The effects of Modified Citrus Pectin on hepatic response as a result of exposure to aluminium in rats

In this study, aluminum (Al) toxicity model was formed by applying aluminum chloride (AlCl3) orally for 30 days to Sprague Dawley rats and the regulatory effects of modified citrus pectin (MCP) on changes in the liver were investigated. Group I (Control: 0.9% NaCl); Group II (34 mg / kg / day AlCl3); Group III (50 mg / kg / day MCP); Group IV (2 hours intervals and respectively 34 mg / kg / day AlCl3 + 50 mg / kg / day MCP) was studied in 4 groups (n = 6). Superoxide dismutase (SOD), catalase (CAT) and lipid peroxidation were measured biochemically. Histological changes were evaluated. Proliferating cell nuclear antigen (PCNA) was performed for determining the proliferation status of liver cells; Immunofluorescence analyzes of BRCA1 and BRCA2 proteins were performed to evaluate DNA repair. According to the findings, MCP prevents pathological changes such as steatosis and necrosis in liver tissue and suppresses lipid peroxidation. In addition, MCP has a protective effect against DNA damage and alterations in cellular structure and physiology as a result of aluminum toxicity. Metal chelating and endogenous antioxidant properties of MCP are thought to play role together in the realization of these effects. Keywords: Aluminium, Hepatotoxicity, Modified citrus pectin, BRCA, PCNA