The protective effect ofleaf extract against lead acetate-induced nephrotoxicity and hepatotoxicity in mice ().
Vet World. 2021 Jan ;14(1):250-258. Epub 2021 Jan 27. PMID: 33642811
Wiwik Misaco Yuniarti
Aim: The liver and kidneys are the most sensitive organs to lead exposure. Drugs that inhibit the actions of lead in the liver and kidneys are required to protect them from such an exposure. This study investigates the protective effect of the leaf extract of(OS) against lead acetate-induced nephrotoxicity and hepatotoxicity in mice.
Materials and Methods: A total of 20 male mice were divided into five equal groups for the 24-day testing period. The negative control group was administered Tween-80 1% orally for 24 days. The positive control group was administered Tween-80 1% orally for 24 days and, starting on day 4, 20 mg/kg BW lead acetate orally once a day for 21 days 1 h after the administration of Tween-80 1%. The other three treatment groups were administered BW OS leaf extract orally in the amount of 140, 280, and 560 mg/kg once a day for 24 days and, starting on day 4, 20 mg/kg BW lead acetate orally for 21 days 1 h after the administration of OS leaf extract. On day 25, the mice were sacrificed to assess the levels of blood urea nitrogen (BUN), creatinine, malondialdehyde (MDA), serum glutamic-oxaloacetic transaminase (SGOT), and serum glutamic-pyruvic transaminase (SGPT) as well as the histopathological changes.
Results: The OS leaf extract caused a decrease in the scores for hepatocyte degeneration and portal inflammation (p<0.05) but not for hepatic necrosis (p>0.05) in mice exposed to lead. Similar patterns were observed in the effect of OS leaf extract on the renal morphofunction. The OS leaf extract decreased the scores for hydropic degeneration, tubular necrosis, and glomerular necrosis. The levels of MDA, SGOT, SGPT, BUN, and creatinine decreased in the lead-exposed mice treated with OS leaf extract (p<0.05).
Conclusion: The administration of OS leaf extract has a protective effect against lead acetate-induced hepatotoxicity and nephrotoxicity in mice.