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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 
 

Effect of sulfur dioxide inhalation on the glutathione redox system in mice and protective role of sea buckthorn seed oil.

This study investigated the effects of sulfur dioxide (SO2) inhalation and protection by sea buckthorn seed oil from oxidative damage caused by SO2 in male Kunming-strain mice. One approach was set up to study the effects of SO2 inhalation on changes of the mice antioxidant defense system. SO2 at different concentrations (22 +/- 2, 64 +/- 3, and 148 +/- 23 mg/m3) was administered to animals in treatment groups for 7 days, 6 h per day, while control groups were exposed to filtered air under the same condition. The activities of glutathione-S-transferase ( GST) and glucose-6-phosphate dehydrogenase ( G6PD) and the contents of reduced glutathione (GSH) in brain, lung, heart, liver, and kidney of mice were measured. In the case of inhalation of a SO2 concentration of 148 +/- 23 mg/m3, the activities of GST and G6PD and contents of GSH in the brain, lung, heart, liver, and kidney were significantly decreased. Dose-dependent relations were found between various SO2-exposed concentrations and the activities of GST and G6PD and the content of GSH. Meanwhile another approach was taken to determine whether sea buckthorn seed oil could maintain the glutathione redox system and prevent the oxidative damage of lung induced by SO2. In groups given a high dosage (6 or 8 ml/kg) intraperitoneally, the level of TBARS (thiobarbituric acid-reactive substances) was decreased significantly (p < 0.05) by the injection of sea buckthorn seed oil, and the activity of GST was increased significantly (p < 0.05). Overall GST activity and TBARS level exhibited a significant negative correlation (r = 0.891, p < 0.05). The observations showed that SO2 inhalation resulted in a significant change in the glutathione redox system and indicated that sea buckthorn seed oil could contribute to the antioxidant effects in the case of SO2 exposure.[1]

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