Department of Clinical Biochemistry, Ardabil University of Medical Sciences, P.O. Box, 56189-85991, Ardabil, Iran.
Faculty of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran.
Biol Trace Elem Res. 2022 Nov;200(11):4726-4732. doi: 10.1007/s12011-021-03046-w. Epub 2022 Apr 27.
Lead acetate-motivated oxidative stress can affect all organ systems, particularly the liver. Glutamine (Gln) has both antioxidant and chelating properties. Therefore, we investigated for the first time the effect of Gln on the biochemical and histopathological alternations in a rat model of lead toxicity. Thirty-two rats were divided into four groups (eight rats in each): untreated normal, lead poisoning, and two similar groups receiving Gln (0.1% in drinking water for 4 weeks). To induce lead poisoning, rats received 50 mg/L lead acetate in drinking water for 4 weeks. Oxidative stress indices (total glutathione, the ratio of reduced glutathione to oxidized glutathione, advanced protein oxidation products, malondialdehyde, and ferric ion reducing power) and inflammatory markers (hepatic nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) were measured. Furthermore, biochemical markers of hepatotoxicity (alanine transaminase, aspartate transaminase, alkaline phosphatase, gamma-glutamyl transpeptidase, total bilirubin, total protein, albumin, and globulins) were measured. Histopathological examination evaluated lead-induced liver damage. The treatment compensated lead-induced biochemical and histopathological alternations in rat liver. Furthermore, it decreased lead acetate level, the NF-kβ gene expression, oxidative stress, and inflammatory markers. Moreover, the treatment elevated total glutathione and reduced glutathione in the sera and liver homogenates of treated groups (p < 0.001). Glutamine could protect the liver against lead intoxication via antioxidant, anti-inflammatory, and chelating properties. In addition, its downregulating effect on the hepatic NF-kβ signaling pathway confirms its hepatoprotective activity.
醋酸铅引起的氧化应激会影响所有器官系统，尤其是肝脏。谷氨酰胺 (Gln) 具有抗氧化和螯合作用。因此，我们首次研究了 Gln 对铅中毒大鼠模型生化和组织病理学变化的影响。32 只大鼠分为四组（每组 8 只）：未处理的正常组、铅中毒组和两组类似的 Gln 组（4 周内饮用 0.1%的 Gln）。为了诱导铅中毒，大鼠饮用含 50mg/L 醋酸铅的水 4 周。测量氧化应激指标（总谷胱甘肽、还原型谷胱甘肽与氧化型谷胱甘肽的比值、高级蛋白质氧化产物、丙二醛和铁离子还原能力）和炎症标志物（肝核因子-κβ表达、白细胞介素 1β 水平和髓过氧化物酶活性）。此外，还测量了肝毒性的生化标志物（丙氨酸氨基转移酶、天冬氨酸氨基转移酶、碱性磷酸酶、γ-谷氨酰转肽酶、总胆红素、总蛋白、白蛋白和球蛋白）。组织病理学检查评估了铅引起的肝损伤。治疗补偿了铅引起的大鼠肝生化和组织病理学变化。此外，它降低了醋酸铅水平、NF-κβ 基因表达、氧化应激和炎症标志物。此外，治疗还提高了血清和肝匀浆中总谷胱甘肽和还原型谷胱甘肽的水平（p<0.001）。谷氨酰胺可以通过抗氧化、抗炎和螯合作用保护肝脏免受铅中毒。此外，其对肝 NF-κβ 信号通路的下调作用证实了其肝保护活性。
