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.
Highlights
Mercury, a toxic heavy metal and a widespread environmental pollutant, poses a serious health hazard [1,2]
The expression of Bcl-2, Mcl-1, and Mdm-2 were showed an obvious decreased (Figure 3A), while that of p53 dramatically increased; these changes were accompanied by a marked up-regulation of caspase-3 and caspase-7 gene expression levels in the isolated islets of mice exposed to MeHgCl or HgCl2. These results indicate that exposure to mercuric compounds in vivo can cause injury to pancreatic islets, leading to a pathophysiological state associated with apoptosis
The growing studies have shown that the toxicological effects of MeHgCl (2–26 mg/kg/day) or HgCl2 (5–10 mg/kg/day) induced by long-term exposure within the cerebral cortex, liver, kidney, and lung of experimental animals were accompanied by a significant production of reactive oxygen species (ROS) [24,25,26,27]
Summary
A toxic heavy metal and a widespread environmental pollutant, poses a serious health hazard [1,2]. Mercury is normally present in 3 forms-elemental mercury (Hg0), inorganic mercury (Hg2+ and Hg+), and organic mercury (methylmercury, MeHg)-all of which can produce varying degrees of toxic effects in many organs or systems. These effects include cardiovascular disease, endocrine system disruption, neurotoxicity, and immunotoxicity [3,4,5]. The organic form of mercury, MeHg, causes an irreversible neurotoxic disorder in mammals through biotransformation in the food chain, such as consumption of contaminated fish, seafood, and aquatic mammals [6,7]. The pancreatic islet cells destroyed and an increased incidence of diabetes mellitus (DM) was found in patients with Minamata disease (MeHg poisoning) in Japan [8,9] The study of Shigenaga [10] found that repeated treatment of rats with
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