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机构地区:[1]华南师范大学生命科学学院广州市亚热带生物多样性与环境生物监测重点实验室,广州510631
出 处:《生态毒理学报》2016年第2期666-671,共6页Asian Journal of Ecotoxicology
基 金:广东省自然科学基金(s2013010013183);广州市科技计划项目(201510010107)
摘 要:双酚A是一种日常生活中无处不在的环境雌激素,具有生殖和神经毒性,但低剂量长期暴露对发育期青少年的危害性常常被低估或忽视。本研究以4周龄雄性清洁级小鼠为实验对象,以茶油作为溶媒对照,分别以双酚A浓度为0μg·m L-1、0.1μg·m L-1、10μg·m L-1和1 000μg·m L-1的茶油灌胃小鼠8周,然后利用彗星电泳法检测各组小鼠脑细胞的DNA损伤。结果显示,不同浓度双酚A暴露8周后,彗星电泳图像显示小鼠脑细胞DNA出现不同程度的损伤,随着暴露剂量的增加,带有彗尾的脑细胞比率从对照组小鼠的9.5%分别升高到暴露组小鼠的34.5%、36.0%和50.5%,细胞总体的尾部DNA含量、尾长和尾矩也都逐渐增加,而且各双酚A暴露组小鼠与溶媒对照组小鼠脑细胞都具有显著性差异(P<0.01),这说明中长期双酚A暴露(包括低浓度环境暴露)会导致雄性幼龄小鼠脑细胞的DNA损伤。Bisphenol A(BPA) is an environmental xenoestrogenic endocrine disruptor and has shown detectable toxicity on biological systems, including the reproduction system, immune system, endocrine system and neurological development. However, the neurotoxicity of low dose BPA to children and youth is often underestimated and few studies were conducted on this aspect. We herein examine the effects of low dose BPA exposure on DNA damage of brain cells of male mice. The adolescent male mice at the age of 4 weeks were divided into four groups, including the control group and three exposure groups, and chronically received systematically varying BPA treatments(0 μg·m L^(-1), 0.1 μg·m L^(-1), 10 μg·m L^(-1)and 1 000 μg·m L^(-1)in tea oil) for 8 weeks. Comet assay was then employed to detect the DNA damages of the brain cells in these mice. After the treatments with BPA, the comet percentages of brain cells increased significantly from 9.5% in the control group to 34.5%, 36.0% and 50.5% in the three exposuregroups respectively, consistent with raised percentages of tail DNA, tail length and tail moment in brain cells. The results show that mid-long term exposure to the low dose BPA lead to DNA damage of brain cells in adolescent male mice and the damage levels increase with the increasing BPA concentrations.
分 类 号:X171.5[环境科学与工程—环境科学]
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