大黄素对高温和氧化应激诱导黄颡鱼雄性化的挽救研究

THE RESCUE OF HIGH TEMPERATURE AND OXIDATIVE STRESS-INDUCED MASCULINIZATION IN YELLOW CATFISH (TACHYSURUS FULVIDRACO) BY EMODIN

  • 摘要: 为探究高温等环境胁迫诱导黄颡鱼(Tachysurus fulvidraco)雄性化的机制及其挽救方法, 研究以XX遗传型黄颡鱼为材料, 利用高温(HT)、过氧化氢(H2O2)和HT-H2O2双重应激进行处理, 并在HT-H2O2处理下试图用大黄素(Emodin)对雄性化进行挽救。实验设置3个雄性化诱导处理组, 分别为HT组(33.5℃)、HP组(1 μmol/L H2O2浸泡)、TP组(33.5℃+1 μmol/L H2O2浸泡), 及一个挽救组: TPE组(33.5℃+1 μmol/L H2O2浸泡+300 mg/kg E拌饲料), 在性别分化时期(12—80DPH)进行处理。结果显示, HT、HP和TP组雄性化比例分别为23.7%、13.9%和41.6%, 而TPE组雄性化比例为6.9%, 且均为间性性腺, 表明大黄素处理显著降低了应激诱导的雄性化。氧化应激指标测定结果显示, 伪雄性CAT、SOD活性和MDA含量较雌性显著上升, TPE组GSH-Px活性较应激组极显著升高, 推测高温或过氧化氢通过提高氧化应激水平诱导黄颡鱼雄性化, 而添加大黄素通过提高抗氧化能力或降低氧化应激水平对雄性化产生挽救效果。进一步, 在池塘培育的XX全雌种群养殖中通过饲料拌喂500 mg/kg大黄素, 结果显示96.4%个体卵巢正常发育, 仅3.6%个体发育为伪雄鱼。研究初步明确了氧化应激参与高温等环境胁迫诱导的雄性化, 而具有抗氧化功能的大黄素能挽救环境胁迫诱导的雄性化。研究结果对于深入理解鱼类性别分化可塑性及性逆转解救提供了重要依据。

     

    Abstract: The masculinization caused by environmental stress, such as high temperatures, has severely impacted aquaculture worldwide, but the mechanisms and rescue methods have not yet been reported. Producing XX genotypic all-female yellow catfish is an important approach for conducting their genetic improvement, however, high water temperatures and other environmental stresses can induce masculinization, which has seriously affected the breeding efficiency based on all-female populations. In the present study, XX genotypic yellow catfish were used as experimental materials and treated with high temperature (HT), hydrogen peroxide (H2O2), and HT-H2O2 dual stress. Under HT-H2O2 treatment, emodin (E, with antioxidant function) was used to rescue masculinization. The experiment set up three masculinization induction treatment groups, i.e. HT group (33.5℃), HP group (1 μmol/L H2O2), TP group (33.5℃+1 μmol/L H2O2), and a rescue group, TPE group (33.5℃+1 μmol/L H2O2+300 mg/kg E mixed with feed), which were treated during the period of sex differentiation (12—80 DPH). The results showed that the masculinization rates in the HT, HP, and TP groups were 23.7%, 13.9%, and 41.6%, respectively. In comparison, the masculinization rate in the TPE group was 6.9%, all with intersex gonads, indicating that emodin treatment significantly reduced stress-induced masculinization. The oxidative stress indicators showed that CAT and SOD activities and MDA content of the pseudo-male increased significantly compared to females (P<0.05). The GSH-Px activity in the TPE group increased significantly compared to the stress group, suggesting that the addition of emodin improved antioxidant capacity and rescued masculinization. Furthermore, field experiments in pond-reared XX all-female stocks demonstrated that feeding fish 500 mg/kg of emodin resulted in 96.4% of individuals exhibiting normal ovarian development, while only 3.6% developed into pseudo-males. This study preliminarily clarifies that oxidative stress is involved in environmental stress-induced masculinization, and emodin with antioxidant function can rescue the masculinization induced by environmental stress. The results provide an important basis for a deeper understanding of sex differentiation plasticity and offer a potential strategy for sex reversal rescue in fish.

     

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