Mercuric Compounds Induce Pancreatic Islets Dysfunction and Apoptosis in Vivo

doi:10.3390/ijms131012349

CSMUIR > College of Health Care and Management > School of Occupational Safety and Health > Journal paper > Item 310902500/20318

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/20318

Title:	Mercuric Compounds Induce Pancreatic Islets Dysfunction and Apoptosis in Vivo
Authors:	Chen, Kuo-Liang;Liu, Shing-Hwa;Su, Chin-Chuan;Yen, Cheng-Chieh;Yang, Ching-Yao;Lee, Kuan-I;Tang, Feng-Cheng;Chen, Ya-Wen;Lu, Tien-Hui;Su, Yi-Chang;Huang, Chun-Fa
Keywords:	mercuric compounds;pancreatic islets;oxidative stress;apoptosis
Date:	2012-10
Issue Date:	2019-08-15T08:36:40Z (UTC)
Publisher:	International journal of molecular sciences
ISSN:	1422-0067
Abstract:	Mercury is a toxic heavy metal that is an environmental and industrial pollutant throughout the world. Mercury exposure leads to many physiopathological injuries in mammals. However, the precise toxicological effects of mercury on pancreatic islets in vivo are still unclear. Here, we investigated whether mercuric compounds can induce dysfunction and damage in the pancreatic islets of mice, as well as the possible mechanisms involved in this process. Mice were treated with methyl mercuric chloride (MeHgCl, 2 mg/kg) and mercuric chloride (HgCl2, 5 mg/kg) for more than 2 consecutive weeks. Our results showed that the blood glucose levels increased and plasma insulin secretions decreased in the mice as a consequence of their exposure. A significant number of TUNEL-positive cells were revealed in the islets of mice that were treated with mercury for 2 consecutive weeks, which was accompanied by changes in the expression of the mRNA of anti-apoptotic (Bcl-2, Mcl-1, and Mdm-2) and apoptotic (p53, caspase-3, and caspase-7) genes. Moreover, plasma malondialdehyde (MDA) levels increased significantly in the mice after treatment with mercuric compounds for 2 consecutive weeks, and the generation of reactive oxygen species (ROS) in the pancreatic islets also markedly increased. In addition, the mRNA expression of genes related to antioxidation, including Nrf2, GPx, and NQO1, were also significantly reduced in these islets. These results indicate that oxidative stress injuries that are induced by mercuric compounds can cause pancreatic islets dysfunction and apoptosis in vivo.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/20318
Relation:	International journal of molecular sciences, vol. 13, issue 10, 12349-12366
Appears in Collections:	[School of Occupational Safety and Health] Journal paper

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