Tamaru N, Watanabe K, Takihara H, Yoshida M
Second Department of Internal Medicine, School of Medicine, Fukuoka University, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1991 Sep;29(9):1126-31.
Paraquat is a herbicide known to cause pulmonary edema in its acute toxic phase. Many investigators showed that paraquat induces morphological changes of alveolar epithelial cells even in its early phase. Controversy still exists, however, as to whether pulmonary vascular endothelial cells are also morphologically vulnerable to paraquat. To test the direct toxicity and metabolic changes of pulmonary vascular endothelial cells after paraquat addition, porcine pulmonary artery endothelial cells (PPAEC) were cultured. Thrombin- or bradykinin-stimulated PGI2 production was enhanced significantly, and the angiotensin converting enzyme (ACE) activity of cell lysate of PPAEC was significantly suppressed after a 24-hour incubation with 10(-4) M of paraquat. No further thrombin-induced enhancement of PGI2 production was noted after a 48-hour incubation. The alterations in arachidonic acid metabolism and ACE activity mentioned above did not result from cytotoxicity of paraquat because LDH release into culture medium was not increased during 72 hours of incubation with paraquat. Longer incubation more than 48 hours, in turn, induces obvious toxic effects on PPAEC.
百草枯是一种除草剂，在其急性中毒阶段可导致肺水肿。许多研究人员表明，百草枯即使在早期阶段也会诱导肺泡上皮细胞发生形态学变化。然而，关于肺血管内皮细胞在形态学上是否也易受百草枯影响仍存在争议。为了测试添加百草枯后肺血管内皮细胞的直接毒性和代谢变化，培养了猪肺动脉内皮细胞（PPAEC）。在与10^(-4) M百草枯孵育24小时后，凝血酶或缓激肽刺激的前列环素（PGI2）生成显著增强，PPAEC细胞裂解物的血管紧张素转换酶（ACE）活性显著受到抑制。在孵育48小时后，未观察到凝血酶诱导的PGI2生成进一步增强。上述花生四烯酸代谢和ACE活性的改变并非由百草枯的细胞毒性引起，因为在与百草枯孵育72小时期间，培养基中乳酸脱氢酶（LDH）的释放并未增加。反过来，孵育超过48小时会对PPAEC产生明显的毒性作用。
