Microplastics are ubiquitous in marine environments and may cause unexpected ecological effects. This study adopted a whole life-cycle exposure to illuminate the impact of polystyrene microplastics on life-history strategies of marine medaka (Oryzias melastigma), including the hatching of embryos, growth and reproduction of F₀ generation, and embryonic and larval development of F₁ offspring. Microplastics accumulated on the eggshell and reduced embryonic hatching rate and larval body length and weight. Similarly, 150 days of microplastic exposure decreased body mass and gonadosomatic index of adult fish, but accelerated sexual maturity of female fish, showing a trade-off between growth and reproduction. Microplastic exposure also caused obvious histopathological damages to gonads and decreased egg productions and fertilization rates. Moreover, parental microplastic exposure induced elevated heartbeats, premature hatching, and slow growth in F₁ offspring. Anti-oxidative stress response, sex hormone disruption, and disturbed transcription of steroidogenic genes in the reproductive axis could partially explain the reproduction impairment and transgenerational trade-offs. Furthermore, transcriptome analysis revealed that the steroid hormone biosynthesis and cytochrome P450 pathways in the testes of male fish were significantly affected after 20 μg/L microplastic exposure. These findings suggest that microplastic pollution may be an emerging threat to the sustainability of marine fish population.

微塑料在海洋环境中无处不在，并可能导致意想不到的生态影响。这项研究采用了整个生命周期暴露，以阐明聚苯乙烯微塑料对海洋花（Oryzias melastigma）的生命历史策略的影响，包括胚胎的孵化，F ₀代的生长和繁殖以及F的胚胎和幼体发育。_1个后代。微塑料积聚在蛋壳上，降低了孵化率，降低了幼虫的体长和体重。同样，暴露于塑料中的150天降低了成鱼的体重和性腺指数，但加速了雌鱼的性成熟，显示出生长和繁殖之间的权衡。暴露于微量的塑料也对性腺造成了明显的组织病理学损害，并降低了产蛋量和受精率。此外，父母暴露于塑料中会引起心跳加快，孵化过早以及F _1的生长缓慢后代。抗氧化应激反应，性激素破坏和生殖轴中类固醇生成基因的转录受阻可以部分解释生殖障碍和跨代折衷。此外，转录组分析显示，暴露于20μg/ L的微塑料后，雄鱼睾丸中类固醇激素的生物合成和细胞色素P450途径受到显着影响。这些发现表明，微塑性污染可能是对海水鱼类种群可持续性的新威胁。