Effect of Oxidative Stress on Secretory Function in Salivary Gland Cells

Abstract

Reactive oxygen species (ROS) such as superoxide radical anion, singlet oxygen, hydrogen peroxide and hydroxyl radical are products of oxidative metabolism (Kourie, 1998). Low levels of ROS contribute to important signaling pathways to regulate key biological responses, including cell migration, mitosis and apoptosis (Goldschmidt-Clermont & Moldovan, 1999). For instance, endogenous oxidants protected the vasculature by inhibiting endothelial exocytosis that would otherwise lead to vascular inflammation and thrombosis, because endogenous hydrogen peroxide inhibited thrombin-induced exocytosis of granules from endothelial cells (Matsushita et al., 2005). In rat aortic smooth muscle cells, reduction in the intracellular concentration of hydrogen peroxide by the overexpression of catalase within cellular peroxisomes resulted in suppression of DNA synthesis and cell proliferation, and induction of apoptotic cell death (Brown et al., 1999). On the other hand, ROS are known to be pathogenic factors that induce cellular alterations in different cell types. For example, ROS are considered to be involved in the pathogenesis of postischemic endothelial dysfunction, because hydrogen peroxide induces Ca2+ oscillations in human aortic endothelial cells (Hu et al., 1998). In pancreatic ┚ cells, hydrogen peroxide interferences glucose metabolism, which leads to the inhibition of insulin secretion (Krippeit-Drews et al., 1999). In mesangial cells, hydrogen peroxide disturbs Ca2+ mobilization, which is considered to be involved in renal injury (Meyer et al., 1996). In neurons, hydrogen peroxide induces apoptotic cell death (Whittemore et al., 1995).