Klaper Rebecca, Rees Christopher B, Drevnick Paul, Weber Daniel, Sandheinrich Mark, Carvan Michael J
Great Lakes WATER Institute, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin, USA.
Environ Health Perspect. 2006 Sep;114(9):1337-43. doi: 10.1289/ehp.8786.
Methylmercury (MeHg) is a known neurotoxic agent, but the mechanisms by which MeHg may act on reproductive pathways are relatively unknown. Several studies have indicated potential changes in hormone levels as well as declines in vertebrates with increasing dietary MeHg exposure.
The purpose of this study was to identify alterations in gene expression associated with MeHg exposure, specifically those associated with previously observed changes in reproduction and reproductive biomarkers. Fathead minnows, Pimephales promelas, were fed one of three diets that were similar to documented concentrations of MeHg in the diets of wild invertivorous and piscivorous fish. We used a commercial macroarray in conjunction with quantitative polymerase chain reaction to examine gene expression in fish in relation to exposure to these environmentally relevant doses of MeHg.
Expression of genes commonly associated with endocrine disruption was altered with Hg exposure. Specifically, we observed a marked up-regulation in vitellogenin mRNA in individual Hg-exposed males and a significant decline in vitellogenin gene expression in female fish with increasing Hg concentrations. Other genes identified by the macroarray experiment included those associated with egg fertilization and development, sugar metabolism, apoptosis, and electron transport. We also observed differences in expression patterns between male and female fish not related to genes specifically associated with reproduction, indicating a potential physiological difference in the reaction of males and females to MeHg.
Gene expression data may provide insight into the mechanisms by which MeHg affects reproduction in fish and indicate how MeHg differs in its effect from other heavy metals and endocrine-disrupting compounds.
甲基汞(MeHg)是一种已知的神经毒性剂,但其作用于生殖途径的机制相对未知。多项研究表明,随着膳食中甲基汞暴露量增加,脊椎动物的激素水平可能发生变化,生殖能力也会下降。
本研究旨在确定与甲基汞暴露相关的基因表达变化,特别是那些与先前观察到的生殖和生殖生物标志物变化相关的基因表达变化。将黑头软口鲦(Pimephales promelas)喂食三种饮食中的一种,这三种饮食的甲基汞浓度与野生食虫和食鱼鱼类饮食中记录的浓度相似。我们使用商业宏阵列结合定量聚合酶链反应来检测鱼类中与这些环境相关剂量的甲基汞暴露相关的基因表达。
与内分泌干扰相关的常见基因的表达随着汞暴露而改变。具体而言,我们观察到暴露于汞的雄性个体中卵黄蛋白原mRNA显著上调,而随着汞浓度增加,雌性鱼类中卵黄蛋白原基因表达显著下降。宏阵列实验鉴定的其他基因包括与卵子受精和发育、糖代谢、细胞凋亡和电子传递相关的基因。我们还观察到雄性和雌性鱼类之间的表达模式差异,这些差异与并非专门与生殖相关的基因无关,这表明雄性和雌性对甲基汞的反应可能存在生理差异。
基因表达数据可能有助于深入了解甲基汞影响鱼类生殖的机制,并表明甲基汞在其作用效果上与其他重金属和内分泌干扰化合物有何不同。