Cadmium Toxicity: An Experimental Study to Illustrate the Toxic Effects of Cadmium Exposure and the Role of BSA to Develop Autoimmunity in the Kidneys of Albino Mice

Cadmium Toxicity and Autoimmunity in Albino Mice

Abstract

Background: Cadmium is a toxic heavy metal that causes nephrotoxicity. Chronic exposures lead to cadmium accumulation in kidneys, causing histopathological and physiological dysfunction. Objective: To assess the nephrotoxic effects of chronic cadmium exposure on the kidneys of albino mice. Study Design: Randomized controlled trial. Settings: University of Health Science, Lahore Pakistan. Duration: Six months from 01-03-2014 to 31-08-2014. Methods: In this study, 48 albino mice were randomly divided into 4 groups (12 each): one control and three experimental groups (A, B, and C). Cadmium exposure, such as cadmium chloride (CdCl₂), was administered orally and intraperitoneally on alternate days for 8 weeks at a 10 mg/kg body weight. Bovine Serum Albumin (BSA) was introduced in the control group to observe the early devastating changes in the glomeruli. Results: The findings of present study presented the mesangial hypercellularity causing glomerular swelling, glomerular bonds, increased thickness of the glomerular capillaries, crescentic nephropathy, tubular dilatation, deterioration of renal tubules, interstitial inflammation and accumulation of protein cast in renal tubules along with many other histopathological changes. Biochemical changes were mainly proteinuria and alterations in serum creatinine. However, all the histopathological lesions and biochemical changes depended on the exposure route. Conclusion: In conclusion, the study found significant kidney histopathological and biochemical damage in mice exposed to cadmium chloride, emphasizing the nephrotoxic nature of cadmium. The route of cadmium administration influenced the extent of the kidney damage, accentuating the need to consider exposure routes in evaluating kidney damage.