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Cyclophosphamide‑induced hepatotoxicity in Wistar rats: The modulatory role of Gallic Acid as a hepatoprotective and chemopreventive phytochemical
(Wolters Kluwer - Medknow, 2016) Oyagbemi, A. A.; Omobowale, O. T.; Asenuga, E. R.; Akinleye, A. S.; Ogunsanwo, R. O.; Saba, A. B.
Background: Gallic acid (GA) is an endogenous plant phenol known to have antioxidant, free radical scavenging ability, anti inflammatory, anti cancer, and anti fungal properties. The aim of this study was to assess the protective effect of GA on cyclophosphamide (CPA) induced hepatotoxicity in male Wistar rats. Methods: Sixty rats were grouped into six groups of 10 rats per group. Group 1 received distilled water. Group 2 received CPA at 200 mg/kg single dose intraperitoneally on day 1. Groups 3 and 4 received a single dose of CPA (200 mg/kg) intraperitoneally on day 1 and then were treated with GA at 60 and 120 mg/kg body weight for 14 days, respectively. Rats in Groups 5 and 6 only received GA at 60 and 120 mg/kg body weight for 14 days, respectively. GA was administered orally. Results: CPA induced hepatic damage as indicated by significant elevation (P < 0.05) in aspartate aminotransferase, organ weight, and evidence by the histological study. CPA also induced hepatic oxidative stress as indicated by significant elevation (P < 0.05) in malondialdehyde content, hydrogen peroxide (H2 O2 ) generation, nitrite level, and the level of glutathione (GSH) peroxidase crashed in the CPA treated group. GA enhanced the antioxidant defense system as indicated by significant elevation (P < 0.05) in GSH level, catalase activity, and GSH S transferase activity. Conclusions: Taken together, the result of this present study shows that GA has a protective effect on CPA induced hepatotoxicity.
Gallic acid protects against cyclophosphamide-induced toxicity in testis and epididymis of rats
(Blackwell Verlag GmbH, 2015) Oyagbemi, A. A.; Omobowale, T. O.; Saba, A. B.; Adedara, I. A.; Olowu, E. R.; Akinrinde, A. S.; Dada, R. O.
The protective role of gallic acid (GA) on reproductive toxicity induced by cyclophosphamide (CPA), an antineoplastic drug, was investigated in male Wistar rats. Sixty rats were grouped into 10 rats per group. Group 1 (control) received distilled water. Rats in groups 2 and 3 received GA alone at 60 and 120 mg kg 1 for 14 consecutive days, respectively. Group 4 received a single intraperitoneal dose of CPA at 200 mg kg 1 on day 1. Groups 5 and 6 received a single dose of CPA (200 mg kg 1 ) intraperitoneally on day 1 followed by treatment with GA at 60 and 120 mg kg 1 for 14 consecutive days, respectively. In testes and epididymis of the treated rats, CPA administration resulted in significant elevation (P < 0.05) in malondialdehyde (MDA), nitrite and hydrogen peroxide levels. There was a significant decrease in the activities of superoxide dismutase and glutathione-S-transferase. Furthermore, there were significant reductions in plasma luteinising hormone (LH), follicle stimulation hormone (FSH) and testosterone levels, which were accompanied by significant decrease in sperm motility and viability in CPA-treated rats. Histological examination revealed marked testicular and epididymal atrophy in CPA alone trea ted rats and these aberrations were reversed by GA. In conclusion, GA has capacity to protect against reproductive toxicity induced by cyclophosphamide.