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首页> 外文期刊>Journal of biochemical and molecular toxicology >Dieldrin elicits a widespread DNA repair and antioxidative response in mouse brain.
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Dieldrin elicits a widespread DNA repair and antioxidative response in mouse brain.

机译：狄氏剂在小鼠脑中引起广泛的DNA修复和抗氧化反应。

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Dieldrin is an organochlorine pesticide that is toxic for monoaminergic neurons. This study was designed to test the hypothesis that a weak DNA repair response to dieldrin by nigrostriatal dopaminergic (DA) neurons results in depletion of striatal DA. The activity of the mammalian base excision repair enzyme oxyguanosine glycosylase was utilized as the index of DNA repair. Other measures of oxidative stress were also studied, including the regional distribution of lipid peroxidation and superoxide dismutase (SOD) activity. The effects of acute and slow infusion of dieldrin on striatal DA levels were biphasic with a transient initial depression followed by increases beyond normal steady-:state levels. Dieldrin administration caused a global oxidative stress evidenced by increased levels of lipid peroxidation in all brain regions, an effect consistent with its capacity to affect mitochondrial bioenergetics. Dieldrin also elicited strong antioxidative and DNA repair responses across the entire mouse brain. Although mitochondrial SOD was not as increased in midbrain as it was in other regions following a cumulative dose of 24 mg/kg, this response, along with the robust DNA repair response, appeared to be sufficient to protect potentially vulnerable DA neurons from cytotoxicity. However, the long-:term consequences of chronic low-:dose dieldrin exposure remain to be studied, especially in light of the concept of "slow excitotoxicity,'' which postulates that even a mild bioenergetic compromise can over time result in the demise of neurons.
机译：狄氏剂是一种有机氯农药，对单胺能神经元有毒。这项研究旨在检验以下假设：黑纹状体多巴胺能（DA）神经元对狄氏剂的弱DNA修复反应会导致纹状体DA耗竭。哺乳动物碱基切除修复酶氧鸟苷糖基化酶的活性被用作DNA修复的指标。还研究了其他氧化应激指标，包括脂质过氧化和超氧化物歧化酶（SOD）活性的区域分布。狄氏剂的急性和缓慢输注对纹状体DA水平的影响是双相的，伴有短暂的初始抑郁，随后增加至超出正常的稳态水平。狄氏剂的使用引起了全球性氧化应激，其在所有脑区域的脂质过氧化水平增加证明了这一作用，其作用与其影响线粒体生物能的能力一致。狄氏剂还引起整个小鼠大脑强烈的抗氧化和DNA修复反应。尽管累积剂量为24 mg / kg后，中脑线粒体SOD的增加没有其他区域增加，但这种反应以及强大的DNA修复反应似乎足以保护潜在的脆弱DA神经元免受细胞毒性作用。但是，长期低剂量狄氏剂长期暴露的长期后果仍有待研究，特别是考虑到“慢兴奋性毒性”的概念，该概念假定即使是轻度的生物能折衷也会随着时间的流逝而导致死亡。神经元。

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