Diclofop-methyl: A phenoxy propionate herbicide with multiple toxic effects in mouse embyro fibroblast (NIH/3T3) cell line

M. Çeliksöz, Bahar Ulus, Ezgi Öztaş, G. Özhan
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Abstract

Diclofop-methyl is a selective post-emergence graminicide from the phenoxy propionate group of herbicides to be developed for control of wild oats, millets, and other annual grass weeds. Diclofop-methyl usage is limited in various grass weed species due to its toxic effect and exposure risks. However, total annual usage of is approximately 750.000 pounds in United States, and more in Asia. Therefore, we aimed to investigate diclofopmethyl’s toxic potentials in vitro and the following assays were used; MTT assay for cytotoxicity, comet assay for genotoxicity, generation of reactive oxygen species (ROS), malondialdehyde (MDA) and glutathione (GSH) for the potential of oxidative damage in mouse embryo fibroblast (NIH/3T3) cell line. Diclofop-methyl was observed to reduce the cell viability in a concentration manner and the half maximal inhibitory concentration (IC50) value was 301.7 μM. Diclofop-methyl caused DNA damage and oxidative stress at the concentrations between 12.5-400 μM. Tail intensities were at the range of 1.24- 58.21% with increasing concentrations, which are approximately ≤ 1.63-fold of the negative control. Also, MDA levels were increased ≥ ³11.4-fold of the negative control that denotes lipid peroxidation was induced. However, there was no significant increment in the ROS and GSH levels at all concentrations. In view of the fact that ROS has not been detected, despite its level of MDA proffers, the idea that oxidative damage may have been caused by other mechanisms. Our results indicate that diclofopmethyl was cytotoxic, genotoxic and might have oxidative damage potential in vitro conditions.
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甲基双氯草:一种对小鼠胚胎成纤维细胞(NIH/3T3)具有多重毒性作用的苯氧基丙酸除草剂
甲基双氯草是丙酸苯氧基除草剂中的一种选择性萌发后除草剂,将被开发用于控制野生燕麦、小米和其他一年生杂草。由于其毒性作用和暴露风险,双氯灭在各种杂草中的使用受到限制。然而,在美国,每年的总使用量约为75万磅,在亚洲则更多。因此,我们旨在研究双氯磷甲基的体外毒性潜势,并采用以下方法:MTT法测定细胞毒性,comet法测定遗传毒性,生成活性氧(ROS)、丙二醛(MDA)和谷胱甘肽(GSH)测定小鼠胚胎成纤维细胞(NIH/3T3)的氧化损伤潜力。双氯吡肟有明显的降低细胞活力的作用,半数抑制浓度(IC50)为301.7 μM。在12.5 ~ 400 μM浓度范围内,甲基双氯草可引起DNA损伤和氧化应激。随着浓度的增加,尾部强度在1.24 ~ 58.21%之间,约为阴性对照的≤1.63倍。MDA水平较阴性对照组升高≥³11.4倍,提示脂质过氧化作用发生。然而,在所有浓度下,ROS和GSH水平均无显著升高。鉴于ROS未被检测到,尽管其MDA水平提供,氧化损伤可能是由其他机制引起的。结果表明,在体外条件下,双氯甲酯具有细胞毒性、遗传毒性和氧化损伤潜力。
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