Antiestrogenicity of clarified slurry oil and two crude oils in a human breast-cancer cell assay

Exposure to crude oil and certain petroleum products can be a serious healt h hazard. Clarified slurry oil (CSO) is a complex mixture of hydrocarbons d erived from the processing of crude oil, and is a known systemic and develo pmental toxicant. mutagen, and carcinogen. In the present study, CSO and tw o crude oils, Belridge heavy crude oil (BHCO) and Lost Hills light crude oi l (LHLCO), were examined for their estrogenic and antiestrogenic properties in a human breast-cancer cell (MCF-7) assay. The MCF-7 focus assay is base d on postconfluent cell growth and tissue restructuring, measured as the po stconfluent development of multicellular nodules or loci. The mutagenicity indices of BHCO and LHLCO also were determined in a modified Ames Salmonell a assay. Oil samples were prepared in dimethyl sulfoxide, resulting in extr action of virtually all of the aromatic compounds including the sulfur- and nitrogen-substituted three- to seven-ring polycyclic aromatic compounds co mprising 62.2% of the CSO, 9% of the BHCO, and 2% of the LHLCO by total wei ght. None of the three samples was estrogenic in the MCF-7 locus assay. In contrast, all of the samples were antiestrogenic; that is, they inhibited t he development of foci induced by 1 nM 17 beta -estradiol (E-2). The potenc ies of the oil samples for both antiestrogenicity and mutagenicity were cor related with the percent of polycyclic aromatic compounds they contained. T wo potential mechanisms for the observed antiestrogenicity were examined. R adiometric analysis of the catabolism of [H-3]E-2 in MCF-7 cell cultures de monstrated that all three samples increased catabolism of E-2. Results from a whole-cell estrogen-receptor (ER) binding assay suggested that metabolit es of compounds in the oil samples might have competed with [H-3]E-2 for ER in the MCF-7 cultures. Thus the antiestrogenicity ui the oil samples may o ccur through at least two mechanisms, increased catabolism of E-2 and antag onistic binding to ER.