Dermal developmental toxicity of N-phenylimide herbicides in rats.

  title={Dermal developmental toxicity of N-phenylimide herbicides in rats.},
  author={S. Kawamura and Terushige Kato and M. Nakaoka and A. Fantel},
  journal={Birth defects research. Part B, Developmental and reproductive toxicology},
  volume={101 2},
BACKGROUND S-53482 and S-23121 are N-phenylimide herbicides and produced embryolethality, teratogenicity (mainly ventricular septal defects and wavy ribs), and growth retardation in rats in conventional oral developmental toxicity studies. Our objective in this study was to investigate whether the compounds induce developmental toxicity via the dermal route, which is more relevant to occupational exposure, hence better addressing human health risks. METHODS S-53482 was administered dermally… Expand
Mechanism of Developmental Effects in Rats Caused by an N-Phenylimide Herbicide: Transient Fetal Anemia and Sequelae during Mid-to-Late Gestation.
Developmental toxicity results from PPO inhibition in primitive erythroblasts, causing transient fetal anemia followed by death, and inhibition of PPO in rats, rabbits, and humans by the herbicides in vitro is proposed. Expand
Maternal and fetal toxicity of Wistar rats exposed to herbicide metolachlor
Exposure of pregnant rats to metolachlor can lead to signs of general toxicity, late embryonic losses and congenital anomalies, as well as teratogenic potential when administered during the period of organogenesis. Expand
Different Effects of an N-Phenylimide Herbicide on Heme Biosynthesis between Human and Rat Erythroid Cells.
It is suggested that the rat would be an inappropriate model for assessing the developmental toxicity of S-53482 in humans as rats are specifically sensitive to PPO inhibition by the herbicide. Expand
Close link between protoporphyrin IX accumulation and developmental toxicity induced by N-phenylimide herbicides in rats.
The peak period of PPIX accumulation corresponded to that of developmental effects, suggesting a close link between PPO inhibition and developmental abnormality. Expand
What happens in the skin? Integrating skin permeation kinetics into studies of developmental and reproductive toxicity following topical exposure.
Physiologically-based pharmacokinetic models enable the integration of available in vivo, in vitro and in silico data to quantitatively predict the kinetics of uptake at the site of interest, as needed for 21st century toxicology and risk assessment. Expand
Nanopesticides: preparation, targeting, and controlled release
Abstract Nanoformulations applied in biomedicine and agriculture are designed to decrease dose-dependent toxicity by the reduced amount of an applied compound, which is realized by increasing theExpand


Difference in developmental toxicity among structurally similar N-phenylimide herbicides in rats and rabbits.
The mechanism of action of developmental toxicity by S-53482 should account for the compound-specific difference as well as species difference between rats and rabbits and the difference in developmental toxicity in rats was striking among N-phenylimide herbicides. Expand
Species Difference in Developmental Toxicity of an N‐Phenylimide Herbicide between Rats and Rabbits and Sensitive Period of the Toxicity to Rat Embryos
It is likely that there is a common mechanism for the three types of developmental toxicity and that S‐53482 does not produce VSD by its direct damage to embryonic heart tissue. Expand
Teratogenicity study of N-methylpyrrolidone after dermal application to Sprague-Dawley rats.
Maternal toxicity was indicated at 750 mg of N-methylpyrrolidone/kg by reduced body weight gain during gestation and treatment at the high dosage level resulted in fewer live fetuses per dam, an increase in the percentage of resorption sites and skeletal abnormalities. Expand
Species difference in protoporphyrin IX accumulation produced by an N-phenylimide herbicide in embryos between rats and rabbits.
The species difference in PPIX accumulation corresponded very well to that of the developmental toxicity exhibited by S-53482, an N-phenylimide photobleaching herbicide between rats and rabbits. Expand
The effects on rat pups when nitrofen (4-(2,4-dichlorophenoxy)nitrobenzene) was applied dermally to the dam during organogenesis.
Nitrofen (4-(2,4-dichlorophenoxy)nitrobenzene; TOK herbicide) was administered dermally as an aqueous dilution of an emulsifiable concentrate on Day 6-15 of gestation to pregnant Sprague-Dawley ratsExpand
Histological changes in rat embryonic blood cells as a possible mechanism for ventricular septal defects produced by an N-phenylimide herbicide.
The herbicide may induce VSD due to hematological dysfunction caused by the inhibition of heme biosynthesis rather than by direct injurious effects on the heart. Expand
Developmental toxicity of four glycol ethers applied cutaneously to rats.
EGEE- and EGEEA-treated rats showed a reduction in body weight relative to water controls that was associated with completely resorbed litters and significantly fewer live fetuses per litter and Fetal body weights were also significantly reduced in those groups. Expand
Proceedings of the workshop on the acceptability and interpretation of dermal developmental toxicity studies
It is concluded that dermal developmental toxicity studies without any indication of maternal or developmental toxicity are inadequate for risk assessment unless accompanied by absorption data, and absorption data and limited pharmacokinetic data should be collected in every der mal developmental toxicity study. Expand
Proceedings of the Workshop on the Acceptability and Interpretation of Dermal Developmental Toxicity Studies.
  • C. Kimmel, E. Francis
  • Medicine
  • Fundamental and applied toxicology : official journal of the Society of Toxicology
  • 1990
It was concluded that dermal developmental toxicity studies without any indication of maternal or developmental toxicity are inadequate for risk assessment unless accompanied by absorption data, and absorption data and limited pharmacokinetic data should be collected in every der mal developmental toxicity study. Expand
Protoporphyrinogen oxidase inhibition by three peroxidizing herbicides: Oxadiazon, LS 82‐556 and M&B 39279
Three chemically unrelated peroxidizing molecules, namely oxadiazon, LS 82‐556, M&B 39279 and 5‐amino‐4‐cyano‐1‐(2,6‐dichloro‐ 4‐trifluoromethylphenyl)pyrazol, are potent inhibitors of plant, yeast and mouse protoporphyrinogen oxidase. Expand