Essay: The toxicity effect of cadmium chloride

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Cadmium chloride may induce oxidative stress leading to the generation of free radicals and alteration in oxygen free radical scavenging enzyme system or antioxidant and damage membrane structure [1,2]. In the current study, we evaluated the protective role of chitosan nanoparticle against the oxidative stress changes in the gastric tissue resulting from the administration of cadmium chloride in rats. The biochemical mechanisms involved in the gastric toxicity of cadmium chloride were studied by measuring the levels of MDA and by screening the activities of primary antioxidant enzymes such as SOD and GPx. It also gastric tissue samples was investigated for histopathological studies and inhibition of gastric ulcer.
 
These results showed that cadmium chloride administration significantly decreased the SOD, GPx and increased MDA levels. Cadmium chloride also increased ulcer index and altered histopathological gastric compared to the negative control group. Cadmium chloride-induced gastric damages have been attributed, at least in part, to toxicant-induced oxidative stress. It results suggest that cadmium chloride induces the formation of ROS, thus inducing damage of various tissues resulting in loss of membrane functions. Long-term exposure to cadmium increases MDA or lipid peroxidation and causes inhibition of SOD activity inducing oxidative damage in gastric [2,3,22]. The various toxic effects caused by cadmium chloride in biological systems, can increase MDA or lipid peroxidation, as an early and sensitive consequences of cadmium exposure. Cadmium chloride toxicity leads to the production of free radical, that consists of hydroperoxides, singlet oxygen, and hydrogen peroxides, evaluated by MDA levels as the products of lipid peroxidation, and the direct decrease of antioxidant reserves [1]. The present study shown in significantly increased of MDA levels in the gastric of cadmium chloride-treated rats in comparison to the negative control. This means that it increased the oxidative stress in the cadmium chloride-treated rats. Therefore, the significantly lower levels of MDA in the gastric tissues of chitosan nanoparticle treated groups as compared with the cadmium chloride group indicate attenuation of lipid peroxidation. It is known that cadmium chloride-induced oxidative stress and tissue damage could be caused by increased production of free radicals and by causing direct decrease of antioxidant reserves [1,2]. Intense lipid peroxidation caused by cadmium exposure may affect the cytoplasmic membranes and mitochondrial , causing damage of the tissues and releasing lipid hydroperoxides into circulation which reflects the induction of oxidative stress [2]. The chitosan nanoparticle, which behaves as a powerful antioxidant and free radical scavenger, can decrease the MDA level perturbed by cadmium chloride in rats gastric, as observed in this study. Treatment of rats with chitosan nanoparticle at a dose of 600 mg/kg BW prevented the levels of MDA to rise when the rats were challenged with cadmium chloride. This means that chitosan nanoparticle minimized the toxic effect of cadmium chloride via its antioxidant activity. The antioxidant protective mechanism decreases the ROS and scavenges the free radical responsible for the gastric damage and thus inhibit the lipid peroxidation as measured by MDA levels [3]. The findings of this study suggest that chitosan nanoparticle

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