Alana Castro Panzenhagen , Fernanda dos Santos Petry , Alexsander Alves-Teixeira, Lucas Santos, Flávio Gabriel Carazza-Kessler, Daniel Pens Gelain, José Cláudio Fonseca Moreira
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引用次数: 0
Abstract
The issue of MeHg contamination is a significant concern due to its detrimental impact on the environment. This study aimed to thoroughly investigate the effects of MeHg on neurodevelopmental biomarkers, as there is a lack of systematic reviews in this area. We conducted a comprehensive search of three databases (PubMed, Scopus, and Web of Science) and found 522 records, which were then meticulously reviewed by two independent reviewers. A total of 66 studies were included, with biomarkers related to oxidative stress, neurotransmission, inflammation, epigenetics, and apoptosis being the most prominent. The results of both in vitro and in vivo models indicate that antioxidant enzymes and other oxidative stress-related markers are indeed, altered following MeHg exposure. Moreover, MeHg exposure causes significant disruptions to neurotransmitter levels, activities of neurotransmitter synthesis enzymes, receptor densities, and proteins involved in synaptic function. Proinflammatory biomarkers are consistently overexpressed in both MeHg-treated cells and the brains of exposed rats. Furthermore, studies on DNA methylation and biomarker activity suggest that MeHg exposure may lead to neurotoxicity and neurodevelopmental issues via perturbations to epigenetic markers and the apoptosis pathway.
由于甲基汞对环境的有害影响，甲基汞污染问题备受关注。本研究旨在深入研究甲基汞对神经发育生物标志物的影响，因为该领域缺乏系统性综述。我们对三个数据库（PubMed、Scopus 和 Web of Science）进行了全面检索，共找到 522 条记录，然后由两名独立审稿人对这些记录进行了仔细审阅。共纳入了 66 项研究，其中与氧化应激、神经传递、炎症、表观遗传学和细胞凋亡有关的生物标志物最为突出。体外和体内模型的研究结果表明，接触甲基汞后，抗氧化酶和其他与氧化应激相关的标志物确实发生了改变。此外，接触甲基汞会严重破坏神经递质水平、神经递质合成酶的活性、受体密度以及参与突触功能的蛋白质。经甲基汞处理过的细胞和接触过甲基汞的大鼠大脑中，促炎生物标志物都持续过度表达。此外，对 DNA 甲基化和生物标志物活性的研究表明，接触甲基汞可能会通过扰乱表观遗传标志物和细胞凋亡途径，导致神经毒性和神经发育问题。
期刊介绍：
Food and Chemical Toxicology (FCT), an internationally renowned journal, that publishes original research articles and reviews on toxic effects, in animals and humans, of natural or synthetic chemicals occurring in the human environment with particular emphasis on food, drugs, and chemicals, including agricultural and industrial safety, and consumer product safety. Areas such as safety evaluation of novel foods and ingredients, biotechnologically-derived products, and nanomaterials are included in the scope of the journal. FCT also encourages submission of papers on inter-relationships between nutrition and toxicology and on in vitro techniques, particularly those fostering the 3 Rs.
The principal aim of the journal is to publish high impact, scholarly work and to serve as a multidisciplinary forum for research in toxicology. Papers submitted will be judged on the basis of scientific originality and contribution to the field, quality and subject matter. Studies should address at least one of the following:
-Adverse physiological/biochemical, or pathological changes induced by specific defined substances
-New techniques for assessing potential toxicity, including molecular biology
-Mechanisms underlying toxic phenomena
-Toxicological examinations of specific chemicals or consumer products, both those showing adverse effects and those demonstrating safety, that meet current standards of scientific acceptability.
Authors must clearly and briefly identify what novel toxic effect (s) or toxic mechanism (s) of the chemical are being reported and what their significance is in the abstract. Furthermore, sufficient doses should be included in order to provide information on NOAEL/LOAEL values.
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