Azam Hosseinzadeh1, Gholamreza Houshmand2, Mehdi Goudarzi3, Seyed Hashem Sezavar4, Saeed Mehrzadi1, Esrafil Mansouri5, Mojtaba Kalantar6. 1. Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran. 2. Department of Pharmacology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. 3. Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. 4. Research Center for Prevention of Cardiovascular Disease, Institute of Endocrinology and Metabolism, Iran University of Medical Sciences, Tehran, Iran. 5. Cellular and Molecular Research Center, Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. 6. Shoushtar University of Medical Sciences, Shoushtar, Iran. Electronic address: kalantar-m@ajums.ac.ir.
Abstract
AIM: Arsenic is an important toxic chemical affecting millions of people around the world. Exposure to inorganic arsenic results in various health problems including skin lesions, hypertension, hematological disturbance, cardiovascular disease, spleen enlargement and cancer. Gallic acid (GA) is an important phenolic compound possessing various pharmacological properties including anti-inflammatory, antioxidant and free radical scavenging activities. The present study investigated effects of GA against sodium arsenite (SA)-induced spleno-, cardio- and hemato-toxicity. MAIN METHODS: Thirty-five adult male Wistar rats were randomly divided into five groups; group I received normal saline (2 ml/kg/day, p.o.) for 21 days, group II received SA (10 mg/kg/day, p.o.) for 14 days, group III and IV were treated with GA (10 and 30 mg/kg/day, respectively) for 7 days prior to receive SA and treatment was continued up to 21 days in parallel with SA administration, group V received GA (30 mg/kg/day, p.o.) for 21 days. The level of MDA, NO and glutathione (GSH) and the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase were measured in heart and spleen tissues. Creatine kinase-MB (CK-MB) activity and hematological and histopathological parameters were also assessed. KEY FINDINGS: GA significantly decreased SA-induced elevation of MDA and NO levels and reduction of GSH level and GPx and SOD activity in heart and spleen tissues. Furthermore, GA improved SA-induced alteration in hematological and histopathological parameters and reduced SA-induced elevation of serum CK-MB activity. SIGNIFICANCE: Our results suggest that GA inhibits SA-induced spleno-, cardio- and hemato-toxicity through reducing oxidative stress.
AIM: Arsenic is an important toxic chemical affecting millions of people around the world. Exposure to inorganic arsenic results in various health problems including skin lesions, hypertension, hematological disturbance, cardiovascular disease, spleen enlargement and cancer. Gallic acid (GA) is an important phenolic compound possessing various pharmacological properties including anti-inflammatory, antioxidant and free radical scavenging activities. The present study investigated effects of GA against sodium arsenite (SA)-induced spleno-, cardio- and hemato-toxicity. MAIN METHODS: Thirty-five adult male Wistar rats were randomly divided into five groups; group I received normal saline (2 ml/kg/day, p.o.) for 21 days, group II received SA (10 mg/kg/day, p.o.) for 14 days, group III and IV were treated with GA (10 and 30 mg/kg/day, respectively) for 7 days prior to receive SA and treatment was continued up to 21 days in parallel with SA administration, group V received GA (30 mg/kg/day, p.o.) for 21 days. The level of MDA, NO and glutathione (GSH) and the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase were measured in heart and spleen tissues. Creatine kinase-MB (CK-MB) activity and hematological and histopathological parameters were also assessed. KEY FINDINGS:GA significantly decreased SA-induced elevation of MDA and NO levels and reduction of GSH level and GPx and SOD activity in heart and spleen tissues. Furthermore, GA improved SA-induced alteration in hematological and histopathological parameters and reduced SA-induced elevation of serum CK-MB activity. SIGNIFICANCE: Our results suggest that GA inhibits SA-induced spleno-, cardio- and hemato-toxicity through reducing oxidative stress.