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代森锰锌增强内吸磷对艾氏腹水癌细胞细胞毒性的作用机制。

Mechanism of potentiation of endosulfan cytotoxicity by thiram in Ehrlich ascites tumor cells.

机构信息

Department of Food Protectants and Infestation Control, Central Food Technological Research Institute (CSIR), Mysore, India.

出版信息

Toxicol In Vitro. 2010 Feb;24(1):40-4. doi: 10.1016/j.tiv.2009.09.012. Epub 2009 Sep 23.

Abstract

Cytotoxicity of the two pesticides, thiram and endosulfan, have been studied in Ehrlich ascites tumor cells. Thiram cytotoxicity was much lower than that of endosulfan with LC(50) (1h exposure) of 4.02 and 1.12mM, respectively. The cytotoxic action of the pesticides on the cells were characterised by glutathione depletion, induction of reactive oxygen species (ROS). The cell death induced by the pesticides was of necrotic type as confirmed by lactate dehydrogenase (LDH) leakage. At non-cytotoxic concentration, thiram potentiated the cytotoxicity of endosulfan when cells were exposed to a mixture of both chemicals. The mechanisms involved in the potentiation of cytotoxicity include excessive glutathione depletion and induction ROS which were higher than the additive effects of individual chemicals. The study demonstrates the importance of pesticide interactions in toxicity risk assessment.

摘要

两种农药(代森锰锌和硫丹)的细胞毒性已在艾氏腹水癌细胞中进行了研究。代森锰锌的细胞毒性远低于硫丹,其 LC50(1 小时暴露)分别为 4.02 和 1.12mM。这些农药对细胞的细胞毒性作用表现为谷胱甘肽耗竭和活性氧(ROS)的诱导。通过乳酸脱氢酶(LDH)漏出证实,农药诱导的细胞死亡为坏死型。在非细胞毒性浓度下,当细胞暴露于两种化学物质的混合物中时,代森锰锌增强了硫丹的细胞毒性。这种增效作用的机制包括谷胱甘肽过度耗竭和 ROS 诱导,其水平高于两种化学物质的相加效应。该研究表明了在毒性风险评估中农药相互作用的重要性。

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