Abstract

This study aimed to know the effect of cadmium on hematology, oxidative stress liver and kidney function in rats. The study utilized a sample of thirty male Sprague Dawley Albino rats, aged 2-3 months, who were in good health. The rats had an average weight of 180 grams. These were divided into 2 groups (15 rats in each group). Group 1 (G1): involved the administration of a daily dose of 1 mg CdCl2/kg in a 0.9% NaCl solution via subcutaneous injection for a duration of two weeks. This approach was employed to ensure that the application of Cd2+ was carefully regulated and maintained at a consistent level. Group 2 (G2): consisted of rats that were administered equal amounts of sterile 0.9% sodium chloride solution via subcutaneous injections. Following a period of two weeks, the animals underwent anesthesia using pentobarbital (0.6 ml/kg). Subsequently, blood samples were obtained via heart puncture and divided into 2 parts first part were used for hematology by using hemolyser and second part for serum collection. This separated serum was then utilized for biochemical estimations, specifically for assessing liver and kidney function (AST, ALT, BUN, Creatinine) as well as total antioxidant. Following the sacrifice of the rats, the liver and kidney samples were subjected to fixation and subsequently embedded in paraffin blocks. Sections measuring 5 mm in thickness were then prepared from these blocks. These sections were stained using the (H&E) staining method. The current results showed that WBCs were decreased significantly in G1 as compared with another, while other parameters RBCs, PCV, Hb, MCV showed no significant differences between both groups. The present results showed a significant increase in AST and ALT in G1 as compared with control group, while the total antioxidant activity exhibit significant decrease in G1 as compared with control group. Histopathological investigations revealed evidence of hepatic and renal damage induced by exposure to cadmium. The hepatic damage observed following exposure to Cd was characterized by widespread degeneration and necrosis of hepatocytes, along with inflammation, cytoplasmic vacuolization, and the presence of various cellular debris within the central liver vein, as compared to the control group. The rats that were exposed to Cd intoxication exhibited cellular changes in the glomeruli, congestion in the cortex, and outer medulla. These changes included loss of the tubular brush border, interstitial edema, and necrosis of the epithelium, these observations were in contrast to the control group. In conclusion, our study has provided confirmation that Cadmium (Cd) exhibits interactions within environmental conditions. The present study demonstrates that the interaction observed in the liver is primarily synergistic, as evidenced by both histological and biochemical findings. Furthermore, an antagonistic relationship was observed between the two toxic metals in relation to kidney markers, specifically urea levels.

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