Nitrofen이 백서의 횡격막 발달에 미치는 영향에 관한 연구
Effect of the Nitrofen on Diaphragmatic Development of Rat
정화순, 장우현,
소속 상세정보
정화순 ( )
한양대학교 의과대학 해부학교실
장우현 ( )
서울대학교 의과대학 병리학교실
KMID : 0357919840180020122
Abstract
Enormous increase of use of herbicide was brought to problem with adverse effect on
environment and its inhabitant. And the teratogenic effects of a few herbicides were
reported.
Nitrofen, 2,3-dictlorphenyl-p, nitrophenyl ether is an organic chemical placed in
nitrophenol/aniline group. This chemical has wren one of mast widely used herbicides in
Korea.
Initial toxicity study of nitrofen was done by Ambrose with lung toxicity. Respiratory
distress and cyanosis of neonatal rats following nitrofen exposure in uterus was
described by Kimbrough et at and suggested that nitrofen might be affecting surfactant
production. Later, it was reported that cardiac anomaly accounted for the neonatal
distress and death.
This experiment wart attempted to produce diaphragmatic defect in offsprings of rots
by nitrofen administration orally in early developmental stage and to find characteristics
of diaphragmatic defect.
Following results and conclusions were made.
1) Nitrofen was a potent teratogenic agent in rats in dose of 350 ㎎/㎏ at 10th day of
gestation.
It was fairly selective in producing diaphragmatic defect. The overall frequency of
diaphragmatic defect was 66.3%.
2) Diaphragm was the primary target organ in nitrofen induced neonatal death, and
pulmonary hypoplasia due to diaphramatic defect was major contributor of direct cause
of neonatal death.
3) In majority the defect was in the posterolateral(Bochdalek) portion of the diaphragm
and in some cases, diaphragmatic defect was due to attenuation of central tendon.
4) The difference in the sidedness of the defect was obviously noted ; in group of
administration of 250 ㎎/㎏ at gestation 11 th day, the great majority were right
sided(92%), while in group of administration of 350 ㎎/㎏ at gestation 10 th day no
difference was observed.
5) Pathogenesis of nitrofen induced diaphragmatic defect was thought probable due to
delay or arrest of development of pleuroperitoneal fold.
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