百草枯对培养的肺细胞中磷脂代谢的破坏作用。

Disruption of phospholipid metabolism by paraquat in cultured pneumocytes.

作者信息

Saito K, Parker W B, Menzel D B

出版信息

J Toxicol Environ Health. 1982 Apr;9(4):527-34. doi: 10.1080/15287398209530185.

DOI:10.1080/15287398209530185

Abstract

Paraquat (PQ) has specific pneumotoxicity in humans. Its effects on phospholipid metabolism in type 2 pneumocytes, A-549, and in lung fibroblasts, WI-38, were examined. PQ inhibited the incorporation of palmitic acid into phosphatidyl-ethanolamine by 42%, but did not inhibit the incorporation into phosphatidylcholine. PQ also inhibited the incorporation of acetate into phosphatidylcholine and ethanolamine by 82-88% in A-549 cells and by 92% in WI-38 cells. PQ inhibited the incorporation of choline into phosphatidylcholine and ethanolamine by 55 and 73%, respectively. Phosphatidylcholine was detected in the medium of A-549 cells. PQ completely inhibited this phosphatidylcholine secretion. These results suggest that PQ has inhibitory effects on phospholipid synthesis and excretion in human type 2 pneumocytes.

摘要

百草枯（PQ）对人类具有特定的肺毒性。研究了其对II型肺细胞A-549和肺成纤维细胞WI-38中磷脂代谢的影响。PQ使棕榈酸掺入磷脂酰乙醇胺的量减少了42%，但不抑制其掺入磷脂酰胆碱。PQ还使A-549细胞中乙酸掺入磷脂酰胆碱和乙醇胺的量减少了82 - 88%，在WI-38细胞中减少了92%。PQ使胆碱掺入磷脂酰胆碱和乙醇胺的量分别减少了55%和73%。在A-549细胞的培养基中检测到了磷脂酰胆碱。PQ完全抑制了这种磷脂酰胆碱的分泌。这些结果表明，PQ对人II型肺细胞中的磷脂合成和排泄具有抑制作用。