2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can induce drug transporter genes such as the ATP-binding cassette G member 2 (ABCG2), which contributes to multidrug resistance. We investigated the effect of TCDD pretreatment on drug transporters induction from cancer cells of various origins. Cell viabilities after treatment of cisplatin were measured to evaluate acquiring cisplatin resistance by TCDD. Acquring cisplatin resistance was found only in cisplatin senstivie cancer cells including gastric SNU601, colon LS180, brain CRT-MG and lymphoma Jurkat cells which showed a significant increase in cell viability after combined treatment with TCDD and cisplatin. High increase of ABCG2 gene expression was found in SNU601 and LS180 cells with a mild increase in the expression of the ABCC3, ABCC5,and SLC29A2 genes in SNU601 cells, and of major vault protein (MVP) in LS180 cells. The AhR inhibitor kaempferol suppressed the upregulation of ABCG2 expression and reversed the TCDD-induced increase in cell viability in LS180 cells. However, in CRT-MG cells, other transporter genes including ABCC1, ABCC5, ABCA3, ABCA2, ABCB4, ABCG1, and SLC29A1 were up-regulated. These findings suggested the acquiring cisplatin resistance by TCDD associated with cancer cell-type-specific induction of drug transporters.Graphical Abstract

No abstract

No abstract

The ovarian function decreases with age, and various markers, such as follicle stimulating hormone, inhibin B, antral follicle count, and anti-Müllerian hormone, are used for its evaluation. Recently, exposure to various environmental pollutants in daily life has been reported as an important cause of ovarian function decline. Therefore, the present study aimed to confirm the effect of environmental pollutants on the relationship between age and decline in ovarian function. The exposure levels of 16 environmental pollutants were evaluated in women aged 26-40 years, and the AMH levels and FSH/AMH ratios were used as markers for the decline of ovarian function. The participants were divided into two groups: low-level or high-level for each environmental pollutant if their exposure level was below or above the median respectively. The slope of the decrease or increase in the AMH level and FSH/AMH ratio of each group with age was evaluated. The FSH/AMH ratio better presented the difference in the rate of change with age in each group than did AMH alone. In particular, the rate of change in the FSH/AMH ratio increased 5.2 and 3.7 times (p<0.05) in the group exposed to high levels of the volatile organic compound metabolite, trans, trans-muconic acid and the polycyclic aromatic hydrocarbons metabolite, 2-hydroxynaphthalene, respectively, than in the low-level exposure groups for those metabolites. This study confirmed that environmental pollutants influenced the rate of change in the FSH/AMH ratio with age. Further studies on larger populations are necessary in the future.