A marked increase in erythrocyte PMRS activity was observed

A marked increase in erythrocyte PMRS activity was observed in HgCl2 challenged rats as compared to control (P<0.0001) (Fig. 5), in contrast, no significant activation of erythrocyte PMRS activity were observed when treated alone with onion, catechin and quercetin (Fig. 5A). A significant decrease in the PMRS activity was observed in HgCl2 challenged rats when co-treated with onion extract (P<0.001), catechin or quercetin (P<0.0001) compared to HgCl2 group (Fig. 5B).
Discussion Oxidative stress is a deleterious condition that occurs when there is damage to cellular components, including proteins, lipids, and DNA [6]. Mercuric chloride (HgCl2) is one of the most toxic forms of mercury and once absorbed into blood stream combines with proteins in the plasma or enters the red orexin manufacturer [14]. Previous studies have shown that mercuric chloride toxicity in rats results in the production of reactive oxygen species (ROS) which in turn generates oxidative stress [9]. In the present study, our observation of a marked reduction in body weight of rat exposed to HgCl2 after 30 days is supported by previous published report [15]. Weight loss is known to be the basic aspect of mercury toxicity and has been attributed to reduced food intake. The antioxidant capacity of plasma is the primary measure and a reliable marker to evaluate the extent of oxidative stress in induced pathological events. The present study demonstrates a decrease in antioxidant capacity in terms of FRAP value in mercuric chloride treated rats, however supplementation with flavonoids caused improvement of antioxidant potential in HgCl2 treated rats. The results are in agreement with a previous report which shows that oral administration of flavonoids (quercetin) enhanced the antioxidative ability of rat plasma, indicating that conjugated metabolites participate in the antioxidant defence [16]. Lipid peroxidation (LPO) is the process of oxidative degradation of polyunsaturated fatty acids and its occurrence in biological membranes causes impaired membrane function, structural integrity, decrease in membrane fluidity and inactivation of several membrane bound enzymes [17]. Under oxidative stress, the erythrocyte membrane is prone to lipid peroxidation that involves cleavage of polyunsaturated fatty acids at their double bonds, leading to the formation of MDA; an increased MDA content is an important indicator of lipid peroxidation. Increased level of MDA in erythrocyte has been reported in many disease conditions which are accompanied with oxidative stress [17]. In this study, HgCl2 treatment increased lipid peroxidation by generating free radicals. This toxicity may be due to mercury-induced alterations in membrane integrity via the formation of reactive oxygen species by successive hydroperoxide formation and β cleavage of polyunsaturated fatty acids in vivo or due to perturbation of antioxidant defense mechanisms. Reduced glutathione (GSH) is a primary intracellular antioxidant present in almost all living cells including erythrocytes, which is considered as a biomarker of redox imbalance at cellular level. The glutathione antioxidant system plays a fundamental role in cellular defence against reactive free radicals and other oxidant species. GSH depletion has been shown to intensify lipid peroxidation and predispose cells to oxidant damage [17]. A significant (P<0.001) (Fig. 5B) depletion of erythrocyte GSH in HgCl2 treated rats demonstrates that a condition of oxidative stress prevails in rats as a result of mercury toxicity. A single Hg ion can bind to and cause irreversible excretion of up to two GSH molecules. The reason being that mercury has strong affinity for thiol (SH) binding groups, especially on endogenous biomolecules [18]. Released Hg ions form complexes with GSH thereby disturbing its metabolism [14]. As a result of binding of mercury to glutathione and subsequent elimination of intracellular glutathione, levels of GSH are lowered in the cell which manifests as decrease in the antioxidant potential of the cell.