Effects of Essential Trace Elements and Oxidative Stress on Endemic Arsenism Caused by Coal Burning in PR China.

Abstract

Few studies have investigated the association between essential trace elements and oxidative stress in environmental media and populations with endemic arsenism caused by coal burning. Element contents and oxidative stress indicators were measured. Moreover, the expression of genes related to the nuclear factor E2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1)-antioxidant response element (ARE) signaling pathway and Nrf2-ARE binding ability is detected. The results show that the contents of arsenic, copper, iron, and chromium were increased in environmental media from the arsenism area compared with the control area; however, the selenium content decreased. The arsenic, iron, chromium, and copper contents and the copper/zinc ratio were also increased in the arsenic-exposed population; however, the selenium content decreased. The results also show that the concentrations of arsenic, iron, and chromium and the copper/zinc ratio increased gradually with the severity of arsenism. However, selenium concentrations decreased gradually with the severity of arsenism. The contents of malondialdehyde, 8-hydroxyldeoxyguanosine, and protein carbonyl in plasma increased, while the levels of sulfhydryl, thioredoxin reductase (TrxR), glutathione peroxidase (Gpx), and superoxide dismutase 1 (SOD1) decreased. The mRNA expression of Keap1 and TrxR1 decreased in the blood, while the mRNA expression of Nrf2, GPx1, and SOD1 increased. Moreover, the Nrf2 protein content and Nrf2-ARE binding ability increased, and the Keap1 protein content decreased. In conclusion, our data suggest that the increased arsenic content in environmental media and populations was accompanied by abnormal levels of essential trace elements. Insufficient selenium intake, copper, and chromium overload and a high copper/zinc ratio might be some of the causes of arsenism, which might be related to the Nrf2/Keap1-ARE signaling pathway.