Ministry of Education Key Laboratory for Ecology of Tropical Islands, College of Life Sciences, Hainan Normal University, Haikou, China.
Ministry of Education Key Laboratory for Ecology of Tropical Islands, College of Life Sciences, Hainan Normal University, Haikou, China; Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu, China.
Comp Biochem Physiol C Toxicol Pharmacol. 2019 May;219:59-67. doi: 10.1016/j.cbpc.2019.02.004. Epub 2019 Feb 7.
The red-eared slider (Trachemys scripta elegans), a freshwater turtle, is an invasive species in many parts of the world where it survives in both freshwater and coastal saline habitats. High salinity can induce reactive oxygen species (ROS) production and lead to oxidative damage. In this study, we investigate the antioxidant defense mechanisms of T. s. elegans in response to salinity stress. The results showed that the mRNA expression levels of superoxide dismutase (SODs), catalase (CAT) and glutathione peroxidase (GSH-PXs) were significantly increased in both 5 psu and 15 psu groups at the early stages of salinity exposure (generally 6-48 h), but typically returned to control levels after the longest 30 d exposure. In addition, hepatic and cardiac mRNA levels of the NF-E2-related factor 2 (Nrf2), showed a similar upregulation as an early response to stress, but decreased at 30 d in the 5 psu and 15 psu groups. The mRNA levels of the negative regulator of Nrf2, kelch-like ECH associating protein 1 (Keap1), exhibited the opposite pattern. Moreover, mRNA expression levels of target of rapamycin (TOR) and ribosomal protein S6 kinase 1 (S6K1) in liver and heart showed roughly similar patterns to those for Nrf2. Furthermore, the content of malondialdehyde (MDA) was significantly increased in liver, especially in the 15 psu group by ~2.5-fold. Taken together, these results indicate that T. s. elegans may activate the TOR-Nrf2 pathway to modulate antioxidant genes transcription in order to promote enhanced antioxidant defense in response to salinity stress.
红耳滑龟(Trachemys scripta elegans),一种淡水龟,在世界许多地区都是入侵物种,它既能在淡水栖息地,也能在沿海咸水栖息地生存。高盐度会诱导活性氧(ROS)的产生,导致氧化损伤。在这项研究中,我们研究了 T. s. elegans 对盐度胁迫的抗氧化防御机制。结果表明,在盐度暴露的早期(通常在 6-48 小时),5 psu 和 15 psu 组的超氧化物歧化酶(SODs)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-PXs)的 mRNA 表达水平显著升高,但在最长 30 天的暴露后,通常会恢复到对照水平。此外,肝脏和心脏中核因子 E2 相关因子 2(Nrf2)的 mRNA 水平表现出类似的早期应激上调,但在 5 psu 和 15 psu 组中,在 30 天暴露时下降。Nrf2 的负调控因子 Kelch 样 ECH 相关蛋白 1(Keap1)的 mRNA 水平则呈现相反的模式。此外,肝脏和心脏中雷帕霉素靶蛋白(TOR)和核糖体蛋白 S6 激酶 1(S6K1)的 mRNA 表达水平与 Nrf2 的表达模式大致相似。此外,肝脏中丙二醛(MDA)的含量显著增加,特别是在 15 psu 组中增加了约 2.5 倍。总之,这些结果表明,T. s. elegans 可能激活 TOR-Nrf2 途径来调节抗氧化基因的转录,以促进抗氧化防御系统增强,从而应对盐度胁迫。