Abstract
Diabetes Mellitus (DM) is a condition of hyperglycemia due to defects of insulin secretion and/or insulin action. Toxic metals such as lead, nickel, cadmium, arsenic and mercury have been identified which accumulate in various biological samples from T2D (type 2 diabetes) patients through environmental pollution and food chain. Present study will elucidate the toxicological effects of mercury (II) chloride in the pancreatic islets and liver tissues of rat which leads to dysfunction and degeneration of pancreatic islets and liver. Photomicrograph of histology of treated pancreas exhibited the disruption of islets, disorientation of cells and disruption of connective tissue septa. In mercury (II) chloride treated group pancreatic cells were found to be pyknotic and cellular death was confirmed by membrane rupture and necrosis. Alteration of blood glucose levels were observed by glucose tolerance test. The liver sections of rats treated with mercury (II) chloride showed modification in the structure of this organ. Treated liver showed lower periodic acid/Schiff response. In this study, changes in the architecture of pancreatic islets as well as liver may be the reason behind diabetes.
Highlights
Mercury is an environmental pollutant which produces health hazard (Marx, 2002; Ratcliffe et al, 1996)
Trypan blue (TB) positive response was noticed in majority of treated pancreatic cells (Fig. 1E)
Recent study evidenced that mercuric compounds (MeHgCl and HgCl2) caused pancreatic islet dysfunction by apoptosis [increasing apoptotic (p53, caspase-3) related gene expressions] and Reactive Oxygen Species (ROS) generation in treated mice (Chen et al, 2012)
Summary
Mercury is an environmental pollutant which produces health hazard (Marx, 2002; Ratcliffe et al, 1996).
Published Version
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