We conducted this study to determine the toxicity mechanism of polycyclic aromatic hydrocarbons(PAHs) on the early development of the marine fish Centropristis striata. We analyzed individual exposure tophenanthrene (Phe), pyrene (Py), and benzo(a)pyrene (BaP) and co-exposure of each with α-naphthoflavone (ANF)to assess their toxic effects on early embryonic and larval development of C. striata. The results showed a cleardose-response relationship between Bap and Py concentration and ethoxyresorufin-O-deethylase (EROD) activitycompared with that of Phe. The effects of the PAHs on EROD activity were in the order Bap (857.52% of control)> Py (514.21%) > Phe (280.50%). Maximum EROD activity occurred at the highest concentration comparedwith that of the control group. EROD activity was inhibited (189.27%, 278.55%, and 195.40% of the control)when ANF was added to Bap, Py, and Phe, respectively. Toxicity of the PAHs to hatching rate, deformity index,and early embryo and larval mortality was in the order of Bap > Py > Phe. PAH concentration and the percentageof fertilized eggs and hatching rate were negatively correlated but PAH concentration was positively correlatedwith larval mortality and the deformity index. Bap and Py showed reduced toxicity when combined withANF. These results show that PAHs with different ring structures have obvious toxic effects, although there weredifferences in the mechanisms among them.