The response of gut microbiota to arsenic metabolism is involved in arsenic-induced liver injury, which is influenced by the interaction between arsenic and methionine synthase.

The drivers of changes in gut microbiota under arsenic exposure and the mechanism by which microbiota affect arsenic metabolism are still unclear. Here, C57BL/6 mice were exposed to 0, 5, or 10 ppm NaAsO in drinking water for 6 months. The results showed that arsenic exposure induced liver injury and increased the abundance of folic acid (FA)/vitamin B12 (VB)- and butyrate-synthesizing microbiota.

Urea cycle promotion via ammonia-upregulated CPS1 is involved in arsenite-induced pulmonary fibrosis through enhancing collagen synthesis.

Arsenic exposure is connected with lung toxicity and is related to lung fibrotic changes. Idiopathic pulmonary fibrosis (IPF) is characterized by extracellular matrix (ECM) deposition. Various genetic mechanisms and environmental factors induce or exacerbate pulmonary fibrosis.

Intrauterine arsenic exposure induces glucose metabolism disorders in adult offspring by targeting TET2-mediated DNA hydroxymethylation reprogramming of HNF4α in developing livers, an effect alleviated by ascorbic acid.

Exposure to arsenic during gestation has lasting health-related effects on the developing fetus, including an increase in the risk of metabolic disease later in life. Epigenetics is a potential mechanism involved in this process. Ten-eleven translocation 2 (TET2) has been widely considered as a transferase of 5-hydroxymethylcytosine (5hmC).

As3MT via consuming SAM is involved in arsenic-induced nonalcoholic fatty liver disease by blocking mA-mediated miR-142-5p maturation.

Arsenic, a common environmental hazard, is a risk factor for nonalcoholic fatty liver disease (NAFLD). However, the mechanism remains unclear. Here, we found that chronic exposure to environmental-related doses of arsenic disturbed fatty acid and methionine metabolism in mice, caused liver steatosis, increased arsenic (3) methyltransferase (As3MT), sterol regulatory element binding protein 1 (SREBP1) and lipogenic gene levels, and decreased N6-methyladenosine (mA) and S-adenosylmethionine (SAM) levels.

SIRT1/PGC-1α is involved in arsenic-induced male reproductive damage through mitochondrial dysfunction, which is blocked by the antioxidative effect of zinc.

Exposure to arsenic poses threats to male reproductive system, including impairing the testes and sperm quality. Although an association regarding arsenic exposure and male reproductive damage has been reported, the undergoing molecular mechanisms and interventions for prevention remain unclear. For the present work, male mice were exposed to 0, 2.

As3MT-mediated SAM consumption, which inhibits the methylation of histones and LINE1, is involved in arsenic-induced male reproductive damage.

Studies have demonstrated that arsenic (As) induces male reproductive injury, however, the mechanism remains unknown. The high levels of arsenic (3) methyltransferase (As3MT) promote As-induced male reproductive toxicity. For As-exposed mice, the germ cells in seminiferous tubules and sperm quality were reduced.

Intrauterine exposure of mice to arsenite induces abnormal and transgenerational glycometabolism.

The adverse, transgenerational effects on health caused by environmental pollutants are receiving increasing attention. For humans and mice, inorganic arsenic (iAs), a widespread environmental contaminant, is associated with diabetic phenotypes. However, the transgenerational effects of arsenite-induced changes in glucose metabolism in mice have not been fully investigated.

Bridging therapy and direct mechanical thrombectomy in the treatment of cardiogenic cerebral infarction with anterior circulation macrovascular occlusion.

Background: Intravenous thrombolysis is an important treatment for cerebral infarction. However, it is difficult to achieve good results if the patient is complicated with anterior circulation macrovascular occlusion. In addition, the vascular recanalization rate is low, so mechanical thrombectomy, that is, bridging therapy, is needed.