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首页> 外文期刊>Archives of Toxicology >Decreased plasma thiol antioxidant barrier and selenoproteins as potential biomarkers for ongoing methylmercury intoxication and an individual protective capacity
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Decreased plasma thiol antioxidant barrier and selenoproteins as potential biomarkers for ongoing methylmercury intoxication and an individual protective capacity

机译:血浆硫醇抗氧化剂屏障和硒蛋白的降低,可作为正在进行的甲基汞中毒的潜在生物标志物和个人保护能力

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Manifestation of methylmercury (MeHg) toxicity depends on individual susceptibility to MeHg, as well as MeHg burden level. Therefore, biomarkers that reflect the protective capacity against MeHg are needed. The critical role of oxidative stress in the pathogenesis of MeHg cytotoxicity has been demonstrated. Because MeHg has high affinity for selenohydryl groups, sulfhydryl groups, and selenides, and causes posttranscriptional defects in selenoenzymes, proteins with selenohydryl and sulfhydryl groups should play a critical role in mediating MeHg-induced oxidative stress. Here, plasma oxidative stress markers and selenoproteins were investigated in MeHg-intoxicated rats showing neuropathological changes after 4 weeks of MeHg exposure. The thiol antioxidant barrier (-SHp) level significantly decreased 2 weeks after MeHg exposure, which is an early stage at which no systemic oxidative stress, histopathological changes, or clinical signs were detected. Diacron reactive oxidant metabolite (d-ROM) levels significantly increased 3 weeks after MeHg exposure, indicating the occurrence of systemic oxidative stress. Rats treated with lead acetate or cadmium chloride showed no changes in levels of -SHp and d-ROM. Selenoprotein P1 abundance significantly decreased in MeHg-treated rats, whereas it significantly increased in rats treated with Pb or Cd. Plasma selenium-dependent glutathione peroxidase (GPx3) activity also significantly decreased after MeHg exposure, whereas plasma non-selenoenzyme glutathione reductase activity significantly increased in MeHg-treated rats. The results suggest that decreased capacity of -SHp and selenoproteins (GPx3 and selenoprotein P) can be useful biomarkers of ongoing MeHg cytotoxicity and the individual protective capacity against the MeHg body burden.
机译:甲基汞(MeHg)毒性的表现取决于个人对MeHg的易感性以及MeHg的负荷水平。因此,需要反映针对MeHg的保护能力的生物标记。已证明氧化应激在MeHg细胞毒性发病机理中的关键作用。由于MeHg对硒代氢基,巯基和硒化物具有很高的亲和力,并引起硒代酶的转录后缺陷,因此具有硒代氢基和巯基的蛋白质应在介导MeHg诱导的氧化应激中起关键作用。在这里,在MeHg中毒的大鼠中研究了血浆氧化应激标志物和硒蛋白,显示了MeHg暴露4周后神经病理学改变。甲基汞暴露后2周,硫醇抗氧化剂屏障(-SHp)水平显着降低,这是一个早期阶段,在此阶段未检测到全身性氧化应激,组织病理学变化或临床体征。 MeHg暴露后3周,Diacron反应性氧化剂代谢产物(d-ROM)含量显着增加,表明发生了全身性氧化应激。用醋酸铅或氯化镉处理的大鼠的-SHp和d-ROM水平无变化。硒蛋白P1的丰度在用MeHg治疗的大鼠中显着降低,而在用Pb或Cd治疗的大鼠中则明显升高。 MeHg暴露后,血浆硒依赖性谷胱甘肽过氧化物酶(GPx3)活性也显着降低,而在MeHg治疗的大鼠中血浆非硒代酶谷胱甘肽还原酶活性显着增加。结果表明,-SHp和硒蛋白(GPx3和硒蛋白P)的能力下降可能是正在进行的MeHg细胞毒性和对MeHg身体负担的个体保护能力的有用生物标志物。

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