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海湾扇贝生理反应的时间变化:抗氧化机制对栖息地盐度突然变化的响应表现

Temporal Changes in Physiological Responses of Bay Scallop: Performance of Antioxidant Mechanism in in Response to Sudden Changes in Habitat Salinity.

作者信息

Song Jin Ah, Choi Cheol Young

机构信息

Division of Marine BioScience, National Korea Maritime and Ocean University, Busan 49112, Korea.

出版信息

Antioxidants (Basel). 2021 Oct 24;10(11):1673. doi: 10.3390/antiox10111673.

Abstract

Changes to habitat salinity may induce oxidative stress in aquatic organisms. The effect of salinity on the antioxidant function of bay scallops was investigated at 55, 70, 85 and 120% of seawater salinity (SW), with 100% SW as the control. The scallops were sampled 0, 6, 12, 24, 48 and 72 h after the salinity change to measure superoxide dismutase (SOD), catalase (CAT), hydrogen peroxide (HO), and lipid peroxidation (LPO) levels, as well as apoptosis in the digestive diverticula and/or hemolymph. The SOD immunohistochemistry and apoptotic response were assessed at 55% and 120% SW at 12 h. Antioxidant expressions at 55% and 70% SW peaked at 24 h or 48 h, and then decreased. At 120% SW, they increased with exposure time. The HO and LPO levels at each SW increased significantly with time. A comet assay also revealed that changes in salinity increased the rate of nuclear DNA damage in all the salinity groups. Thus, variations in salinity result in significant physiological responses in bay scallops. A change in habitat salinity of 15% or more produces oxidative stress that cannot be resolved by the body's antioxidant mechanism, suggesting that excessive generation of reactive oxygen species can lead to cell death.

摘要

栖息地盐度的变化可能会在水生生物中引发氧化应激。以100%海水盐度(SW)为对照,研究了在55%、70%、85%和120%海水盐度下盐度对海湾扇贝抗氧化功能的影响。在盐度变化后的0、6、12、24、48和72小时对扇贝进行采样,以测量超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、过氧化氢(HO)和脂质过氧化(LPO)水平,以及消化盲囊和/或血淋巴中的细胞凋亡情况。在12小时时对55%和120%海水盐度下的SOD免疫组织化学和凋亡反应进行评估。55%和70%海水盐度下的抗氧化剂表达在24小时或48小时达到峰值,然后下降。在120%海水盐度下,它们随暴露时间增加。每个海水盐度下的HO和LPO水平均随时间显著增加。彗星试验还表明,盐度变化增加了所有盐度组中核DNA损伤的速率。因此,盐度变化会导致海湾扇贝产生显著的生理反应。栖息地盐度变化15%或更多会产生氧化应激,而机体的抗氧化机制无法解决这种应激,这表明活性氧的过度产生会导致细胞死亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc16/8615089/76b5866b58a4/antioxidants-10-01673-g001.jpg

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