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水生缺氧扰乱日本沼虾(Macrobrachium nipponense)睾丸发育:跨代研究。

Aquatic hypoxia disturbs oriental river prawn (Macrobrachium nipponense) testicular development: A cross-generational study.

机构信息

Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources, Ministry of Education, Shanghai Ocean University, Shanghai, 201306, China; International Research Center for Marine Biosciences at Shanghai Ocean University, Ministry of Science and Technology, China; National Demonstration Center for Experimental Fisheries Science Education, Shanghai Ocean University, Shanghai, China.

Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources, Ministry of Education, Shanghai Ocean University, Shanghai, 201306, China.

出版信息

Environ Pollut. 2020 Nov;266(Pt 3):115093. doi: 10.1016/j.envpol.2020.115093. Epub 2020 Jun 29.

Abstract

Recently, we reported that hypoxia disrupts the endocrine system and causes metabolic abnormalities in prawns. Although transgenerational impairment effects of hypoxia have become a hot topic in vertebrate, it is unknown whether hypoxia could exert cross-generational effects on testicular function crustaceans. The present study aimed to investigate hypoxia's toxic effects on the testicular function of oriental river prawns (Macrobrachium nipponense) and offspring development. Hypoxia disrupted testicular germ cells quality, caused sex hormone imbalance (testosterone and estradiol), and delayed testicular development. The F1 generation derived from male prawns exposed to hypoxia showed retarded embryonic development, and reduced hatching success and larval development, despite not being exposed to hypoxia. Analysis of the transcriptome the F0 generation (exposed to hypoxia) showed that the impaired testicular functions were associated with changes to mitochondrial oxidative phosphorylation, apoptosis, and steroid biosynthesis. Interestingly, quantitative real-time PCR confirmed that hypoxia could significantly suppress the expression of antioxidant and gonad development-related genes in the testis of the F1 generations, with and without continued hypoxia exposures. In addition, paternal exposure to hypoxia could result in a higher production of reactive oxygen species in offspring testis tissue compared with those without hypoxia exposure. The cross-generational effects of testicular function implied that the sustainability of natural freshwater prawn populations would be threatened by chronic hypoxia.

摘要

最近,我们报道了低氧会破坏虾类的内分泌系统并导致代谢异常。尽管低氧对脊椎动物的跨代损伤效应已成为一个热门话题,但低氧是否会对甲壳类动物的睾丸功能产生跨代效应尚不清楚。本研究旨在探讨低氧对日本沼虾(Macrobrachium nipponense)睾丸功能和后代发育的毒性作用。低氧破坏了睾丸生殖细胞的质量,导致性激素失衡(睾酮和雌二醇),并延迟了睾丸发育。尽管未暴露于低氧,但来自雄性虾暴露于低氧的 F1 代表现出胚胎发育迟缓,孵化成功率和幼虫发育降低。对 F0 代(暴露于低氧)的转录组分析表明,受损的睾丸功能与线粒体氧化磷酸化、细胞凋亡和类固醇生物合成的改变有关。有趣的是,定量实时 PCR 证实,低氧可显著抑制 F1 代睾丸中抗氧化和性腺发育相关基因的表达,无论是否继续暴露于低氧。此外,与未暴露于低氧的雄性虾相比,父本暴露于低氧会导致其后代睾丸组织中产生更高水平的活性氧。睾丸功能的跨代效应表明,慢性低氧会威胁到天然淡水虾种群的可持续性。

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