PubMed · 574716
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K W Kang, J C Christian. 1979. Twin data analysis.. https://pubmed.ncbi.nlm.nih.gov/574716/
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Comparative molecular field analysis (CoMFA) was performed on polyhalogenated dibenzo-p-dioxins, dibenzofurans, and biphenyls for Ah (dioxin) receptor binding and associated enzyme inducing activities determined by others using in vitro assays. Since various members of all three classes of compounds have been shown to produce qualitatively similar toxicities, a separate CoMFA was performed on each class of compounds and combinations of the different classes for each bioactivity which included combining all three classes of molecules in one CoMFA study. For the Ah receptor binding, the CoMFA-derived QSARs for all three classes of compounds and combinations thereof showed strong crossvalidated correlations indicating that they are highly predictive. For enzyme induction, the CoMFA-derived QSARs were highly predictive for the dibenzofurans but were only partially successful for the dioxins. For the biphenyls, the results were clearly unpredictive. The overall results of these CoMFA studies which include both steric and electrostatic considerations are compared and contrasted to other SAR models that have met with some success in making qualitative predictions about the potential for receptor binding and associated toxicity in these classes of compounds. The CoMFA-derived QSAR for the dioxin series of molecules in most cases significantly overestimates the enzyme inducing ability of the ortho-substituted biphenyls. This weak inducing activity of the o-biphenyls is, however, consistent with their relatively low dioxin-like toxicity as measured in other biological systems. Fundamentally different mechanisms may be operating in the expression of dioxin-like toxic responses for the o-biphenyls, and their direct, dioxin-like toxic equivalency perhaps needs to be reconsidered in this light.
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Induction of aryl hydrocarbon hydroxylase (AHH) activity in the placenta as a result of maternal exposure to polycyclic aromatic hydrocarbons contained in cigarette smoke has been well documented. Furthermore, calcifications are more prevalent in the placentas of pregnant smokers than in those of non-smokers. The present study examines whether this latter relationship could be explained by the induction of AHH activity in the placenta. AHH levels were determined at birth in 141 unselected pregnant women admitted for delivery. Macroscopic placental examination was performed for vascular lesions, abnormalities of placental shape, of the cord and parameters of placental maturity such as basal and parenchymatous calcifications. Significant increases in the prevalence of calcifications of the placental basal plates and parenchyma with the induction of placental AHH were found. A similar significant association between smoking and AHH activation was also observed. These findings remained unchanged when controlling for smoking status assessed both by questionnaire and presence of cotinine in mother's urine. Moreover, the apparent association between smoking 'factor' and calcifications disappeared when controlling for AHH induction. Therefore, the association between smoking and placental calcifications previously related could be mediated by the AHH induction.