Experimental findings demonstrate oxidative stress and histopathological damage in Wistar rats, highlighting cadmium's toxicity.
Cadmium (Cd) is a heavy metal that is a persistent environmental contaminant. Cd has gained global attention due to its widespread use in industries and represents an occupational hazard. Humans are exposed to Cd via the oral route throughout their lifetime, which can adversely affect their health. The present study was done to delineate the mechanism of acute toxicity of cadmium chloride (CdCl 2 ) on rat intestine. Adult male Wistar rats were given a single oral dose of CdCl 2 at 30, 60, 90, and 120 mg/kg body weight. The administration of CdCl 2 impaired the enzymatic and non‐enzymatic antioxidant defense systems, which lowered the total antioxidant capacity of intestinal cells. The oxidation of lipids, proteins, and thiol groups was significantly increased. The activities of enzymes of the brush border membrane and glucose metabolism were also altered. DNA strand scission and DNA‐protein cross‐linking were enhanced in CdCl 2 ‐treated rats. Histopathologic images supported the biochemical findings and showed detrimental changes in the intestine of CdCl 2 ‐treated rats. All effects were seen in a CdCl 2 dose‐dependent manner. The results of this study strongly suggest that the toxic effects of CdCl 2 in rat intestine are due to the induction of oxidative stress that lowers the antioxidant defense system, leading to tissue damage.
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Iqbal et al. (2025) studied this question.
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