除草剤パラコートの肺毒性
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概要
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Paraquat (1,1'-dimethyl-4,4'-bipyridylium), a widely used and effective herbicide, can cause a severe lung injury in both humans and experimental animals. The injury is characterized by initial damage to the alveolar epithelium and capillary endothelium with the development of hemorrhagic pulmonary edema, followed by development of intra-alveolar and interstitial fibrosis. Although the lung is thought to be a primary target organ for paraquat toxicity, the mechanism of action of this herbicide remains to be uncertain. A possible mechanism of selective toxicity to the lung is the accumulation of paraquat in the lung. Data from experimental animals in vivo and in vitro indicate the accumulation of paraquat in the lung by an energy-dependent transport system. However, paraquat does not appear to be selectively concentrated by the lung in human paraquat poisoning. A widely accepted theory regards lipid peroxidation and NADPH depletion as the basic mechanism of paraquat toxicity. According to this theory, paraquat can be reduced by microsomal enzymes and undergoes a cyclic reduction and reoxidation, giving rise to a reactive oxygen radical. This continuous generation of oxygen radicals within the cells of the lung then in turn destroy this tissue through various mechanisms of oxidative damage such as lipid peroxidation and NADPH depletion. However, there are data in the literatures that contradict the active oxygen species theory of paraquat toxicity. Most of these findings show a lack of extensive oxidative damage to the lung. Extent of lipid peroxidation and NADPH depletion is not always correlated with that of lung tissue damage. Moreover, the mechanism of paraquat toxicity leading to the development of lung fibrosis have not been fully elucidated. Recent studies suggest that inflammatory cells such as polymorphonuclear leukocytes and alveolar macrophage, and chemical mediators released by these cells may play an important role in lung fibrosis caused by paraquat. To sum up, the mechanism of selective lung toxicity in paraquat poisoning is not clearly explained by the theory mentioned above. Study on the secondary pulmonary response following cell injury directly caused by paraquat may become a clue to elucidate this mechanism.
- 公益社団法人日本薬学会の論文
- 1989-08-31
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