Asian Journal of Pharmaceutical Research and Health Care

Turki M. Al-Shaikh ¹, Mahmoud M. E. Mudawi ², Abdelhadi Y. A. Yassin ², Rami S. Habeballa ², Vijay R. Chidrawar ²

Affiliations
1 Department of Biological Sciences, Northern Border University, Arar, SA
2 Department of Pharmacology and Toxicology, Northern Border University, SA

Abstract

Many patients may administered medications like captopril (ACE inhibitor) for treatment of chronic diseases and may also take Paracetamol as an Over The Counter (OTC) drug which may interact with captopril. Therefore, the aim of this study is to evaluate of the hepatoprotective effect of captopril on liver toxicity induced by low and high dose of paracetamol in rats. This study was conducted in two phases: first study for low dose of paracetamol (300 mg/kg); animals were divided into 4 groups of 6 rats each (n = 6); all groups were treated orally either 0.9 % Normal Saline (NS), captopril 20 mg/kg, paracetamol 300 mg/kg or captopril 20 mg/kg plus paracetamol 300 mg/kg for 10 consecutive days. Second study for single high dose of paracetamol (3000 mg/kg); animals were divided into 4 groups of 6 rats each (n = 6); all groups were pretreated orally either 0.9 % Normal Saline (NS) or captopril 20 mg/kg for 7 consecutive days followed by single oral administration of Paracetamol 3000 mg/kg or normal saline. The administration of Paracetamol or normal saline was performed 24 hours after the last administration of captopril. After 48 hours of hepatic injury induction, the animals were then sacrificed and the liver was removed for histopathological studies. Low dose (300 mg/kg) for 10 days and high single dose (3000 mg/kg) of paracetamol produced hepatotoxic effects. While captopril 20 mg/kg showed marked protection against changes induced by low and high dose of paracetamol on the liver.

Keywords

Acetaminophen, Captopril, Hepatoprotective, Hepatotoxicity, Paracetamol.

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Turki M. Al-Shaikh ¹

Affiliations
1 Department of Biology, College of Science and Arts at Khulis, University of Jeddah, Jeddah, SA

Abstract

Tartrazine is a common artificial food and pharmaceutical additive and has become a part of daily intake values. However, the actual daily intake is much higher than the recommended value. A higher intake is shown to exhibit carcinogenic, mutagenic, and allergic effects. The present work aimed to research whether antioxidant vitamin E (Vit E) therapy would impact liver damage induced by Tartar-Zine (TZ). Twenty-eight mice were used in this experimental study. Mice were categorized into four groups; group (A) in which mice served as control were orally administered distilled water for 28 days. Group (B) in which mice administered daily 100 mg/kg vitamin E orally for 28 days. Group (C) in which mice administered daily 300 mg/kg tartrazine dissolved in distilled water orally for 28 days. Group (D), mice received orally both 100mg/kg vitamin E and 300mg/kg tartrazine concomitantly for 28 days. Biochemical parameters in serum including liver function enzymes aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP), glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione S-transferase (GST) and catalase (CAT) had been inspected. Histological and immunological studies were done including Cyclooxygenase-2 (COX-2). Results showed that TZ treatment initiates hepatic disorders indicated by elevation of liver enzymes and oxidative stress markers in treated mice. Oral administration of Vit E diminished the activities of ALP, AST, and ALT compared to treated mice. Besides, Vit E effectively reduced oxidative stress as indicated by elevated GSH, SOD, GST, CAT, and decreased MDA. Histologically, TZ+Vit E delineated moderate potential improvement of hepatic tissue architecture. Immunologically revealed that TZ+Vit E treated mice showed reduction in COX-2 immuno-expression in hepatic cords sinusoids and hepatocytes versus TZ group. In conclusion, treatment with Vit E could improve all deviated biochemical, immunological, and histological changed induced by tartrazine consumption.

Keywords

Hepatoxicity, Tartrazine E102, Vitamin E

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