Li Lanlan, Liu Zhe, Zhao Guiyan, Quan Jinqiang, Sun Jun, Lu Junhao
College of Animal Science & Technology, Gansu Agricultural University, No. 1 Yingmen Village, Anning District, Lanzhou, 730070, Gansu Province, China.
Biol Trace Elem Res. 2023 Dec;201(12):5805-5815. doi: 10.1007/s12011-023-03637-9. Epub 2023 Mar 27.
The cold-water fish rainbow trout (Oncorhynchus mykiss) shows poor resistance to heat, which is the main factor restricting their survival and yield. With the advancement of nanotechnology, nano-selenium (nano-Se) has emerged as a key nano-trace element, showing unique advantages, including high biological activity and low toxicity, for studying the response of animals to adverse environmental conditions. However, little is still known regarding the potential protective mechanisms of nano-Se against heat stress-induced cellular damage. Herein, we aimed to investigate the mechanism underlying the antagonistic effects of nano-Se on heat stress. Four groups were assessed: CG18 (0 μg/mL nano-Se, 18 °C), Se18 (5.0 μg/mL nano-Se, 18 °C), CG24 (0 μg/mL nano-Se, incubated at 18 °C for 24 h and then transferred to 24 °C culture), and Se24 (5.0 μg/mL nano-Se, incubated at 18 °C for 24 h and then transferred to 24 °C culture). We found that after heat treatment (CG24 group), T-AOC, GPx, and CAT activities in rainbow trout hepatocytes showed a decrease of 36%, 33%, and 19%, respectively, while ROS and MDA levels showed an increase of 67% and 93%, respectively (P < 0.05). Meanwhile, the mRNA levels of the apoptosis-related genes caspase3, caspase9, Cyt-c, Bax, and Bax/Bcl-2 in the CG24 group were 41%, 47%, 285%, 65%, and 151% higher than those in the CG18 group, respectively, while those of PI3K and AKT were 31% and 17% lower, respectively (P < 0.05). Besides, flow cytometry analysis showed an increase in the level of apoptotic cells after heat exposure. More importantly, we observed that nano-Se cotreatment (Se24 group) remarkably attenuated heat stress-induced effects (P < 0.05). We conclude that heat stress induces oxidative stress and apoptosis in rainbow trout hepatocytes. Nano-Se ameliorates heat stress-induced apoptosis by activating the PI3K/AKT pathway. Our results provide a new perspective to improve our understanding of the ability of nano-Se to confer heat stress resistance.
冷水鱼虹鳟(Oncorhynchus mykiss)对热的耐受性较差,这是限制其生存和产量的主要因素。随着纳米技术的发展,纳米硒(nano-Se)已成为一种关键的纳米微量元素,在研究动物对不利环境条件的反应方面显示出独特优势,包括高生物活性和低毒性。然而,关于纳米硒对热应激诱导的细胞损伤的潜在保护机制仍知之甚少。在此,我们旨在研究纳米硒对热应激的拮抗作用机制。评估了四组:CG18(0μg/mL纳米硒,18°C)、Se18(5.0μg/mL纳米硒,18°C)、CG24(0μg/mL纳米硒,在18°C孵育24小时,然后转移至24°C培养)和Se24(5.0μg/mL纳米硒,在18°C孵育24小时,然后转移至24°C培养)。我们发现,热处理后(CG24组),虹鳟肝细胞中的总抗氧化能力(T-AOC)、谷胱甘肽过氧化物酶(GPx)和过氧化氢酶(CAT)活性分别下降了36%、33%和19%,而活性氧(ROS)和丙二醛(MDA)水平分别升高了67%和93%(P<0.05)。同时,CG24组中凋亡相关基因caspase3、caspase9、细胞色素c(Cyt-c)、Bax以及Bax/Bcl-2的mRNA水平分别比CG18组高41%、47%、285%、65%和151%,而磷脂酰肌醇-3激酶(PI3K)和蛋白激酶B(AKT)的mRNA水平分别低31%和17%(P<0.05)。此外,流式细胞术分析显示热暴露后凋亡细胞水平增加。更重要的是,我们观察到纳米硒联合处理(Se24组)显著减轻了热应激诱导的影响(P<0.05)。我们得出结论,热应激诱导虹鳟肝细胞氧化应激和凋亡。纳米硒通过激活PI3K/AKT途径改善热应激诱导的凋亡。我们的结果为增进对纳米硒赋予热应激抗性能力的理解提供了新视角。