Accumulation of di(2‐ethylhexyl) phthalate causes endocrine‐disruptive effects in marine medaka (Oryzias melastigma) embryos

Abstract

Di (2-ethylhexyl) phthalate (DEHP) is extensively distributed in marine environments. However, limited research on the toxicological and molecular effects of DEHP on marine organisms has been conducted. Our study investigated the accumulation, elimination, and endocrine-disruptive effects of DEHP on embryonic marine medaka (Oryzias melastigma). The medaka embryos were continuously exposed to DEHP (0.01, 0.1, and 1 mg/L) or 17β-estradiol (E2, 0.01 mg/L) until hatching, and the newly hatched larvae were then transferred to clean sea water for 12 days of depuration. DEHP and E2 appeared to have no significant effects on the mortality and hatching rates of medaka embryos, but E2 exposure significantly delayed the hatching. Significantly higher DEHP embryonic burdens were detected in the group treated with higher DEHP (0.1 and 1 mg/L) at 10 dpf (days post fertilization). The recovered larvae showed an elimination tendency of DEHP during the recovery period. DEHP had no significant effects on the transcriptional responses of endocrine-disrupting biomarker genes in the 3-dpf embryos. Treatment with 0.1 and 1 mg/L DEHP elicited a significant induction of transcriptional responses of ER, PPAR, and the CYP19 genes in a concentration-dependent manner at 10 dpf, indicating endocrine disruption may be due to bioaccumulation of DEHP. With the elimination of DEHP during the depuration period, all of the effects on these genes showed no significant effects. However, 0.1 mg/L E2 significantly affected the expression of ER, PPAR, and the CYP19 genes in the exposed embryos at both 3 and 10 dpf and recovered larvae. Therefore, these results demonstrate that accumulation of DEHP caused endocrine disruption in medaka embryos and that recovery in clean sea water may weaken the endocrine-disrupting effects.

Mediating Roles of PPARs in the Effects of Environmental Chemicals on Sex Steroids

“…In our study, PPAR γ was thought to transduce the toxicity of DEHP at 0.2–2 μ M in both primary cultured endometrial cells and endometrial adenocarcinoma cell line (ishikawa) [ 23 ]. We also obtained consistent results in a marine fish model where the expressions of PPAR γ and aromatase were both enhanced after fish embryo exposure to DEHP at 0.1–1 mg/L [ 24 ]. In vivo, DEHP is metabolized to mono(2-ethylhexyl) phthalate (MEHP) which could activate both PPAR α and PPAR γ and then suppress the transcription of aromatase and estradiol production in the ovary.…”

The Effects of Disturbance on Hypothalamus-Pituitary-Thyroid (HPT) Axis in Zebrafish Larvae after Exposure to DEHP

“…Wang et al . reported that the accumulation of DEHP caused endocrine disruption in medaka embryos [ 22 ]. Zhai et al .…”

Raw and biologically treated paper mill wastewater effluents and the recipient surface waters: Cytotoxic and genotoxic activity and the presence of endocrine disrupting compounds

“…Although present in surface waters in low concentrations BEHP, DBP and NP are posing possible health hazards, while they tend to accumulate in aquatic organisms (Wofford et al, 1981;Lee et al, 2015) and thus can reach the food chain through digestion of fish or when river water is used for irrigating of nearby fields. Published data show that BEHP, DBP, and NP or their metabolites in addition to the disruption of endocrine system (Kloas et al, 1999;Christen et al, 2011;Ye et al, 2016) induce genotoxic and even mutagenic effects (Phillips et al, 1982;Agarwal et al, 1985;Kleinsasser et al, 2001;Frassinetti et al, 2011).…”