Hypoxic and temporal variation in the endocrine disrupting toxicity of perfluorobutanesulfonate in marine medaka(Oryzias melastigma)

Perfluorobutanesulfonate(PFBS)is an emerging pollutant capable of potently disrupting the sex and thyroid endocrine systems of teleosts.However,the hypoxic and temporal variation in PFBS endocrine disrupting toxicity remain largely unknown.In the present study,adult marine medaka were exposed to environmentally realistic concentrations of PFBS(0 and 10μg/L)under normoxia or hypoxia conditions for 7 days,aiming to explore the interactive behavior between PFBS and hypoxia.In addition,PFBS singular exposure was extended till 21days under normoxia to elucidate the time-course progression in PFBS toxicity.The results showed that hypoxia inhibited the growth and caused the suspension of egg spawn regardless of PFBS exposure.With regard to the sex endocrine system,7-day PFBS exposure led to an acute stimulation of transcriptional profiles in females,which,subsequently,recovered after the 21-day exposure.The potency of hypoxia to disturb the sex hormones was much stronger than PFBS.A remarkable increase in estradiol concentration was noted in medaka blood after hypoxia exposure.Changes in sex endocrinology of coexposed fish were largely determined by hypoxia,which drove the formation of an estrogenic environment.PFBS further enhanced the endocrine disrupting effects of hypoxia.However,the hepatic synthesis of vitellogenin and choriogenin,two commonly used sensitive biomarkers of estrogenic activity,failed to initiate in response to the estrogen stimulus.Compared to sex endocrine system,disturbances in thyroidal axis by PFBS or hypoxia were relatively mild.Overall,the present findings will advance our toxicological understanding about PFBS pollutant under the interference of hypoxia.

Exposure to methylparaben at environmentally realistic concentrations significantly impairs neuronal health in adult zebrafish

Methylparaben(MeP)is an emerging aquatic pollutant that is found to impact neural functions.However,it still lacks a comprehensive understanding about its neurotoxicology.The present study exposed adult zebrafish to environmentally realistic concentrations(0,1,3,and 10μg/L)of MeP for 28 days,with objectives to elucidate the neurotoxic effects andmechanisms.Proteomic profiling found that MeP pollutant induced distinct mechanism of neurotoxicity as a function of sex.MeP pollutant appeared to preferentially target the neurotransmission cascade via synapse junctions.In male brain,glutamatergic neural signaling was enhanced by 10μg/L of MeP in characteristics of higher glutamate neurotransmitter content(by 61.9%)and up-regulated glutamate receptor expression by 2.6-fold relative to the control.In MeP-exposed female brain,biomarker proteins of synapse formation and regeneration had significantly lower abundance,accounting for the blockage of synaptic neurotransmission.Furthermore,under the stress of MeP pollutant,both male and female zebrafish initiated a negative feedback mechanism along stress neuroendocrine axis by down-regulating the transcriptions of corticotropin-releasing hormone and its binding protein,which subsequently decreased blood cortisol concentrations.MeP subchronic exposure also disturbed innate immune function.In particular,significant increases in lipopolysaccharide(LPS)content by 15.6%were caused by MeP exposure in male brain,thereby inducing the synthesis of pro-inflammatory cytokines.In contrast,female brain was able to adaptively up-regulate the protein expression of blood brain barrier to inhibit the infiltration of LPS endotoxin into brain.Overall,the present findings pinpoint the potent neurotoxicity of MeP pollutant even at environmentally realistic concentrations.