الفهرس 
Evaluation of the protective and therapeutic potential of echinochrome against 7,12-dimethylbenz[a]anthracene-induced pre-cancerous hepatorenal toxicity in Wistar rats
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Abstract
One of the main causes of hepatorenal toxicity is 7,12 dimethylbenz [a] anthracene (DMBA). On the other hand, echinochrome (Ech) pigment, which is extracted from sea urchins, is one of the marine natural products, which possess antioxidant, antimicrobial, and anti-inflammatory activities. So, the present study aims to evaluate both the protective and curative effects of Ech on the hepatorenal toxicity induced by DMBA in albino Wistar rats. Thirty-six rats were divided into two main groups, the protective and curative group. Each group was subdivided into three subgroups, control, hepatorenal toxicity model and hepatorenal toxicity treatment groups were treated with Ech. In the protective group, Ech was received (1 mg/Kg body weight, orally) for 14 days before a single dose of DMBA (15 mg/Kg body weight, orally), the rats were then euthanized 4 days after DMBA administration. While the curative group received Ech (1 mg/Kg body weight, orally) for 14 days after 4 days from a single dose of DMBA (15 mg/Kg body weight, orally). Ech treatment groups have shown a significant decrease in the concentrations of aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), urea, creatinine, uric acid in the serum and the liver and kidney malondialdehyde (MDA). Additionally, Ech treatment caused an increase in the liver and kidney concentrations of glutathione reduced (GSH) as well as catalase (CAT). Moreover, histological examination showed a great improvement in the liver and kidney structure of Ech treated rats as compared to DMBA treated rats. These results demonstrated the capability of Ech to treat hepatorenal toxicity by increasing the antioxidant activity and inhibiting DMBA bioactivation by binding to both CYP1B1 and mEH enzymes which responsible for the metabolism of DMBA and DMBA-diol preventing the formation of ROS