The Effect of Vitamin E on the Composition of inflammatory Cells in Alveoli after Paraquat Intoxication in Rats

Abstract

Background : Acute pulmonary injury by paraquat are caused by multiple mechanisms including direct injury with oxygen free radicals and several mediators released from inflammatory cells. In order to clarify whether vitamin E could reduce tissue damages induced by intraperitoneal administration of paraquat and to investigate the pathogenetic mechanisms of paraquat-induced pulmonary injury, vitamin E as a free radical scavenger was administered. Method : Rats were divided into three groups (group 1 : control, group 2 : paraquat treated group, group 3 : paraquat and vitamin E treated group). Animals were sacrificed on day 1, day 2, day 3, and day 8 after the administration of saline, paraquat, or paraquat/vitamin E. Results : Treatment with vitamin E decreased the death rate of rats treated with paraquat. Comparing with control group (), mean total cell counts recovered from the lavage fluid from animals treated with paraquat() were increased(p=0.06). Magnitudes of increment of the total cell counts on the Day 8 in the vitamin E treated group were smaller than those of the animals treated with paraquat alone. The neutrophils began to appear in significant amounts in the lavage fluid on Day 8 after the administration of paraquat(37.0+12.7%). A significant decreasing neutrophil concentration at Day 8 was observed in the paraquat/vitamin E treated group(20.6+13.4%). Histologically the degree of pulmonary fibrosis was most prominent in the paraquat treated group while diffuse alveolar damage was continuously observed in the paraquat/vitamin E treated group and extensive interstitial lymphocytic infiltration was seen in the paraquat/vitamin E treated group. The paraquat/vitamin E treated group showed the less histologic changes. Conclusion : In this study vitamin E acting as a scavenger of neutrophil-derived free radicals and suppressant of lipid peroxidation, seemed to be the effective antioxidant in the inhibition of paraquat-induced pulmonary injury.