Affiliation: | a High-Tech Research Center, Institute of Biosciences, Azabu University, Fuchinobe, Sagamihara, Kanagawa 229-8501, Japan b Laboratory of Pathobiochemistry, Department of Pathology, School of Veterinary Medicine, Azabu University, Fuchinobe, Sagamihara, Kanagawa 229-8501, Japan c Laboratory of Biochemistry, Division of Applied Life Science, Graduate School of Agriculture, Kyoto University, Kyoto 606-8502, Japan |
Abstract: | Endocrine disrupters such as sex hormone-like chemicals and the non-physiological ligands for aryl hydrocarbon receptor (AhR) exert many adverse biological effects. The ligands for AhR disturb gene expression downstream of the gene induced by estrogen receptor at a very low concentration. Thus, transepithelial transport and cellular accumulation of cortisol (COR) and estrogen as congeners of sex hormone-like chemicals, and 3,3′,4,4′-tetrachlorobiphenyl (TeCB) as one of the ligands for AhR were examined in a monolayer of porcine kidney cells transfected with human P-glycoprotein (LLC-COL). The net basal-to-apical transport of COR increased in LLC-COL compared to that in the wild type cells (LLC-PK1) the same as in vinblastine, whereas the net transport of estradiol (EST) was not detected in either cell group. Though the diffusion transports of EST for both directions, basal-to-apical and apical-to-basal, were higher than that of COR, cellular accumulation of EST was higher than that of COR. Transepithelial transport of TeCB was very low and the net basal-to-apical transport was not detected, while it was highly accumulated in the epithelial cells. The accumulation was slightly higher in LLC-COL than in LLC-PK1 at high dose. |