Uranium and Lead Intoxication Hazards Induce Hepatotoxicity In Rats; Biochemical, Histochemical And Histopathological Studies | ||||
| Egyptian Journal of Chemistry | ||||
| Article 52, Volume 64, Issue 8, August 2021, Page 4545-4556 PDF (1 MB) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/ejchem.2021.82995.4079 | ||||
 View on SCiNiTO | ||||
| Author | ||||
Hazem K A. Sarhan 
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| Medical and radiation research Dep. Research Sector, Nuclear Material Authority, Cairo, Egypt | ||||
| Abstract | ||||
| Depleted uranium (DU) used in each of civilian and military activities and contributes to health problems. Uranium is an element of heavy metals with chemical and radiological nature that have made it useful in industry and commerce, but toxic at sufficiently high doses to both humans and the environment. Also, Lead is one of the naturally occurring environmental heavy metals. This experimental study was designed to evaluate uranium and lead-induced hepatotoxicity. Material and Methods: This study was conducted in the Medical and Radiation Research Department, Research Sector, Nuclear Material Authority, Cairo, Egypt. from September to December 2020 on 30 normal healthy adult male albino rats divided into three equal groups each of 10 rats. Control group rats were kept on a normal diet and pure distilled water (Group A). The 2 experimental groups were kept on a normal diet and rats were administered with 50 mg/kg body weight of lead acetate only for 45 days, (Group B) and rats were administered with 40 mg/kg body weight of uranyl acetate only for 45 days (Group C). Animals were sacrificed and livers were removed and used to identify microscopic changes. Specimens were stained with Hematoxylin and eosin, with Masson trichrome stain for the study of fibrous tissue. Results: Mild lymphocytic infiltration, vacuolar degeneration, and mild increase of periportal fibrosis with mild depletion of glycogen significance and partial disappearance of glycogen vacuoles were reported in animals that received lead acetate contaminated water for 6 weeks. Animals that received uranyl acetate contaminated water for 6 weeks showed hepatic changes in the form of abundant lymphocytic infiltration, increased cellular polymorphism, pyknotic nuclei, and areas of cell necrosis with evident moderate periportal fibrosis and marked vacuolar degeneration associated with marked depletion of glycogen level. Conclusion: It could be concluded that exposure to uranium as compared to lead imposes a potent toxic effect on liver cells listing as glycogen depletion, cellular infiltration, and liver architecture in the form of initiation of periportal fibrosis that may progress to liver cirrhosis. | ||||
| Keywords | ||||
| Heavy metal; Uranium acetate; Lead acetat; Hepatotoxicity; Antioxidants; histopathology; and Rats | ||||
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