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耐热性:DNA损伤、抗氧化防御和应激基因调控的综合分析

Heat Tolerance in : Integrative Analysis of DNA Damage, Antioxidant Defense, and Stress Gene Regulation.

作者信息

Yao Tuo, Wang Xiaodi, Lu Jie, Fu Shengli, Cheng Changhong, Ye Lingtong

机构信息

Key Laboratory of South China Sea Fishery Resources Exploitation & Utilization, Ministry of Agriculture and Rural Affairs, South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou 510300, China.

Sanya Tropical Fisheries Research Institute, Sanya 572018, China.

出版信息

Antioxidants (Basel). 2025 Sep 2;14(9):1075. doi: 10.3390/antiox14091075.

Abstract

Water temperature stands as a crucial environmental element, exerting an impact on the survival and growth of organisms in aquaculture. Heat stress poses a significant threat to the survival and aquaculture of the Hong Kong oyster (also known as ), yet the underlying physiological and molecular mechanisms remain poorly understood. This study investigated the effects of elevated temperatures (35 °C and 37 °C) on survival, DNA damage, antioxidant enzyme activities, and gene expression related to apoptosis, inflammation, and heat shock proteins (HSPs) in . The median lethal temperature (LT50) of was determined to be 37.09 °C, with significant mortality observed at 35 °C compared with the control (29 °C). Antioxidant enzyme activities (SOD, CAT, and GPx) and T-AOC were up-regulated initially but exhibited divergent patterns under prolonged stress, indicating a temperature-dependent threshold for oxidative defense. Comet assay results also showed that heat stress induced severe DNA damage in hemocytes. Moreover, heat stress significantly up-regulated mRNA expression of apoptosis-related genes (, , , and ), inflammatory genes (, , and ), and HSP family members (, , , and ). The expression peaks of these genes were generally earlier and more pronounced at 37 °C, reflecting intensified cellular damage and protective responses. Collectively, this study demonstrates that employs integrated antioxidant, apoptotic, inflammatory, and HSP-mediated mechanisms to counteract heat stress, but temperatures exceeding 35 °C disrupt these defenses, leading to survival impairment. These findings provide critical insights into the heat adaptation strategies of and serve as a scientific foundation for developing sustainable aquaculture practices to mitigate summer heat stress.

摘要

水温是一个关键的环境因素,对水产养殖中生物的生存和生长产生影响。热应激对香港牡蛎(也称为 )的生存和养殖构成重大威胁,但其潜在的生理和分子机制仍知之甚少。本研究调查了高温(35°C和37°C)对香港牡蛎的生存、DNA损伤、抗氧化酶活性以及与细胞凋亡、炎症和热休克蛋白(HSPs)相关的基因表达的影响。香港牡蛎的半数致死温度(LT50)被确定为37.09°C,与对照组(29°C)相比,在35°C时观察到显著的死亡率。抗氧化酶活性(SOD、CAT和GPx)和总抗氧化能力(T-AOC)最初上调,但在长期应激下呈现出不同的模式,表明氧化防御存在温度依赖性阈值。彗星试验结果还表明,热应激诱导血细胞中严重的DNA损伤。此外,热应激显著上调了细胞凋亡相关基因( 、 、 、和 )、炎症基因( 、 、和 )以及HSP家族成员( 、 、 、和 )的mRNA表达。这些基因的表达峰值通常在37°C时更早且更明显,反映出细胞损伤和保护反应的加剧。总体而言,本研究表明香港牡蛎采用综合的抗氧化、凋亡、炎症和HSP介导的机制来应对热应激,但超过35°C的温度会破坏这些防御机制,导致生存受损。这些发现为香港牡蛎的热适应策略提供了关键见解,并为制定可持续的水产养殖实践以减轻夏季热应激提供了科学依据。

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