Table 2.

Effects of steroid biosynthetic enzyme inhibitors

Treatment groupsCortical 3α, 5α, THP (ng/gm)Plasma Progesterone (ng/ml)Plasma Corticosterone (ng/ml)n
Saline1.93  ± 0.343.40  ± 0.9098.5  ± 2314
Ethanol10.5  ± 0.8787.6  ± 7.3476  ± 2918
Ethanol + trilostane10.4  ± 0.9237.3  ± 7.3*7
Ethanol + finasteride5.9  ± 1.0*66.7  ± 8.9202  ± 1.0*6
Ethanol + indomethacin14.9  ± 89*72.3  ± 1332.4  ± 13*7
  • *Significantly different from ethanol alone p < 0.01.

  • Steroid biosynthetic enzyme inhibitors differentially alter ethanol effects on cerebral cortical 3α,5α-THP levels. Ethanol (2 gm/kg, i.p.) was administered, and 3α,5α-THP levels were measured in cerebral cortex 1 hr after ethanol administration. Trilostane was administered 30 mg/kg, i.p. 1 hr before ethanol. The 5α-reductase inhibitor finasteride was administered 25 mg/kg, s.c., 4 and 1.5 hr before ethanol. The 3α-hydroxysteroid oxidoreductase inhibitor indomethacin was administered 0.1 mg/kg, i.p., 20 min before ethanol (Morrow et al., 1998). Cortical allopregnanolone levels were significantly decreased with finasteride pretreatment and significantly increased with indomethacin pretreatment, one-way ANOVA,F = 30.99, df = 4,47, p < 0.0001 with Dunnett's multiple comparison post hoc(p < 0.05 for both finasteride and indomethacin). Pretreatment with trilostane increased plasma progesterone levels, one-way ANOVA, F = 26.05, df = 4,47, p < 0.0001 with Dunnett's multiple comparisonpost hoc (p < 0.01). Pretreatment with finasteride and indomethacin decreased plasma corticosterone levels, one-way ANOVA, F = 34.29, df = 3.41,p < 0.0001 with Dunnett's multiple comparisonpost hoc (p < 0.01 for both finasteride and indomethacin).