Vitamin E Protects Against Lipid Peroxidation Due to Cold-SO2 Coexposure in Mouse Lung

• Published in: Inhalation toxicology Vol. 19; no. 2; pp. 161 - 168
• Main Authors: Ergonul, Zuhal, Erdem, Ay en, Balkanci, Zeynep Dicle, Kilinc, Kamer
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01-02-2007; Taylor & Francis
• Subjects: Administration, Inhalation; Air Pollutants - toxicity; Animals; Antioxidants - pharmacology; Cold Temperature - adverse effects; Drug Therapy, Combination; Female; Glutathione Peroxidase - metabolism; Heart - drug effects; Injections, Intraperitoneal; Lactic Acid - metabolism; Lipid Peroxidation - drug effects; Lipid Peroxidation - physiology; Lung - drug effects; Lung - metabolism; Lung - pathology; Male; Mice; Myocardium - metabolism; Myocardium - pathology; Oxidative Stress - drug effects; Oxidative Stress - physiology; Silicon Dioxide - toxicity; Superoxide Dismutase - metabolism; Thiobarbituric Acid Reactive Substances - metabolism; Vitamin E - pharmacology
• ISSN: 0895-8378; 1091-7691
• DOI: 10.1080/08958370601051883

Exposure to sulfur dioxide (SO2) and cold increases especially in the winter. SO2 or cold exposure destroys the oxidant/antioxidant balance and increases lipid peroxidation. However, the effect of coexistence of both factors has not been studied yet. Therefore, we investigated the effect of SO2 and/or repeated short-term cold exposure on the oxidant-antioxidant status and the possible protective role of vitamin E in the cardiopulmonary tissues of mice. Swiss albino mice of both sexes were assigned to eight groups. Four groups were kept at room temperature, injected either with saline or vitamin E (100 mg/kg) in the presence or absence of SO2 exposure (10 ppm, 1 h/day, 30 days). The remaining four groups received the same protocol but were exposed to cold (4 ± 1°C, 1 h/days, 30 days) instead of room temperature. On day 30, the lung and heart tissues were removed for biochemical analysis. SO2 and cold coexposure increased lactate level in the lung, and elevated thiobarbituric acid-reactive substance (TBARS) and reduced glutathione levels in both tissues, while vitamin E treatment reversed TBARS increment predominantly in the lung. In conclusion, cold and SO2 coexposure exerts more deleterious effects in the cardiopulmonary tissues, while vitamin E treatment seems to be protective, particularly in the lung.