Selenium Supplementation Protects Against Arsenic-Trioxide-Induced Cardiotoxicity Via Reducing Oxidative Stress and Inflammation Through Increasing NAD+ Pool.

Arsenic is an environmental contaminant, and accumulating evidence has indicated that exposure to arsenic can cause various diseases, especially cardiotoxicity. Selenium (Se) exerts a vital role in the regulation of multiple physiological activities. Recently, several studies highlighted that Se treatment can effectively antagonize the toxic effects induced by arsenic. However, the exact underlying effect and mechanism of Se on Arsenic-induced cardiotoxicity has not been explored. In the current study, the arsenic trioxide (ATO)-triggered heart damage mice model was used to explore whether Se exerts protective roles in ATO-related cardiotoxicity and its potential mechanism. Our data showed that Se treatment significantly alleviated ATO-mediated cardiotoxicity evidenced by increased weight, decreased myocardial damage markers, and improved heart functions in mice. Furthermore, we demonstrated that Se remarkably inhibited ATO-mediated oxidative stress and inflammatory responses in heart tissues. Mechanistically, we showed that Se upregulated the levels of NAD+ in cardiomyocytes of the mice challenged by ATO, and this effect involved in the activation of the NAD+ biosynthesis through the salvage pathway. Collectively, our findings demonstrated that Se protected against ATO-mediated cardiotoxicity by antioxidant and anti-inflammatory effects via increasing the NAD+ pool in mice.

Selenium Attenuates Doxorubicin-Induced Cardiotoxicity Through Nrf2-NLRP3 Pathway.

Selenium (Se), an essential nutrient for humans, has been reported to possess cardioprotective effect. However, the protective effects of Se against doxorubicin (DOX)-induced cardiotoxicity and the underlying mechanism are rarely reported. In this study, we sought to explore whether Se protected against DOX-induced cardiotoxicity by inhibiting Nrf2-NLRP3 pathway. We found that Se treatment effectively alleviated DOX-induced myocardial dysfunctions, decreasing plasma markers associated with myocardial injury. Moreover, Se treatment significantly inhibited DOX-induced oxidative damages and pro-inflammatory cytokine expression in heart tissues. Furthermore, Se treatment markedly promoted the expression of Nrf2 and prevented the activation of NLRP3 inflammasome. Importantly, suppression of Nrf2 abolished the cardioprotective effects of Se and diminished the inhibition of Se on NLRP3 inflammasome. Collectively, our study demonstrated that Se might protect against DOX-induced cardiotoxicity via regulating Nrf2-NLRP3 pathway. Se supplementation may be a potential therapeutic strategy to protect against DOX-induced cardiac injury.

Effects of habitat fragmentation on the population genetic diversity of the Amur minnow (Phoxinus lagowskii).

Phoxinus lagowskii is a freshwater fish that is widely distributed in China. In this study, a comparative analysis of the mtDNA control region (D-loop) was performed to analyze the natural population structure and genetic diversity of 54 individuals from eleven locations (T1, T2, T3, T4, T5, T6, T7, T8, T9, T10 and T11) which was divided with reservoirs. The estimated haplotype and nucleotide diversity were 0.734 and 0.03514, respectively. An AMOVA indicated that 79.78% of the total variation originated from individual populations and 20.22% came from variation within the 11 geographic populations, which showed high genetic differentiation among the 11 geographic groups. A test of neutral evolution and mismatch distribution indicated that historical expansion occurred in these populations. However, the findings of low genetic diversity and high genetic differentiation demonstrated that the reproduction isolated by reservoir has showed a certain effect for the development of the populations, and the results should provide new information for the conservation and exploitation of this species.