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Pakistan Journal of Nutrition

Year: 2018 | Volume: 17 | Issue: 2 | Page No.: 89-101
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Authors

Abdullah G. Alkushi

Abdullah G. Alkushi

Mustafa M. Sinna

Mohammed EL-Hady

Naser A. ElSawy

Keywords

Background and Objective: Cadmium (Cd) is a natural heavy metal with no known positive biological function in humans. Therefore, it is not normally found in body fluids or tissues. However, its presence in the body of humans and animals can produce acute and chronic poisoning, leading to bony lesions, liver damage and much more. Biochemical, histopathological and histochemical liver changes due to injection of CdCl2 in rats were examined as a model of chronic exposure and toxicity. In addition, possible recovery from the toxic effects of this heavy metal after withdrawal was also investigated. Materials and Methods: A total of 48 adult male rats albino were divided into two groups and subcutaneously injected every other day with equivalent volumes of saline solution (control group, n = 16) or CdCl2 (experimental group, n = 32 total) for a total of 45 days. Experimental rats were further subdivided into subgroups A and B (n = 16 each). Rats in subgroup A were injected subcutaneously with 1/8 the median lethal dose of CdCl2, while subgroup B was given a double dose of CdCl2 (1/4 median lethal dose). On day 20, 30 and 45, 4 rats from each group were sacrificed and blood and liver samples were taken. The remaining 4 rats in each group were left for an additional 30 days without injection before blood and liver tissue were collected to evaluate possible signs of recovery. Functional, histological and histochemical examination of blood and liver tissue was conducted at each time-point. Results: Significant elevation of liver function was found in both experimental groups as indicated by increased serum alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase levels. Histopathologically, liver samples showed many displaced lesions, ranging from hydropic degeneration to cellular necrosis and most of the portal vein radicals were dilated and congested. The extent of damage was more severe in rats treated for a longer period of time and a higher Cd dose. Mild recovery was observed in specimens examined 30 days after CdCl2 withdrawal, especially in subgroup A. Histochemistry showed a gradual decrease in hepatocyte carbohydrate, DNA, RNA and total protein content over time, reaching a minimum by injection day 45 for subgroup B. While partial recovery of these factors was observed in hepatic cells 30 days after CdCl2 withdrawal, especially in subgroup A, they never returned to control levels. Conclusion: The present study revealed that chronic subcutaneous exposure to CdCl2 causes significant hepatotoxicity in less than a month. Therefore, workers dealing with Cd in industrial settings should use proper precautions and safety measures to avoid Cd exposure. Furthermore, cigarette smoke is known to contain Cd, antismoking programs should be implemented to reduce mortality from cardiovascular and respiratory diseases associated with Cd toxicity.
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