Altered gene expression: a mechanism for reproductive toxicity in zebrafish exposed to benzo[a]pyrene

Exposure of fish to polycyclic aromatic hydrocarbons (PAHs) has consistently been shown to have a negative impact on reproduction (e.g. decreased spawning success, decreased ovarian somatic index (OSI) and lower circulating levels of 17beta-estradiol and vitellogenin). While an understanding of the mechanism behind these changes has yet to be fully elucidated, it has been proposed that PAHs can alter the expression of genes important in regulating reproduction. The objectives of this study were to: (1) determine the effect of exposure to waterborne benzo[a]pyrene (B[a]P) (0, 1.5 and 3.0 microg/L) for 56 days on egg production and OSI in female zebrafish (Danio rerio) and (2) determine the effect of B[a]P on transcription of genes involved in reproduction including gonadotropins (follicle stimulating hormone (FSH) and luteinizing hormone (LH)), steroidogenic enzymes (CYP11A1, CYP17, CYP19A1, CYP19A2 and 20beta-HSD), estrogen receptor beta (ERbeta) and vitellogenin. Cytochrome P4501A1 (CYP1A1) was also measured in the liver and heads as an indicator of exposure to B[a]P. A reduction in total egg output was observed in B[a]P exposed fish as well as a decrease in OSI in fish exposed to 3.0 microg/L B[a]P. A significant increase in CYP1A1 expression in the heads as compared to the control was observed whereas no significant difference in CYP1A1 was detected in livers. A significant increase in 20beta-HSD mRNA occurred in heads and pre-vitellogenic oocytes from fish exposed to 1.5 and 3.0 microg/L as compared to the controls. CYP19A2 and vitellogenin were significantly increased following exposure to 3.0 microg/L in the heads and liver, respectively. No effects on the expression of FSH, LH, CYP19A1 or ERbeta were observed. Results from this study demonstrate that reproduction in zebrafish is affected by waterborne exposure to B[a]P and that altered transcription of genes important in regulating reproduction (20beta-HSD, CYP19A2 and vitellogenin) may be one of the underlying mechanisms of B[a]P-induced reproductive toxicity.