BPB Reports

Paper Details

BPB Reports
Vol. 5 No. 4 p.74-79 2022
Report
Effects of the Interplay between Selenocystine and Methylmercury on Their Cytotoxicity and Glucose-Driven Insulin Secretion from Mouse Insulinoma Cells
  • Takashi Toyama (Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical Sciences, Tohoku University / takashi.toyama.c6@tohoku.ac.jp)
  • Yoshiro Saito (Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical Sciences, Tohoku University / yoshiro.saito.a8@tohoku.ac.jp)
Daichi Chida , Takashi Toyama , Takanori Chiba , Takayuki Kaneko , Kotoko Arisawa , Yoshiro Saito
Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical Sciences, Tohoku University
Received: April 26, 2022;   Accepted: June 27, 2022;   Released: July 12, 2022
Keywords: Selenocystine, Methylmercury, Diabetes
Abstracts

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