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Fajun Li¹, Xiaocui Cui¹, Chunpeng Fu¹

¹Shandong Peninsula Engineering Research Center of Comprehensive Brine Utilization, Weifang University of Science and Technology, Shouguang 262700, PR China.

Comparative biochemistry and physiology. Part D, Genomics & proteomics

|March 26, 2024

概括

在Macrobrachium nipponense中,饥饿会导致氧化应激,导致DNA损伤和亡. 抗氧化酶最初保护细胞,但长时间的禁食会诱导自和细胞死亡.

科学领域:

甲动物生理学甲动物生理学
水生物质毒理学研究
分子生物学分子生物学

背景情况:

食物剥夺是类在自然环境和水产养殖环境中的重要环境压力因素.
了解对饥饿的生理反应对于类水产养殖和保护至关重要.
在甲类动物的饥饿压力背后的分子机制在很大程度上仍然未被阐明.

研究的目的:

为了研究马克罗布拉基乌尼波尼尼斯对饥饿的生理和分子反应.
为了检查氧化应激,DNA损伤,自和禁食期间的亡的作用.
为了阐明饥饿引起的压力的调节机制,在这个经济上重要的甲动物物种.

主要方法:

在四个禁食条件 (0,7,14,21天) 下,对来自Macrobrachium nipponense的肝胰腺组织进行转录组分析.
评估反应性氧物种 (ROS) 生产,抗氧化酶活性,DNA损伤和亡标志物.
传输电子显微镜用于识别自解体和亡体.

主要成果:

饥饿会触发ROS介导的反应,最初会激活抗氧化酶.
长时间的禁食会导致ROS的产生增加,导致肝细胞的自.
在晚期饥饿阶段的高ROS水平会诱导显著的DNA损伤和细胞亡.

结论:

一个ROS介导的调节机制是 Macrobrachium nipponense.中饥饿反应的核心.
该研究显示,随着饥饿持续时间的增加,氧化应激和抗氧化剂防御向自,DNA损伤和亡的进展.
这些发现为了解饥饿压力分子机制提供了基础,并为水产养殖禁食策略提供了指导.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.自自是一种自的过程.马克罗布拉基乌尼波尼尼尼斯氧化应激是一种氧化应激.饥饿饥饿饥饿饥饿饥饿

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