Independently of their ability to activate the AhR, benzonaphthothiophene, 2,1-naphthylbenzothiophene, 3,1-naphthylbenzothiophene, and 3,2-naphthylbenzothiophene inhibited gap junctional intercellular communication in a model of rat liver epithelial cells.

Benzonaphthothiophene and 3,2-naphthylbenzothiophene elicited AhR-mediated activity only in the rat liver cell model, while dibenzothiophene and 3,1-naphthylbenzothiophene were inactive in either cell type. Benzonaphthothiophene, benzonaphthothiophene, 2,2-naphthylbenzothiophene, and 2,1-naphthylbenzothiophene were newly identified as efficient AhR agonists in both rat and human AhR-based reporter gene assays, with 2,2-naphthylbenzothiophene being the most potent compound identified in both species. Here, we studied the aryl hydrocarbon receptor (AhR)-mediated activity of dibenzothiophene, benzonaphthothiophenes, and naphthylbenzothiophenes, as well as their presence in two types of environmental matrices: river sediments collected from both rural and urban areas, and in airborne particulate matter (PM 2.5) sampled in cities with different levels and sources of pollution. Polycyclic aromatic sulfur heterocyclic compounds (PASHs) belong among ubiquitous environmental pollutants however, their toxic effects remain poorly understood.

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