The failure of the swim bladder to inflate during fish development is a common and sensitive response to exposure to petrochemicals. Here, we review potential mechanisms by which petrochemicals or their toxic components (polycyclic aromatic hydrocarbons; PAHs) may affect swim bladder inflation, particularly during early life stages. Surface films formed by oil can cause a physical barrier to primary inflation by air gulping, and are likely important during oil spills. The act of swimming to the surface for primary inflation can be arduous for some species, and may prevent inflation if this behavior is limited by toxic effects on vision or musculature. Some studies have noted altered gene expression in the swim bladder in response to PAHs, and Cytochrome P450 1A (CYP1A) can be induced in swim bladder or rete mirabile tissue, suggesting that PAHs can have direct effects on swim bladder development. Swim bladder inflation failure can also occur secondarily to the failure of other systems; cardiovascular impairment is the best elucidated of these mechanisms, but other mechanisms might include non-inflation as a sequela of disruption to thyroid signaling or cholesterol metabolism. Failed swim bladder inflation has the potential to lead to chronic sublethal effects that are as yet unstudied.

在鱼类发育过程中，游泳膀胱无法充气是对暴露于石化产品的常见且敏感的反应。在这里，我们回顾了石化产品或其有毒成分（多环芳烃； PAHs）可能影响游泳膀胱充气的潜在机制，特别是在生命早期。由油形成的表面膜可能会由于空气吞咽而对初次膨胀造成物理屏障，并且在溢油期间可能很重要。对于某些物种而言，游泳到水面进行初次充气的行为可能很艰巨，如果这种行为受到对视力或肌肉系统的毒性影响所限制，则可能会阻止充气。一些研究指出，响应PAHs，游泳膀胱中的基因表达发生了变化，并且可以在游泳膀胱或网状奇迹组织中诱导细胞色素P450 1A（CYP1A），提示多环芳烃对游泳膀胱发育有直接影响。游泳膀胱充气失败也可能次于其他系统的失败。可以通过这些机制来最好地阐明心血管损害，但其他机制可能包括非通货膨胀，这是破坏甲状腺信号传导或胆固醇代谢的后遗症。游泳膀胱充气失败有可能导致尚未被研究的慢性亚致死作用。