Effects of the Interplay between Selenocystine and Methylmercury on Their Cytotoxicity and Glucose-Driven Insulin Secretion from Mouse Insulinoma Cells

We’ve previously shown that high levels of selenoprotein P (SeP), a major in plasma, can be risk factor type 2 diabetes. It was also thought inhibition insulin secretion caused by over-supplementation selenium SeP to pancreatic β cells contributed the progress On other hand, methylmercury, which is an environmental pollutant, known cancel action via covalent modification. Therefore, we interaction between and methylmercury could associated with pathogenesis To address hypothesis, MIN6 cells, mouse β-cell line, were treated selenocystine (as donner) then examined release from cells. Selenocystine (400–1200 nM), corresponds concentration diabetic patients, shows cytotoxicity inhibited glucose-driven secretion. Methylmercury rescued induced selenocystine, however it affected depressed at little intense. These data indicate mechanisms underlying are independent cytotoxicity, cannot expected restore or suppress diabetes as neutlizer.