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首页> 外文期刊>Clinical kidney journal. >Metabolic adaptability in hexavalent chromium-treated renal tissue: an in vivo study
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Metabolic adaptability in hexavalent chromium-treated renal tissue: an in vivo study

机译：在六价铬治疗的肾脏组织中的代谢适应性：一项体内研究

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Background Hexavalent chromium [Cr(VI)], an environmental pollutant that originates mostly from anthropogenic sources, is a serious threat to human health. After entering into cells, Cr(VI) is capable of producing excessive free radicals and causing tissue damage. The present study aims to reveal the toxic manifestation of Cr(VI) on the metabolic activity of renal tissue. Methods Male Swiss albino mice were treated orally with potassium dichromate (K2Cr2O7) at a dose of 10?mg/kg body weight for a period of 30 days. Important tricarboxylic acid (TCA) cycle enzyme activities like isocitrate dehydrogenase, succinate dehydrogenase and malate dehydrogenase, as well as the activities of enzymes involved in oxidative phosphorylation such as Nicotinamide adenine dinucleotide (NADH) dehydrogenase, were measured. Additionally, transaminase and protease (pronase, cathepsin and trypsin) activities, tissue protein and free amino nitrogen were estimated in renal tissue. Glucose-6-phosphatase, glucose-6-phosphate dehydrogenase and alkaline phosphatase activities, as well as lactic acid, pyruvic acid and chromium contents, of kidneys were determined following standard protocols. Kidney histology was performed by hematoxylin and eosin staining. Results Cr(VI) suppresses the rate-limiting enzymes of the TCA cycle and oxidative phosphorylation indicating an inhibition of renal ATP production. It decreases protease activity by eliminating the protein substrates and alters the gluconeogenic pathway. Cr(VI) worsens the normophysiological attributes of renal tissue by enhancing the activity of alkaline phosphatase, pointing towards kidney disease. Histopathological observations confirmed these biochemical results through the presence of chronic tubular nephritis and altered glomerular structure. Cr(VI) retention occurs to a greater extent in renal tissue, which intensifies the toxic manifestation of this pollutant in the kidney. Conclusions Cr(VI) disrupts the metabolic interaction between carbohydrates and proteins in mammalian renal tissue.
机译：背景技术六价铬[Cr（VI）]是一种主要来自人为来源的环境污染物，对人类健康构成严重威胁。进入细胞后，Cr（VI）能够产生过多的自由基并引起组织损伤。本研究旨在揭示六价铬对肾脏组织代谢活性的毒性表现。方法对瑞士白化病雄性小鼠口服重铬酸钾（K 2 Cr 2 O 7 ），剂量为10？mg / kg体重体重持续30天。测量了重要的三羧酸（TCA）循环酶活性，如异柠檬酸脱氢酶，琥珀酸脱氢酶和苹果酸脱氢酶，以及涉及氧化磷酸化的酶（如烟酰胺腺嘌呤二核苷酸（NADH）脱氢酶）的活性。另外，估计了肾组织中的转氨酶和蛋白酶（链酶，组织蛋白酶和胰蛋白酶）活性，组织蛋白和游离氨基氮。根据标准方案测定肾脏的葡萄糖6-磷酸酶，葡萄糖-6-磷酸脱氢酶和碱性磷酸酶活性以及乳酸，丙酮酸和铬含量。通过苏木精和曙红染色进行肾脏组织学检查。结果Cr（VI）抑制了TCA循环的限速酶和氧化磷酸化，表明肾脏ATP生成受到抑制。它通过消除蛋白质底物降低蛋白酶活性，并改变糖异生途径。 Cr（VI）通过增强碱性磷酸酶的活性而恶化了肾脏组织的正常生理特性，从而导致肾脏疾病。组织病理学观察通过慢性肾小管肾炎和肾小球结构改变证实了这些生化结果。 Cr（VI）保留在肾脏组织中发生的程度更大，这加剧了该污染物在肾脏中的毒性表现。结论Cr（VI）破坏了哺乳动物肾组织中碳水化合物和蛋白质之间的代谢相互作用。

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