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首页> 外文期刊>International Journal of Pharmacy and Pharmaceutical Sciences >ALTERATION IN CARBOHYDRATE METABOLISM BY SUB-ACUTE LEAD EXPOSURE: A DOSE-DEPENDENT STUDY
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ALTERATION IN CARBOHYDRATE METABOLISM BY SUB-ACUTE LEAD EXPOSURE: A DOSE-DEPENDENT STUDY

机译:亚急性铅暴露引起的碳水化合物代谢改变:剂量依赖性研究

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摘要

Objective: The study was conducted to evaluate the dose-dependent effects of sub-acute lead exposure on certain aspects of carbohydrate metabolism. Methods: Swiss albino male mice (weighing 30-35 g) were selected for the present study and divided into five groups; one control group and others lead-treated groups i.e. Group A (5 mg/kg body weight), Group B (10 mg/kg body weight), Group C (15 mg/kg body weight) and Group D (20 mg/kg body weight). Parameters like blood and liver glucose, glycogen and pyruvic acid contents were determined in liver tissue. The enzyme activities like pyruvate dehydrogenase, malate dehydrogenase and glucose 6-phosphatase were recorded in that tissue. Additionally, free amino acid nitrogen content and transaminase enzyme activities were also evaluated in liver tissue of mice. Results: The study reveals that lead caused a significant diminution of blood and hepatic glucose levels and fall in liver glycogen content in a dose-dependent manner, the highest effect was observed in animals treated with lead at a dose of 20 mg/kg body weight. Glucose 6-phosphatase activity was decreased significantly in all the treated groups. There was a dose-dependent increase in pyruvic acid content whereas pyruvate dehydrogenase, malate dehydrogenase and transaminase enzyme activities were significantly depressed in a dose-dependent fashion in all the treated animals. Additionally, lead treatment significantly (p<0.001) enhanced free amino acid nitrogen in the liver to provide a substrate for gluconeogenesis. Conclusion: It is suggested that an adaptive mechanism is initiated by stimulating and retarding glycogenolytic and glycolytic activity and also by rising in the content of free amino acid nitrogen to recover from the lead stressed toxic manifestation
机译:目的:进行这项研究以评估亚急性铅暴露对碳水化合物代谢某些方面的剂量依赖性作用。方法:选择瑞士白化病雄性小鼠(体重30-35 g)用于本研究,分为5组,每组5只。一个对照组和其他铅治疗组,即A组(5 mg / kg体重),B组(10 mg / kg体重),C组(15 mg / kg体重)和D组(20 mg / kg体重)。确定肝脏组织中的血液和肝葡萄糖,糖原和丙酮酸含量等参数。在该组织中记录了诸如丙酮酸脱氢酶,苹果酸脱氢酶和葡萄糖6-磷酸酶的酶活性。另外,还评估了小鼠肝脏组织中的游离氨基酸氮含量和转氨酶活性。结果:研究表明,铅导致血液和肝葡萄糖水平显着降低,并以剂量​​依赖性方式降低肝糖原含量,在以20 mg / kg体重的铅治疗的动物中观察到最高的效果。在所有治疗组中,葡萄糖6-磷酸酶活性均显着降低。丙酮酸含量呈剂量依赖性增加,而丙酮酸脱氢酶,苹果酸脱氢酶和转氨酶活性均以剂量依赖性方式显着降低。另外,铅治疗显着(p <0.001)增强了肝脏中的游离氨基酸氮,为糖异生提供了底物。结论:提示通过刺激和延迟糖原分解和糖酵解活性,以及​​通过增加游离氨基酸氮的含量以从铅胁迫的毒性表现中恢复来启动适应机制。

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