Departamento de Biología Celular y Ultraestructura, Centro de Investigación Biomédica, Facultad de Medicina, Universidad Autónoma de Coahuila Unidad Torreón, Gregorio A. García No. 198 sur. Colonia centro, Torreón, Coahuila, CP 27000, México.
Centro de Investigación Biomédica del Noreste, Instituto Mexicano del Seguro Social, Monterrey, Nuevo León, Mexico.
Sci Rep. 2021 Apr 15;11(1):8276. doi: 10.1038/s41598-021-87677-y.
An emerging concern is the influences of early life exposure to environmental toxicants on offspring characteristics in later life. Since recent evidence suggests a transgenerational transference of aberrant phenotypes from exposed-parents to non-exposed offspring related to adult-onset diseases including reproductive phenotype. The transgenerational potential of arsenic a well know genotoxic and epigenetic modifier agent has not been assessed in mammals until now. In this experimental study, we evaluated the transgenerational effects of arsenic in a rat model with chronic exposure to arsenic. Rats chronically exposed to arsenic in drinking water (1 mg AsO/mL) (F0) were mated to produce the arsenic lineage (F1, F2, and F3). The arsenic toxic effects on were evaluated over the four generations by analyzing the DNA methylation percentage, genotoxicity in WBC and physical and reproductive parameters, including sperm quality parameters and histopathological evaluation of the gonads. Chronic exposure to arsenic caused genotoxic damage (F0-F3) different methylation patterns, alterations in physical and reproductive parameters, aberrant morphology in the ovaries (F0 and F1) and testicles (F1-F3), and a decrease in the quality of sperm (F0-F3, except F2). Parental chronic arsenic exposure causes transgenerational genotoxicity and changes in global DNA methylation which might be associated with reproductive defects in rats. Combined with recent studies reveal that disturbances in the early life of an individual can affect the health of later generations.
一个新出现的问题是，早期暴露于环境毒物会对后代后期的特征产生影响。由于最近的证据表明，暴露于父母的异常表型会通过代际传递给未暴露的后代，与包括生殖表型在内的成年发病疾病有关。砷作为一种众所周知的遗传毒性和表观遗传修饰剂，其在哺乳动物中的代际潜力直到现在才得到评估。在这项实验研究中，我们评估了砷在慢性接触砷的大鼠模型中的代际效应。大鼠长期通过饮用水（1mg AsO/mL）暴露于砷（F0），然后进行交配，产生砷系（F1、F2 和 F3）。通过分析 DNA 甲基化百分比、白细胞的遗传毒性以及身体和生殖参数，包括精子质量参数和性腺的组织病理学评估，评估了砷在四代中的毒性作用。慢性砷暴露（F0-F3）引起遗传毒性损伤、不同的甲基化模式、身体和生殖参数的改变、卵巢（F0 和 F1）和睾丸（F1-F3）的形态异常，以及精子质量下降（F0-F3，除了 F2）。父母慢性砷暴露会导致代际遗传毒性和全基因组 DNA 甲基化的改变，这可能与大鼠的生殖缺陷有关。结合最近的研究表明，个体早期的干扰可能会影响后代的健康。
