Ali A Shati1. 1. Department of Biology, College of Science, King Khalid University, Abha, Kingdom of Saudi Arabia. shati100@yahoo.com
Abstract
OBJECTIVE: To evaluate the effect of Origanum majorana L. (OM) against cadmium (Cd)-induced hepatotoxicity and nephrotoxicity. METHODS: This study was performed at King Khalid University, Abha, Kingdom of Saudi Arabia from September to December 2010. Thirty-six male albino rats were divided into 6 groups: control, Cd, OM, OM+Cd, OM pre-treated (received OM extract for 14 days followed by Cd for 14 days), OM post-treated (received Cd for 14 days followed by OM extract for 14 days). All treatments were orally administered once a day (Cd: 5 mg/kg by weight [b.w] and OM: 1 g/kg b.w) for 28 days. Changes in liver biochemical markers namely, alanine transaminase, aspartate aminotransferase, alkaline phosphatase (ALP) and gamma-glutamyltransferase (GGT), and levels of total protein, urea, and creatinine in the serum were determined. Levels of liver and kidney antioxidants namely, glutathione, superoxide dismutase and catalase, and lipid peroxidation (LPO) were estimated. Differential display using 3 primers: chi 25, 5.8S and NS3 was performed for liver homogenates. RESULTS: Exposure to Cd increased the levels of liver biochemical markers, urea, and creatinine, and lowered total protein levels. Exposure to Cd lowered activities of liver and kidney antioxidants, while it increased LPO levels. Levels of all disrupted parameters were alleviated by co-administration and post-administration of OM extract. The NS3 primer was able to show genetic variability in livers of all experimental groups. CONCLUSION: The OM showed apparent protective and curative effect on Cd-induced hepatotoxicity and nephrotoxicity.
OBJECTIVE: To evaluate the effect of Origanum majorana L. (OM) against cadmium (Cd)-induced hepatotoxicity and nephrotoxicity. METHODS: This study was performed at King Khalid University, Abha, Kingdom of Saudi Arabia from September to December 2010. Thirty-six male albino rats were divided into 6 groups: control, Cd, OM, OM+Cd, OM pre-treated (received OM extract for 14 days followed by Cd for 14 days), OM post-treated (received Cd for 14 days followed by OM extract for 14 days). All treatments were orally administered once a day (Cd: 5 mg/kg by weight [b.w] and OM: 1 g/kg b.w) for 28 days. Changes in liver biochemical markers namely, alanine transaminase, aspartate aminotransferase, alkaline phosphatase (ALP) and gamma-glutamyltransferase (GGT), and levels of total protein, urea, and creatinine in the serum were determined. Levels of liver and kidney antioxidants namely, glutathione, superoxide dismutase and catalase, and lipid peroxidation (LPO) were estimated. Differential display using 3 primers: chi 25, 5.8S and NS3 was performed for liver homogenates. RESULTS: Exposure to Cd increased the levels of liver biochemical markers, urea, and creatinine, and lowered total protein levels. Exposure to Cd lowered activities of liver and kidney antioxidants, while it increased LPO levels. Levels of all disrupted parameters were alleviated by co-administration and post-administration of OM extract. The NS3 primer was able to show genetic variability in livers of all experimental groups. CONCLUSION: The OM showed apparent protective and curative effect on Cd-induced hepatotoxicity and nephrotoxicity.