砷和二(2-乙基己基)邻苯二甲酸盐联合暴露引起大鼠脑atp酶的反应,不同于肝脏和肾脏的活性

O. Afolabi, R. Ugbaja, O. Ademuyiwa
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引用次数: 3

摘要

砷和邻苯二甲酸二(2-乙基己基)酯(DEHP)是环境上普遍存在的、流行病学上重要的有毒物质,目前全世界有数百万人接触到它们。虽然暴露于砷或DEHP的不利影响有文献记载,但共同暴露于这些物质的毒理学影响在很大程度上是未知的。在本研究中,研究了暴露于这些化学物质对大鼠脑、肝和肾三磷酸腺苷酶活性的影响。雄性Wistar大鼠每天分别或同时暴露于100 mg L-1砷(通过饮用水)和100 mg DEHP (kg-1体重)玉米油中,持续30天。毒性评估通过评估身体和器官重量的变化,以及Na+/K+-, Ca2+-, Mg2+-和总atp酶活性在脑,肝和肾。暴露于砷或DEHP导致所调查的室室中酶的活性急剧降低,除了在大脑中Na+/K+-和Mg2+- atp酶的活性显著增加。此外,DEHP对肾脏和大脑的总atp酶和Ca2+ atp酶分别没有影响。有趣的是,共同接触这些有毒物质会显著刺激大脑中所有这些酶的活动。在这个隔间中,联合处理导致毒物之间的加性相互作用和砷对DEHP的增强效应,分别与Na+/K+- atp酶活性和Ca2+- atp酶活性有关。我们的研究结果表明,大鼠对砷和DEHP联合暴露的组织特异性反应与其他隔间的影响明显不同。关键词:砷,邻苯二甲酸二(2-乙基己基)酯,Na+/K+- atp酶,Ca2+- atp酶,共暴露
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Combined arsenic and di-(2-ethylhexyl) phthalate exposure elicits responses in brain ATPases different from hepatic and renal activities in rats
Arsenic and di-(2-ethylhexyl) phthalate (DEHP) are environmentally ubiquitous and epidemiologically important toxic agents that millions of people are currently exposed to, worldwide. Although the adverse impact due to exposure to either arsenic or DEHP are documented, the toxicological effects of co-exposure to these agents are largely unknown. In this study, exposure to these chemicals was investigated for their effects on ATPase activities in the brain, liver and kidney of rats. Male Wistar rats were exposed daily to 100 mg L-1 arsenic via drinking water and to 100 mg DEHP kg-1 body weight in corn oil either individually or concurrently for 30 days. Toxicity was assessed by evaluating changes in body and organ weights, as well as, Na+/K+-, Ca2+-, Mg2+- and total ATPase activities in the brain, liver and kidney. Exposure to either arsenic or DEHP resulted in drastic reduction in activities of the enzymes in the compartments investigated, except in the brain where Na+/K+- and Mg2+- ATPases had their activities significantly increased. Also, DEHP displayed no effect on the total ATPase and Ca2+ ATPase in the kidney and brain, respectively. Interestingly, co-exposure to these toxicants significantly stimulated the activities of all these enzymes in the brain. In this compartment, combined treatment resulted in an additive interaction between the toxicants and a potentiation effect of arsenic on DEHP with regards to the Na+/K+- ATPase activity and Ca2+- ATPase activity, respectively. Our findings demonstrate tissue specific response to combined arsenic and DEHP exposure in rats with the effect on the brain significantly different from other compartments. Key words: Arsenic, di-(2-ethylhexyl) phthalate, Na+/K+-ATPase, Ca2+-ATPase, co-exposure.
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