In recent years increased frequencies of malformations among eelpout fry living in coastal areas with high anthropogenic input have been observed. Eelpout (Zoarces viviparous) is the only viviparous fish species in Northern Europe, which makes this species very suitable for investigation of mother-offspring interactions and effects in the offspring upon maternal exposure to various chemicals. In oviparous fish species malformations can be induced by exposure to chemicals, including endocrine disrupting substances. Hence the malformations observed in wild eelpout could be due to anthropogenic chemicals. The specific chemicals or group of chemicals causing the malformations observed in nature are not known, but similar malformations upon exposure of pregnant eelpout to octylphenol (OP) and 17β-estradiol (E2) in high concentrations have recently been observed in the laboratory. In the current two experiments pregnant eelpout with newly fertilized eggs were exposed to 5.7-133 ng E2/L (autumn 2011) and 6.25-50 µg 4-t-OP/L, 500 ng pyrene/L or 5 ng EE2/L (autumn 2012) for 6 weeks in order to establish no effect concentrations for the teratogenic effect (fry malformations) of E2 and OP in eelpout and to investigate if two environmental chemicals with known endocrine disrupting effects, the PAH pyrene and the synthetic hormone 17α-ethinylestradiol (EE2), could induce similar teratogenic effects. Exposure of female eelpouts to environmentally realistic concentrations of E2 during early pregnancy increased the abundance of larvae malformations and the amount of ovarian fluid was signicficantly reduced. Plasma levels of E2 and vitellogenin increased with increasing E2 exposure. Similar endpoints were investigated in the experiment with OP, pyrene and EE2. The results also indicate that there is a sensitive window for induction of malformations in eelpout fry.