Bipyridylium herbicide toxicity in vitro: comparative study of the cytotoxicity of paraquat and diquat toward the pulmonary alveolar macrophage.

Bipyridylium herbicide toxicity in vitro: comparative study of the cytotoxicity of paraquat and diquat toward the pulmonary alveolar macrophage.
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联吡啶鎓除草剂体外毒性:百草枯和敌草快对肺泡巨噬细胞细胞毒性的比较研究。

DOI:
10.1080/15287398609530880
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发表时间:
1986
期刊:
Journal of toxicology and environmental health
影响因子:
--
通讯作者:
Stevens,JB
Stevens,JB
中科院分区:
--
文献类型:
--
作者:
Wong,RC;Stevens,JB

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成年大鼠肺泡巨噬细胞体外暴露于百草枯或双菊枯均可导致浓度依赖性细胞毒性(细胞死亡)。然而,从统计上看,除草剂百草枯比diquat对这些细胞更有效。测定百草枯(暴露8小时,37°C)的LC50值为0.94 mM[95%置信区间(ci)]。diquat的LC50值为1.97 mM (C.I. 1.58-2.51 mM)。有趣的是,迪奎特进入这些细胞的程度比百草枯要大得多。后一项数据虽然看起来与上述发现相矛盾,但与本研究中报道的其他发现一致,即通过耗氧量损失来测量的细胞呼吸对diquat比对百草枯更敏感。此外,发现只有百草枯的细胞毒性依赖于氧张力,并且可以通过培养基中抗氧化酶的存在而改变。然而,这两种化合物都被发现对纯化的线粒体具有同等效力。百草枯和双菊枯都能解偶联氧化磷酸化,并从该细胞器中诱导活性氧(超氧阴离子和过氧化氢)。由此得出结论,自由基病理是百草枯对这些细胞具有细胞毒性的最可能的作用机制,但百草枯中毒可能源于其他一些作用方式。
In vitro exposure of adult rat alveolar macrophages to either paraquat or diquat resulted in concentration dependent cytotoxicity (cell death). The herbicide paraquat, however was statistically significantly more potent toward these cells than was diquat. The LC50 value for paraquat (8‐h exposure, 37°C) was determined to be 0.94 mM [95% confidence interval (C.I.) 0.79–1.12 mM], whereas the corresponding LC50 value for diquat was 1.97 mM (C.I. 1.58–2.51 mM).Interestingly, diquat was shown to enter these cells to a much greater extent than was paraquat. The latter data, while seemingly contradictory to the above findings, is consistent with other reported findings in this study that show that cell respiration, as measured by loss of oxygen consumption, was more sensitive to diquat than it was to paraquat. Also, only paraquat cytotoxicity was found to be dependent on oxygen tension and could be altered by the presence of antioxidant enzymes in the culture medium. Both compounds, however, were found to be equipotent toward purified mitochondria. Both paraquat and diquat were able to uncouple oxidative phosphory‐lation and induce active oxygen species (superoxide anions and hydrogen peroxide) from this organelle. It is concluded that free‐radical pathology is the most likely mechanism of action by which paraquat is cytotoxic toward these cells, but that diquat poisoning probably originates from some other mode of action.
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