Indices of the DNA repair system in the brain of fish as a biomarker of inorganic mercury burden

V. Nedzvetsky, V. Gasso, R. Novitskyi, I. Hasso
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Abstract

Mercury is a widespread heavy metal that causes a stable and prolonged environmental pollution. Low concentrations of inorganic and organic mercury compounds are found in almost all water bodies. The high level of mercury bioaccumulation is a cause of tissue-specific toxicity, including neurotoxicity. Absorbed in nervous tissue mercury can cause brain disorders both in neural and glial cells. The brain of fish is considered one of the most susceptible targets for cytotoxicity of mercury in aquatic ecosystems. Taking into account that different forms of mercury have widespread distribution and exhibit a strong neurotoxic effect, the assessment of mercury cytotoxicity in the brain of fish is relevant and extremely important. Rainbow trout Oncorhynchus mykiss was exposed to mercury chloride in the dose range of 5-20 μg/L for 60 days to study the chronic exposure of low doses. In this paper, we studied the influence of inorganic mercury on oxidative stress, DNA repair proteins – ERCC1 and PARP1 in the trout’s brain. The results obtained have shown that the chronic effect of inorganic mercury causes dose-dependent oxidative stress in the fish brain. In addition, low concentrations of mercury (10 and 20 μg/L) caused a decrease in the content of ERCC1 in the brain of fish. On the contrary, the same doses have caused an increase in PARP1 expression. That is the chronic influence of low concentrations of inorganic mercury has a negative effect in the fish brain. Observed results showed that inorganic mercury has a potential for suppressing DNA repair and, therefore, increases the instability of genome. Thus, ERCC1 and PARP1 can be considered as the sensitive biomarkers of mercury cytotoxicity in the fish brain. A further study of mercury neurotoxicity is needed to find out the hazard of mercury environmental pollution as well as a validation of biomarkers of their impact.
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鱼类脑内DNA修复系统指标作为无机汞负荷的生物标志物
汞是一种广泛存在的重金属,对环境造成稳定和长期的污染。在几乎所有的水体中都发现低浓度的无机和有机汞化合物。高水平的汞生物蓄积是组织特异性毒性的一个原因,包括神经毒性。被神经组织吸收的汞可引起神经细胞和神经胶质细胞的脑部紊乱。鱼类的大脑被认为是水生生态系统中汞细胞毒性最易受影响的目标之一。考虑到不同形式的汞分布广泛,并表现出强烈的神经毒性作用,对鱼类大脑中汞细胞毒性的评估是相关的,也是极其重要的。以虹鳟(Oncorhynchus mykiss)为研究对象,在5 ~ 20 μg/L剂量范围内连续暴露60 d,研究低剂量的慢性暴露。本文研究了无机汞对鳟鱼大脑氧化应激、DNA修复蛋白ERCC1和PARP1的影响。所获得的结果表明,无机汞的慢性效应引起鱼脑剂量依赖性氧化应激。此外,低浓度汞(10和20 μg/L)导致鱼脑ERCC1含量下降。相反,相同剂量会导致PARP1表达增加。即低浓度无机汞的慢性影响对鱼的大脑有负面影响。观察结果表明,无机汞具有抑制DNA修复的潜力,因此增加了基因组的不稳定性。因此,ERCC1和PARP1可以被认为是鱼脑汞细胞毒性的敏感生物标志物。需要进一步研究汞的神经毒性,以发现汞环境污染的危害,并验证其影响的生物标志物。
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