Laboratorio de Toxicología Molecular, Centro de Investigación Aplicada en Ambiente y Salud (CIAAS), Coordinación para la Innovación y Aplicación de la Ciencia y la Tecnología (CIACYT), Universidad Autónoma de San Luis Potosí, Avenida Sierra Leona No. 550, Colonia Lomas Segunda Sección, 78210, San Luis Potosi, SLP, Mexico.
Facultad de Medicina, Universidad Autónoma de San Luis Potosí, San Luis Potosi, Mexico.
Environ Sci Pollut Res Int. 2017 Dec;24(36):28036-28045. doi: 10.1007/s11356-017-0367-6. Epub 2017 Oct 6.
Recently, a great number of epidemiological studies have shown evidence that exposure to inorganic arsenic could have harmful effects on the cardiovascular system of humans. However, the underlying mechanisms through which arsenic induces cardiovascular toxic effects remain unclear. In this regard, epigenetic mechanisms have emerged as a probable connection between environment and disease phenotypes, including cardiovascular diseases. Therefore, this study aimed to evaluate epigenetic changes related to cardiotoxicity (miR-126 and miR-155 expression levels) in children from San Luis Potosi, Mexico exposed to inorganic arsenic. From 2014 to 2015, in a cross-sectional study, children (aged 6-12 years; n = 73) attending public schools at the studied sites were enrolled to take part in this study. Urinary arsenic was used as an exposure biomarker and analyzed by an atomic absorption spectrophotometry technique. On the other hand, miR-126 and miR-155 expression levels were evaluated by qRT-PCR. A mean urinary arsenic level of 30.5 ± 25.5 μg/g of creatinine was found. Moreover, the data showed a significant negative association (p < 0.05) between urinary arsenic concentrations and plasma miR-126 levels. However, an association between urinary arsenic concentrations and plasma miR-155 levels was not found (p > 0.05). In this regard, some investigations have shown an association between diminished plasma miR-126 levels and cardiovascular illnesses. The results found in this study are of concern. However, more similar studies including a larger sample size are necessary in order to clarify the real significance of the data.
最近，大量的流行病学研究表明，接触无机砷可能对人类的心血管系统造成有害影响。然而，砷诱导心血管毒性作用的潜在机制仍不清楚。在这方面，表观遗传机制已成为环境与疾病表型（包括心血管疾病）之间的可能联系。因此，本研究旨在评估暴露于无机砷的墨西哥圣路易斯波托西儿童的心脏毒性相关的表观遗传变化（miR-126 和 miR-155 表达水平）。在 2014 年至 2015 年期间，进行了一项横断面研究，在研究地点的公立学校中招募了年龄在 6-12 岁的儿童（n=73）参加这项研究。将尿砷作为暴露生物标志物，并采用原子吸收分光光度法进行分析。另一方面，通过 qRT-PCR 评估 miR-126 和 miR-155 的表达水平。发现平均尿砷水平为 30.5±25.5μg/g 肌酐。此外，数据显示尿砷浓度与血浆 miR-126 水平之间存在显著负相关（p<0.05）。然而，未发现尿砷浓度与血浆 miR-155 水平之间存在关联（p>0.05）。在这方面，一些研究表明血浆 miR-126 水平降低与心血管疾病之间存在关联。本研究的结果令人担忧。然而，为了澄清数据的真正意义，需要进行更多类似的研究，包括更大的样本量。
