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QUANTITATIVE STRUCTURE-TOXICITY RELATIONSHIPS FOR A SERIES OF PRIMARY ALCOHOLS IN A MAMMALIAN VIRAL HOST CELL REACTIVATION ASSAY
Citation:
Benane, S.G., A. Richard, C. Blackman, AND C. Lytle. QUANTITATIVE STRUCTURE-TOXICITY RELATIONSHIPS FOR A SERIES OF PRIMARY ALCOHOLS IN A MAMMALIAN VIRAL HOST CELL REACTIVATION ASSAY. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-94/410 (NTIS PB95125365), 1994.
Description:
Structure-toxicity relationships for alcohols in a wide variety of systems have been found to depend primarily on the effective molar concentration of alcohol that penetrates to a lipid site of action in the cell, and not on specific structural features. n contrast, a structure-activity cutoff based on alcohol chain length has been reported for permeability of bacterial membranes. n te present study, structure-toxicity relationships for inhibition of DNA repair in mammalian cells were investigated for 16 aliphatic alcohols using a monkey kidney fibroblast - herpes simplex virus (HSV) assay. thanol had been studied previously an found to inhibit repair of damaged DNA. ell toxicity and DNA repair inhibition were determined by adding individual alcohols to cell monolayers infected with intact HSV or UV-damaged HSV (UV-HSV), respectively, and measuring reduction in viral plaque formation. og-log plots of 1/[alcohol concentrations yielding 20% reduction in HSV plaque formation of 50% inhibition of US-HSV survival] versus log (octanol/water partition coefficients) yielded highly significant correlations (R2=0.98) in each case. hese quantitative structure-activity relationships imply similar rate limiting steps and re consistent with a baseline molar toxicity model that further validates the HSV repair inhibition assay for toxicity investigations.