• Tuberculosis and Respiratory Diseases
• /
• v.41 no.3
• /
• pp.222-230
• /
• 1994

Background: Paraquat, a widely used herbicide, is extremely toxic, causing multiple organ failure in humans. Paraquat especially leads to irreversible progressive pulmonary fibrosis, which is related to oxygen free radicals. However, its biochemical mechanism is not clear. Natural mechanisms that prevent damage from oxygen free radicals include changes in glutathione level, G6PDH, superoxide dismutase(SOD), catalase, and glutathione peroxidase. The authors think catalase is closely related to paraquat toxicity in the lungs Method: The effects of 3-amino-1,2,4-triazole(aminotriazole), a catalase inhibitor, on mice administered with paraquat were investigated. We studied the effects of aminotriazole on the survival of mice administered with paraquat, by comparing life spans between the group to which paraquat had been administered and the group to which a combination of paraquat and aminotriazole had been administered. We measured glutathion level, glucose 6-phosphate dehydrogenase(G6PDH), superoxide dismutase(SOD), catalase, and glutathione peroxidase(GPx) in the lung tissue of 4 groups of mice: the control group, group A(aminotriazole injected), group B(paraquat administered), group C(paraquat and aminotriazole administered). Results: The mortality of mice administered with paraquat which were treated with aminotriazole was significantly increased compared with those of mice not treated with aminotriazole. Glutathione level in group B was decreased by 20%, a significant decrease compared with the control group. However, this level was not changed by the administration of aminotriazole(group C). The activity of G6PDH in all groups was not significantly changed compared with the control group. The activities of SOD, catalase, and glutathione peroxidase(GPx) in the lung tissue were significantly decreased by paraquat administration(group B); catalase showed the largest decrease. Catalase and GPX were significantly decreased by aminotriazole treatment in mice administered with paraquat but change in SOD activity was not significant(group C). Conclusion: Decrease in catalase activity by paraquat suggests that paraquat toxicity in the lungs is closely related to catalase activity. Paraquat toxicity in mice is enhanced by aminotriazole administration, and its result is related to the decrease of catalase activity rather than glutathione level in the lungs. Production of hydroxyl radicals, the most reactive oxygen metabolite, is accelerated due to increased hydrogen peroxide by catalase inhibition and the lung damage probably results from nonspecific tissue injury of hydroxyl radicals.

• Food Science and Preservation
• /
• v.19 no.3
• /
• pp.443-450
• /
• 2012

Recently, NADPH oxidase 4 (NOX4)-mediated generation of intracellular reactive oxygen species (ROS) was proposed to accelerate adipogenesis of 3T3-L1 cell. We have previously shown that Cheonnyuncho (Opuntia humifusa) extract significantly inhibited adipocyte differentiation via downregulation of $PPAR{\gamma}$ (peroxisome proliferator-activated receptor gamma) gene expression. In this study, we focused on the molecular mechanism(s) of NOX4, G6PDH (glucose-6-phosphate dehydrogenase) and antioxidant enzymes in anti-oxidative activities of 3T3-L1 adipocytes. Our results indicate that Cheonnyuncho extracts markedly inhibits ROS production during adipogenesis in 3T3-L1 cells. Cheonnyuncho extracts suppressed the mRNA expression of the pro-oxidant enzyme such as NOX4 and the NADPH-producing G6PDH enzyme. In addition, treatment with Cheonnyuncho extract was found to upregulate mRNA levels of antioxidant enzymes such as Mn-SOD (manganese-superoxide dismutase), Cu/Zn-SOD (copper/zinc-SOD), glutathione peroxidase (GPx), glutathion reductase (GR), and catalase, all of which are important for endogenous antioxidant responses. These data suggest that Cheonnyuncho extract may be effective in preventing the rise of oxidative stress during adipocyte differentiation through mechanism(s) that involves direct down regulation of NOX4 and G6PDH gene expression or via upregulation of endogenous antioxidant responses.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.24 no.6
• /
• pp.848-858
• /
• 1995

The present study was conducted to investigate the effect of dietary vitamin A on the antioxidant status in ethanol-treated rats. Weaning rats were fed a basal diet until they reached about 160-180g body weight. Thereafter, four experimental groups were fed a liquid diet containing 36% ethanol of total calorie and four pair-fed groups were fed isocaloric sucorse instead of ethanol. Additionally, the liquid diet contained adequate amount of ${\beta}-carotene$, retinyl acetate, or 13-cis-retinoic acid except vitamin A deficient diet. The rats were sacrificed after 7 weeks of feedng periods. Significant decrease in hepatic vitamin E content was found in rats treated with chronic ethanol. However, dietary supplementation of retinyl acetate modified the change to some extent. Total vitamin C content of liver increased in vitamin A-deficient or ${\beta}-carotene$ groups with ethanol feeding. The ratio of reduced/oxidized vitamin C increased in the plasma and liver of ${\beta}-carotene$ group with ethanol feeding. Chronic ethanol intake did not change the total glutathione content of rat liver, but increased reduced glutathione(GSH)/oxidized glutathione(GSSG) ratio. This increase in hepatic GSH after chronic ethanol treatment. The changes of Se content in plasma and liver was not consistant. Fe content of liver increased by ethanol treatment, but this increase reduced in rats fed dietary retinyl acetate or 13-cis-retinoic acid. Fe content of plasma increased in vitamin A-deficient and ${\beta}-carotene$ supplemented groups with ethanol intake.