| First Author | Lee YS | Year | 2015 |
| Journal | Toxicol Appl Pharmacol | Volume | 284 |
| Issue | 2 | Pages | 254-61 |
| PubMed ID | 25576766 | Mgi Jnum | J:222600 |
| Mgi Id | MGI:5644915 | Doi | 10.1016/j.taap.2014.12.016 |
| Citation | Lee YS, et al. (2015) Sodium meta-arsenite prevents the development of autoimmune diabetes in NOD mice. Toxicol Appl Pharmacol 284(2):254-61 |
| abstractText | Sodium meta-arsenite (SA) is an orally available arsenic compound. We investigated the effects of SA on the development of autoimmune type 1 diabetes. Female non-obese diabetic (NOD) mice were orally intubated with SA (5mg/kg/day) from 8weeks of age for 8weeks. The cumulative incidence of diabetes was monitored until 30weeks of age, islet histology was examined, and lymphocytes including T cells, B cells, CD4+ IFN-gamma+ cells, CD8+ IFN-gamma+ cells, CD4+ IL-4+ cells, and regulatory T cells were analyzed. We also investigated the diabetogenic ability of splenocytes using an adoptive transfer model and the effect of SA on the proliferation, activation, and expression of glucose transporter 1 (Glut1) in splenocytes treated with SA in vitro and splenocytes isolated from SA-treated mice. SA treatment decreased the incidence of diabetes and delayed disease onset. SA treatment reduced the infiltration of immunocytes in islets, and splenocytes from SA-treated mice showed a reduced ability to transfer diabetes. The number of total splenocytes and T cells and both the number and the proportion of CD4+ IFN-gamma+ and CD8+ IFN-gamma+ T cells in the spleen were significantly reduced in SA-treated NOD mice compared with controls. The number, but not the proportion, of regulatory T cells was decreased in SA-treated NOD mice. Treatment with SA either in vitro or in vivo inhibited proliferation of splenocytes. In addition, the expression of Glut1 and phosphorylated ERK1/2 was decreased by SA treatment. These results suggest that SA reduces proliferation and activation of T cells, thus preventing autoimmune diabetes in NOD mice. |
