PubMed · 3271376
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M Julián. 1988. [Teratogens].. https://pubmed.ncbi.nlm.nih.gov/3271376/
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Postnatal changes in the fiber distribution and release of 5-HT in the somatosensory cortex (Sm) of methylazoxymethanol acetate (MAM)-induced microencephalic rats were studied. A transient accumulation of serotonergic fibers was observed in the Sm of the control and MAM rats in the first 2 weeks following birth. However, the density of serotonergic fibers was higher in the MAM rats than in the controls, and the distribution pattern of serotonergic fibers was more extensive in the MAM rats. The microdialysis indicated a high basal level and a delayed K+ -evoked 5-HT release in the Sm of MAM rats on postnatal day 10. The present results suggest morphological and functional alterations of serotonergic fibers in the Sm of MAM rats during the critical period of cortical formation.
Gestational and lactational exposure to di(n-butyl) phthalate (DBP) at >/=250 mg/kg/day disrupts male rat reproductive development and function. Although this indicates an antiandrogenic mechanism, DBP and its biologically active metabolite do not interact with the androgen receptor (AR) in vitro. In the present study, we compared the effects of DBP and the antiandrogen flutamide using a shorter exposure during the prenatal period of male sexual differentiation in rats. Pregnant CD rats received DBP at 0, 100, 250, or 500 mg/kg/day po (n = 10) or flutamide at 100 mg/kg/day po (n = 5) from Gestation Days 12 to 21. In F1 males, DBP (500 mg/kg/day) and flutamide caused hypospadias; cryptorchidism; agenesis of the prostate, epididymis, and vas deferens; degeneration of the seminiferous epithelium; and interstitial cell hyperplasia of the testis. Flutamide and DBP (250 and 500 mg/kg/day) also produced retained thoracic nipples and decreased anogenital distance. Interstitial cell adenoma occurred at 500 mg DBP/kg/day in two males. The only effect seen at 100 mg DBP/kg/day was delayed preputial separation. In contrast to flutamide, DBP caused a low incidence of prostate agenesis and hypospadias with no vaginal pouch. The low incidence of DBP-induced intraabdominal testes contrasted with the high incidence of inguinal testes seen with flutamide. Thus prenatal male sexual differentiation is a sensitive period for the reproductive toxicity of DBP. A no observed adverse effect level was not established and the lowest observed (adverse) effect level was 100 mg/kg/day. Flutamide and DBP disrupted the androgen signaling necessary for male sexual differentiation but with a different pattern of antiandrogenic effects. DBP is an example of an environmental antiandrogen that disrupts androgen-regulated male sexual differentiation without interacting directly with the AR, as does flutamide.