Two arsenicals induce apoptosis of islet cells

doi:10.3969/j.issn.2095-4344.2014.51.016

Abstract

Abstract:

BACKGROUND: In recent years, epidemiological data show an association between arsenic exposure and diabetes mellitus.

OBJECTIVE: To investigate the underlying mechanism of arsenic-induced apoptosis in pancreatic β cells to elucidate the pathogenesis of arsenic-related diabetes.

METHODS: Rat pancreatic β cells (INS-1) were treated with sodium arsenate (iAs⁵⁺) (50, 100, 200 µmol/L) and dimethylarsinic acid (DMA⁵⁺) (100, 200, 400 µmol/L) for 24 or 48 hours. The cytotoxicity of arsenic was detected by MTT assay in INS-1 cells. The arsenic-induced apoptosis was detected by Annexin V-FITC/PI and Hoechst33258 staining. The intracellular reactive oxygen species level was detected by 2’,7’-dichlorofluorescein staining. The P53 expression level was detected by western blot.

RESULTS AND CONCLUSION: iAs⁵⁺ (> 50 µmol/L), DMA⁵⁺ (> 100 µmol/L) reduced the INS-1 cell viability (P < 0.05, P < 0.01); after treating with iAs⁵⁺ (50-200 µmol/L) and DMA⁵⁺(100-400 µmol/L) for 48 hours, both arsenic compounds induced apoptosis in INS-1 cells. The intracellular reactive oxygen species level increased in a concentration-dependent manner (P < 0.05, P < 0.01), after treating with iAs⁵⁺ and DMA⁵⁺ for 24 hours respectively; the nuclear expression level of P53 protein in INS-1 increased after treating with iAs⁵⁺(P < 0.05,P < 0.01); however, DMA⁵⁺ did not increase the P53 level significantly. In summary, both iAs⁵⁺ and DMA⁵⁺ can induce apoptosis in INS-1 cells, which may be related with arsenic-induced rise in intracellular reactive oxygen species.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

全文链接：

Key words: tissue engineering, arsenic, apoptosis, flow cytometry

CLC Number:

R318

Yao Xiao-feng, Wang Fang-fang, Jiang Li-ping, Geng Cheng-yan, Zhong Lai-fu, Zheng Bai-lu, Yang Guang, Sun Xian-ce. Two arsenicals induce apoptosis of islet cells[J]. Chinese Journal of Tissue Engineering Research, 2014, 18(51): 8286-8291.

Figures/Tables 5

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