Mechanism of Developmental Effects in Rats Caused by an N-Phenylimide Herbicide: Transient Fetal Anemia and Sequelae during Mid-to-Late Gestation.

Background: Rat developmental toxicity including embryolethality and teratogenicity (mainly ventricular septal defects [VSDs] and wavy ribs) was produced by an N-phenylimide herbicide that inhibits protoporphyrinogen oxidase (PPO) common to chlorophyll and heme biosynthesis. Major characteristics of the developmental toxicity included species difference between rats and rabbits, compound-specific difference among structurally similar herbicides, and sensitive period. Protoporphyrin accumulation in treated fetuses closely correlated with the major characteristics.

Maternal exposure to procymidone has no effects on fetal external genitalia development in male rabbit fetuses in a modified developmental toxicity study.

This study was conducted to evaluate the effects of procymidone (PCM) on development of male rabbit fetal external genitalia. PCM was administered once daily by gavage at dose levels of 0 (control) and 125mg/kg/day to pregnant rabbits from gestation day 6 through 28 and fetal external genitalia was observed in detail. This treatment period covered the critical stage of sexual differentiation of fetal external genitalia in rabbits.

New method for detecting antiandrogenic effects through the measurement of external genitalia in rabbits.

The aim of the present study was to develop a quantitative evaluation method for detecting antiandrogenic activity of chemicals in rabbits that are regularly used for developmental toxicity studies. Kbl: New Zealand White rabbits (n = 8-9) were injected intramuscularly with an antiandrogen, cyproterone acetate (CA; 10 mg/kg body weight [BW]/day), on gestation days (GD) 13-24. On GD 29, live fetuses were obtained by cesarean section and sexed by examination of the internal genitalia.