Arsenite-induced transgenerational glycometabolism is associated with up-regulation of H3K4me2 via inhibiting spr-5 in caenorhabditis elegans.

Arsenic (As) is a toxic element that is highly abundant in the environment. However, there has not been sufficient research into the mechanisms of arsenic-induced transgenerational effects. In biomedical and environmental toxicology research field, C. elegans are often used as the ideal model. In this study, F0 generation animals were cultured with arsenite, while subsequent generations animals (F1 - F6) were cultured in the absence of arsenic. Experiments were performed to examine the transgenerational glycometabolism and the associated mechanisms in all seven generations (F0 - F6) of C. elegans. Results show that arsenite exposure increased total glucose content but reduced glucose metabolites in F0 generation C. elegans. The total glucose content was also elevated in subsequent generations probably due to transgenerational downregulation of fgt-1. In addition, arsenite exposure induced transgenerational downregulation of histone demethyltransferase spr-5 and elevated histone dimethylation in F0 generation. This study highlights that single generation exposure to arsenite causes transgenerational changes in glycometabolism in C. elegans, which may be caused by downregulation of spr-5 and elevation of H3K4me2.