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Mercury exposure, epigenetic alterations, and brain tumorigenesis: A possible relationship?
Current Medicinal Chemistry ( IF 4.1 ) Pub Date : 2020-11-30 , DOI: 10.2174/0929867326666190930150159
Geir Bjørklund 1 , Lyudmila Pivina 2, 3 , Maryam Dadar 4 , Yuliya Semenova 2, 3 , Salvatore Chirumbolo 5, 6 , Jan Aaseth 7, 8
Affiliation  

The risk assessment of mercury (Hg), in both wildlife and humans, represents an increasing challenge. Increased production of Reactive Oxygen Species (ROS) is a known Hg-induced toxic effect, which can be accentuated by other environmental pollutants and by complex interactions between environmental and genetic factors. Some epidemiological and experimental studies have investigated a possible correlation between brain tumors and heavy metals. Epigenetic modifications in brain tumors include aberrant activation of genes, hypomethylation of specific genes, changes in various histones, and CpG hypermethylation. Also, Hg can decrease the bioavailability of selenium and induce the generation of reactive oxygen that plays important roles in different pathological processes. Modification of of metals can induce excess ROS and cause lipid peroxidation, alteration of proteins, and DNA damage. In this review, we highlight the possible relationship between Hg exposure, epigenetic alterations, and brain tumors.



中文翻译:

汞暴露,表观遗传学改变和脑肿瘤发生:可能的关系?

野生动植物和人类中汞(Hg)的风险评估都代表着日益严峻的挑战。活性氧(ROS)产量的增加是已知的汞诱导的毒性作用,其他环境污染物以及环境和遗传因素之间的复杂相互作用会加剧这种活性。一些流行病学和实验研究已经研究了脑肿瘤和重金属之间的可能相关性。脑肿瘤的表观遗传修饰包括基因异常激活,特定基因的低甲基化,各种组蛋白的变化以及CpG甲基化。此外,汞会降低硒的生物利用度并诱导活性氧的生成,而活性氧在不同的病理过程中起着重要的作用。金属的修饰会诱导过量的ROS并引起脂质过氧化,蛋白质改变和DNA损伤。在这篇综述中,我们强调了汞暴露,表观遗传学改变和脑肿瘤之间的可能关系。

更新日期:2020-11-25
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