The toxicity effect of cadmium chloride

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 could attenuate oxidative stress by decreasing the lipid peroxidation (MDA level) in the cadmium-treated gastric.

A similar result has shown that vitamin C and vitamin E enhanced the antioxidant status and inhibited lipid peroxidation in rats with cadmium chloride toxicity. These findings indicate that the antioxidant activity of vitamin C and vitamin E are targeted primarily towards the lipid component of cells. Antioxidants such as vitamin C and vitamin E have been reported to inhibit free radical formation and are effective in minimizing lipid peroxidation in several different biological systems [21].

SOD and GPx are important antioxidant enzymes. They constitute a mutually supportive defense mechanism against free radical. SOD decomposes superoxide radicals (O2-) to produce H2O2. GPx is a selenoenzyme which has played a major role in the decrease of H2O2 and hydroperoxide to produce nontoxic products. Therefore, the activities of SOD and GPx have been used to assess oxidative stress in cells [6,12]. It has that cadmium chloride has a high affinity for SH groups in several enzymes such as SOD and GPx, thus it can alter antioxidant activities by inhibiting functional SH groups in these enzymes [2,3]. In the present study, the activity of SOD and GPx in gastric rats was decreased by cadmium chloride treatment. This decreased SOD and GPx activities with cadmium chloride treatment is in agreement with previous studies. This suggested that cadmium chloride exposure induced oxidative stress by inhibiting the activity of this antioxidant enzyme. Interestingly, the administration of chitosan nanoparticle doses-dependent manner increased the activities of SOD and GPx in the gastric of cadmium-treated rats, which might be due to the ability of chitosan nanoparticle to reduce the accumulation of free radicals. Chitosan nanoparticle acts as a scavenger for the oxygen-derived free radicals, thus protecting from gastric damage [9,17].

The decrease in lipid peroxidation due to chitosan nanoparticle has been attributed to alterations in the antioxidant defense system which includes enzymes such as glutathione-S-transferase, catalase (CAT), SOD, GPx, and nonenzymatic molecule such as glutathione, which normally protect against free radical toxicity. The primary mechanism of action of chitosan nanoparticle may involve the scavenging of free radicals which can inhibit free radical formation [17]. It has been found a decrease MDA levels and an increase in the antioxidant enzyme parameters including SOD, CAT, and GPx in the plasma and tissue such as liver, kidney, and brain of animals that were administered chitosan in association with heavy metal, in comparison to the group that was administered heavy metal alone [6,10].

Histopathological results demonstrating structural changes in gastric tissue of heavy metal toxicity such as cadmium chloride were reported by some researchers. In the present study, histopathological view of gastric sections in the cadmium chloride treated group showed the gastric damage and necrosis of gastric mucosa epithelial cell as compared to the negative control group. The rats pretreated with chitosan nanoparticle 600 mg/kg BW demonstrated significantly improved necrosis of gastric mucosal epithelial cell.

In summary, our data indicate that cadmium chloride-induced gastric toxicity might be related to oxidative damage. Co-administration of chitosan nanoparticle lessened the effects of cadmium chloride-induced gastric toxicity possibly by inhibiting free radical-mediated process. Further investigation of these promising protective effects of chitosan nanoparticle against cadmium chloride-induced gastric damage may have a considerable impact on developing clinically feasible strategies to treat patients with cadmium chloride-induced gastric ulcer.


It could be concluded that chitosan nanoparticle may exert its protective actions against cadmium‑induced gastric injury in rats, possibly through its antioxidant mechanisms. Chitosan nanoparticle can be a future natural product for counteracting the cadmium chloride intoxication. These results showed that chitosan nanoparticle has a potential gastroprotective effect in a dose‑dependent manner that minimize or diminish the gastric toxicity effect of cadmium chloride.

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