Effects of ethanol on glutethimide absorption and distribution in relationship to a mechanism for toxicity enhancement

Hetland, L. B.; Couri, Daniel

doi:10.1016/0041-008x(74)90244-0

Cited by 2 publications

(1 citation statement)

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“…Ethanol has been shown to modify cellular membrane structure and composition (Gruber et al 1977; Chin and Goldstein 1977). Acute and chronic ethanol exposure has also been shown to modify membrane permeability (Isselbacher 1977) and alter brain or tissue distribution of various compounds (Paul and Whitehouse 1977; Hetland and Couri 1974; Seidel 1967; Siemens et al 1977). Second, ethanol may have reduced the metabolism of nicotine by the liver.…”

Section: Discussionmentioning

confidence: 99%

Time-course of extracellular nicotine and cotinine levels in rat brain following administration of nicotine: effects of route and ethanol coadministration

et al. 2014

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Rationale Nicotine and ethanol are commonly coabused drugs, and nicotine-laced ethanol products are growing in popularity. However, little is known about time-course changes in extracellular nicotine and cotinine levels in rat models of ethanol and nicotine coabuse. Objectives The objective of the present study was to determine the time-course changes in brain levels of nicotine and cotinine following subcutaneous (SC) and intragastric (IG) nicotine administration in alcohol-preferring (P) and Wistar rats. Methods In vivo microdialysis was used to collect dialysate samples from the nucleus accumbens shell (NACsh) for nicotine and cotinine determinations, following SC administration of (−)-nicotine (0.18, 0.35, and 0.70 mg/kg) in female P and Wistar rats or IG administration of (−)-nicotine (0.35 and 0.70 mg/kg) in 15 % (v/v) ethanol or water in female P rats. Results SC nicotine produced nicotine and cotinine dialysate levels as high as 51 and 14 ng/ml, respectively. IG administration of 15 % EtOH + 0.70 mg/kg nicotine in P rats resulted in maximal nicotine and cotinine dialysate levels of 19 and 14 ng/ml, respectively, whereas administration of 0.70 mg/kg nicotine in water resulted in maximal nicotine and cotinine levels of 21 and 25 ng/ml, respectively. Nicotine and cotinine levels were detectable within the first 15 and 45 min, respectively, after IG administration. Conclusions Overall, the results of this study suggest that nicotine is rapidly adsorbed and produces relevant extracellular brain concentrations of nicotine and its pharmacologically active metabolite, cotinine. The persisting high brain concentrations of cotinine may contribute to nicotine addiction.

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