家对铅诱导的肾脏组织病理学改变进行研究。在Pbi组大鼠的肾脏中，肾小球受损。Gln可预防肾脏损伤并降低肾功能障碍参数。此外，Gln可降低血清和肾脏匀浆中的氧化应激和炎症。此外，它还改善了胰岛素抵抗、血脂异常和羰基应激（p < 0.001）。Gln通过改善胰岛素抵抗和血脂异常、提高抗氧化标志物以及减轻炎症和羰基应激，保护肾脏免受铅中毒。
