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Aluminum-Induced Toxicity and Its Response to Combined Treatment of HEDTA and Propolis in Rats

机译:铝诱导的毒性及其对HEDTA和蜂胶联合治疗的反应

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Our study evaluates the protective effect of the chelating agent N-(2-hydroxy ethyl ethylene diamine tri-acetic acid) [HEDTA] with and without propolis against Al(NO_3)_3-induced toxicity in liver, kidney, and brain. Toxicity was induced by a single administration of A1(NO_3)_3 at a dose of 6.5 mg/kg, intraperitoneally. HEDTA, propolis, and a combination of HEDTA+propolis were administered for 3 days after 24 h of Al exposure. Significant enhancements in AST, ALT, ALP, cholesterol, triglycerides, urea, uric acid, protein, and blood sugar were found, whereas albumin was decreased after Al exposure. The fall in GSH contents and increase in LPO were significant in hepatic, renal, and neuronal tissues. Al(NO_3)_3 caused significant inhibition in the activity of adenosine triphosphatase, superoxide dismutase, and catalase. It inhibited AChE activity in fore-brain, midbrain, and hindbrain. Individual treatment of HEDTA and propolis restored biochemical parameters moderately toward control, but combined treatment of HEDTA+propolis showed better results than mono-therapy. Combined treatment of HEDTA+propolis reduced oxidative stress and regained histological features and metabolic enzymes of liver, kidney, and brain toward control.
机译:我们的研究评估了有和没有蜂胶的螯合剂N-(2-羟乙基乙二胺三乙酸)[HEDTA]对Al(NO_3)_3诱导的肝,肾和脑毒性的保护作用。腹膜内单次给予A1(NO_3)_3剂量为6.5 mg / kg会诱导毒性。铝暴露24小时后,将HEDTA,蜂胶和HEDTA +蜂胶的组合给药3天。发现AST,ALT,ALP,胆固醇,甘油三酸酯,尿素,尿酸,蛋白质和血糖显着增强,而Al暴露后白蛋白下降。肝,肾和神经元组织中GSH含量的下降和LPO的增加是显着的。 Al(NO_3)_3显着抑制了腺苷三磷酸酶,超氧化物歧化酶和过氧化氢酶的活性。它抑制前脑,中脑和后脑的AChE活性。单独治疗HEDTA和蜂胶可以使生化参数适度恢复至对照水平,但是HEDTA +蜂胶的联合治疗比单药治疗效果更好。 HEDTA +蜂胶的联合治疗可减轻氧化应激,并恢复肝,肾和脑的组织学特征和代谢酶,从而达到控制的目的。

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