Linuron is an
herbicide that displays weak
androgen receptor antagonist activity. Male offspring exposed in utero to 50 mg/kg/day
linuron often exhibit malformations in Wolffian duct derivatives (i.e. the epididymis and vas deferens). The objectives of this study were to determine the point during the perinatal period that
linuron-induced epididymal lesions can be identified, to characterize
linuron-mediated perinatal testicular and epididymal pathology, and to determine whether male rat fetuses exposed prenatally to
linuron exhibit decreased intratesticular and serum
testosterone (T) levels. Pregnant rats were administered
corn oil vehicle or
linuron by gavage at 0 or 50 mg/kg/day (n = 3 controls, 5-11
linuron-treated dams per time point) from gestation days (GD) 12 to 21 or to termination. Male fetuses or offspring were necropsied on GD 17, 19, and 21, and postnatal days (PND) 7 and 14. Epididymal malformations were not observed in fetuses from
linuron-treated dams but were seen in
linuron-exposed male offspring on PND 7 and 14. No testicular lesions were observed at any time point. The growth and development of
linuron-exposed fetuses were altered, as evidenced by slight decreases in
fetal weight and increased levels of immunoreactive
proliferating cell nuclear antigen (
PCNA) on GD 21. Intratesticular and serum T levels were not decreased in
linuron-exposed male fetuses. These findings indicate that the adversely altered adult phenotype following in utero exposure to
linuron is very similar to that produced by the
antiandrogens di-n-butyl phthalate (DBP) and di(2-ethylhexyl)
phthalate (
DEHP). However, the absence of testicular lesions or alterations in fetal
testosterone levels would suggest that the effect of
linuron on the developing Wolffian ducts is distinctly different from DBP or
DEHP.