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https://www.selleckchem.com/products/dyngo-4a.html The wide range of industrial applications of chromium (Cr) has led to an increasing risk of water contamination by Cr(Ⅵ). However, efficient methods to remove or decrease the toxicity of Cr(Ⅵ) in situ are lacking. The main aim of this study was to investigate the mechanisms by which selenite alleviates chromium(Ⅵ)-induced toxicity in Chlamydomonas reinhardtii. Our results showed that K2Cr2O7 had toxic effects on both the structure and physiology of C. reinhardtii in a dose-dependent manner. Adding selenite significantly alleviated chromium accumulation and toxicity in cells. RNA-seq data showed that the expression level of selenoproteins such as SELENOH was significantly increased. Both SELENOH-amiRNA knockdown mutants and selenoh insertional mutant produced more reactive oxygen species (ROS) and grew slower than the wild type, suggesting that SELENOH can reduce chromium toxicity by decreasing the levels of ROS produced by Cr(Ⅵ). We also demonstrated that selenite can reduce the absorption of Cr(Ⅵ) by cells but does not affect the process of Cr(Ⅵ) adsorption and efflux. This information on the molecular mechanism by which selenite alleviates Cr(Ⅵ) toxicity can be used to increase the bioremediation capacity of algae and reduce the human health risks associated with Cr(Ⅵ) toxicity.Prior human studies have explored effects of phthalate exposures on thyroid function, but the underlying biological mechanisms remain poorly unclear. We aimed to explore the associations between phthalate exposures and thyroid function among a potentially susceptible population such as patients with thyroid nodules, and further to assess the mediating role of oxidative stress. We measured eight phthalate metabolites, three oxidative stress biomarkers [8-hydroxy-2-deoxyguanosine (8-OHdG), 8-iso-prostaglandin F2α (8-isoPGF2α) and 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)] in urine and three thyroid function biomarkers [thyroid-stimulating

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