N-ACETYLCYSTEINE DELAYS THE INFILTRATION OF INFLAMMATORY CELLS INTO THE LUNGS OF PARAQUAT-INTOXICATED RATS

被引:36
作者
HOFFER, E
AVIDOR, I
BENJAMINOV, O
SHENKER, L
TABAK, A
TAMIR, A
MERZBACH, D
TAITELMAN, U
机构
[1] TECHNION ISRAEL INST TECHNOL,RAMBAM MED CTR,FAC MED,DEPT MICROBIOL,IL-31096 HAIFA,ISRAEL
[2] TECHNION ISRAEL INST TECHNOL,FAC MED,DEPT COMMUNITY MED & EPIDEMIOL,IL-31096 HAIFA,ISRAEL
关键词
D O I
10.1006/taap.1993.1080
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
We investigated a possible role for N-acetylcysteine (NAC), a well-known antioxidant and free radical scavenger, against oxidative lung damage as observed in the in vivo model of paraquatintoxicated rats. The administration of two ip doses of 50 mg/kg NAC to paraquat-intoxicated animals did not change the glutathione status of the lungs, as determined by the measurement of nonprotein sulfhydryl (NP-SH) groups. The administration of NAC did however suppress the paraquat-induced release of chemoattractants for neutrophils in the bronchoalveolar fluid when the lavage was carried out 12 hr after the administration of 30 mg/kg paraquat. Also, in the intoxicated NAC-treated animals, the infiltration of inflammatory cells was significantly reduced, as demonstrated by the examination of the cell composition of the bronchoalveolar lavage (BAL), 24 hr after paraquat. Phorbol myristate acetate-stimulated superoxide anion production from the AM isolated from the HAL of paraquat-intoxicated nontreated animals was lower than that of controls, whereas in the NAC-treated animals, it was close to that of the controls. The obtained results indicate that NAC has a protective effect against oxidative lung damage by delaying inflammation. It also prevents the paraquat-induced reduction of superoxide anion production by stimulated AM. In the present model, however, the NAC administration regimen did not affect the survival rate of paraquat-intoxicated rats. © 1993 Academic Press, Inc.
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页码:8 / 12
页数:5
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