Effects of ethanol and other aliphatic alcohols on NO‐mediated relaxations in rat anococcygeus muscles and gastric fundus strips

Rand, M. J.; Li, Chun Guang

doi:10.1111/j.1476-5381.1994.tb14856.x

Cited by 7 publications

(1 citation statement)

References 19 publications

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“…It has been suggested that ethanol and other aliphatic alcohols might interact chemically with nitric oxide to form nitrosylated compounds such as ethyl nitrite, thus sequestering the nitric oxide and explaining their ability to inhibit nitric oxide‐mediated relaxation of rat anococcygeus muscle and gastric fundus ( Rand & Li, 1994 ). The possible nitrosylation of alkanols by nitric oxide seems to be of little significance for two reasons.…”

Section: Discussionmentioning

confidence: 99%

Effects of short chain alkanols on the inducible nitric oxide synthase in a glial cell line

Syapin

Rendon

Huron

et al. 1999

British J Pharmacology

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1 Ethanol inhibits inducible nitric oxide synthase (iNOS) expression in C6 glioma cells by an unknown mechanism. Because relatively high concentrations are needed for inhibition in drug-naõÈ ve cells (IC 50 &150 mM), suppression due to cytotoxicity is one possible mechanism that has not been ruled out. Therefore, the present study examined the e ects of ethanol and other alkanols on C6 glioma cell viability and iNOS activity to better understand the mechanism for inhibition. 2 iNOS expression was induced in cell culture with lipopolysaccharide and phorbol ester treatment. Nitrite accumulation in culture medium, the in vitro conversion of [ 3 H]-L-arginine to [ 3 H]-Lcitrulline, and immunoblotting were used to quantify iNOS induction and activity. Trypan blue exclusion, extracellular release of lactate dehydrogenase, and quantity of total cell protein were used as measures of viability. 3 Short chain alkanols, methanol through 1-heptanol, concentration-dependently inhibited nitrite accumulation. Longer chain alkanols, 1-octanol and 1-decanol, did not except at cytotoxic concentrations. Experiments indicated short chain alkanol inhibition was not due to direct actions on iNOS catalytic activity, but that it transpires during iNOS induction. Immunoblots showed reduced iNOS protein levels. 4 Correlation analysis ruled out iNOS inhibition as being due to decreased cell number, total cell protein, or cell viability. In contrast, there was signi®cant correlation with physical measures of lipophilicity. 5 In conclusion, inhibition of iNOS expression by ethanol and other short chain alkanols is not due to cytotoxicity. Instead, the strong correlation with lipophilicity suggests the inhibition derives from an interaction with unknown hydrophobic cellular sites.

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Section: Discussionmentioning

confidence: 99%