Nervous system disruption and swimming abnormality in early-hatched pufferfish (Takifugu niphobles) larvae caused by pyrene is independent of aryl hydrocarbon receptors.

Pyrene, a member of the polycyclic aromatic hydrocarbons (PAHs), contributes to abnormality in the size of the brain and the swimming behavior of pufferfish (Takifugu niphobles) larvae. We hypothesized that the aryl hydrocarbon receptor (AHR) may mediate pyrene-induced toxic effects because AHR is assumed to be a candidate for the downstream target of PAHs in many cases. To identify the contribution of AHR on developing pufferfish, we performed exposure experiments using β-naphthoflavone, an agonist of AHR. We found that the toxic effects of pyrene and β-naphthoflavone in pufferfish larvae are fundamentally different. Pyrene specifically induced problems in the developing midbrain and in swimming behavior, while β-naphthoflavone affected the heartbeat rate and the size of the yolk. These results suggest that the behavioral and morphological abnormality caused by pyrene exposure is mediated by an AHR-independent pathway. Alternatively, defects caused by pyrene may be attributed to the inhibition of the FGF signal.