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Possible Interaction: Ethanol and Finasteride



Research Papers that Mention the Interaction

We also examined whether finasteride (a 5-α steroid reductase inhibitor), which blocks the synthesis of some neuroactive steroids, reduces the subjective response to alcohol.
Neuropsychopharmacology  •  2005  |  View Paper
CONCLUSIONS Injection of alcohol and bleomycin (approximately 10% of the volume of ventral prostatic) as well as consuming finasteride can induce a reduction of 1/3, 1/4 and 1/5 in the hypertrophied gland respectively.
Central European journal of urology  •  2017  |  View Paper
LTP inhibition by corticosterone plus ethanol was blocked by finasteride , an inhibitor of 5α-reductase, suggesting a role for neurosteroid synthesis.
Front. Cell. Neurosci.  •  2015  |  View Paper
Incorporation of PG, EtOH or SLS caused a significant increase in FNS solubility both in the solution and on the skin with SLS > EtOH > PG.
The permeation studies demonstrated that FNS permeation fluxes were enhanced only by EtOH vehicles.
Pharmaceutical development and technology  •  2015  |  View Paper
In a recent work we reported … the neonatal administration of AlloP or finasteride (Finas), an inhibitor of the enzyme 5α-reductase … for AlloP synthesis, altered the voluntary consumption of ethanol and the ventrostriatal dopamine (DA) levels in adulthood, suggesting that … NS manipulations can increase alcohol abuse vulnerability in adulthood.
The results revealed that neonatal Finas increased ethanol consumption in some days of the consumption phase, and decreased the DA release in the NAcc in response to solutions (ethanol+glucose) and food presentation.
Behavioural Brain Research  •  2016  |  View Paper
Finasteride (FIN), a 5α-reductase inhibitor that blocks the formation of ALLO and other GABAergic neurosteroids, alters EtOH sensitivity.
Recently, we found that Withdrawal Seizure-Prone mice from the first genetic replicate (WSP-1) exhibited behavioral tolerance to the anticonvulsant effect of intrahippocampal ALLO during EtOH withdrawal and that intrahippocampal FIN significantly increased EtOH withdrawal severity.
Alcoholism, clinical and experimental research  •  2013  |  View Paper
CONCLUSIONS Although the exact mechanism is unclear, FIN and other pharmacological interventions that modulate the GABAergic system may prove useful in curbing ethanol intake acquisition in at-risk individuals.
Alcoholism, clinical and experimental research  •  2008  |  View Paper
The 5alpha-reductase inhibitor finasteride prevented both the increase in the cerebrocortical concentration of 3alpha,5alpha-TH PROG apparent after 4 weeks of ethanol intake and the changes in NPY immunoreactivity and transgene expression induced by ethanol discontinuation.
Journal of neurochemistry  •  2008  |  View Paper
Pretreatment with finasteride increased acute EtOH withdrawal severity in female C57BL/6J and DBA/2J mice but decreased withdrawal severity in male mice of both strains.
Treatment with finasteride during chronic EtOH exposure decreased EtOH withdrawal severity and blood EtOH concentrations (BECs), suggesting an additional effect of finasteride on EtOH pharmacokinetics.
Neuroscience  •  2007  |  View Paper
Moreover, ethanol increased the amplitude of GABA(A) receptor-mediated miniature inhibitory postsynaptic currents recorded from CA1 pyramidal neurones with greater potency in hippocampal slices prepared from socially isolated rats than in those from group-housed rats, an effect inhibited by finasteride.
The ability of ethanol to inhibit isoniazid-induced convulsions is greater in isolated rats than in group-housed animals and this effect is prevented by treatment with finasteride.
Journal of neurochemistry  •  2006  |  View Paper
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