scholarly journals Temporal Changes in Physiological Responses of Bay Scallop: Performance of Antioxidant Mechanism in Argopecten irradians in Response to Sudden Changes in Habitat Salinity

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1673
Author(s):  
Jin Ah Song ◽  
Cheol Young Choi
Keyword(s):  
Oxidative Stress ◽  
Nuclear Dna ◽  
Physiological Responses ◽  
Aquatic Organisms ◽  
Argopecten Irradians ◽  
Salinity Change ◽  
Bay Scallops ◽  
Antioxidant Mechanism ◽  
Seawater Salinity ◽  
Antioxidant Function

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 (H2O2), 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 H2O2 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.

Exposure to domoic acid causes oxidative stress in bay scallops Argopecten irradians

2020 ◽  
Vol 86 (4) ◽  
pp. 701-709 ◽  
Author(s):  
Jin Ah Song ◽  
Cheol Young Choi ◽  
Heung-Sik Park
Keyword(s):  
Oxidative Stress ◽  
Domoic Acid ◽  
Argopecten Irradians ◽  
Bay Scallops

scholarly journals NME3 Regulates Mitochondria to Reduce ROS-Mediated Genome Instability

2020 ◽  
Vol 21 (14) ◽  
pp. 5048
Author(s):  
Chih-Wei Chen ◽  
Ning Tsao ◽  
Wei Zhang ◽  
Zee-Fen Chang
Keyword(s):  
Oxidative Stress ◽  
Dna Repair ◽  
Genome Stability ◽  
Nuclear Dna ◽  
Genome Instability ◽  
Mitochondrial Fission ◽  
Nucleoside Diphosphate Kinase ◽  
Mitochondrial Fusion ◽  
Mitochondrial Outer Membrane ◽  
Mitochondrial Oxidative Stress

NME3 is a member of the nucleoside diphosphate kinase (NDPK) family that binds to the mitochondrial outer membrane to stimulate mitochondrial fusion. In this study, we showed that NME3 knockdown delayed DNA repair without reducing the cellular levels of nucleotide triphosphates. Further analyses revealed that NME3 knockdown increased fragmentation of mitochondria, which in turn led to mitochondrial oxidative stress-mediated DNA single-strand breaks (SSBs) in nuclear DNA. Re-expression of wild-type NME3 or inhibition of mitochondrial fission markedly reduced SSBs and facilitated DNA repair in NME3 knockdown cells, while expression of N-terminal deleted mutant defective in mitochondrial binding had no rescue effect. We further showed that disruption of mitochondrial fusion by knockdown of NME4 or MFN1 also caused mitochondrial oxidative stress-mediated genome instability. In conclusion, the contribution of NME3 to redox-regulated genome stability lies in its function in mitochondrial fusion.

scholarly journals Enhanced Oxidative Stress and Physiological Damage inDaphnia magnaby Copper in the Presence of Nano-TiO2

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
W. H. Fan ◽  
M. M. Cui ◽  
Z. W. Shi ◽  
C. Tan ◽  
X. P. Yang
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species Generation ◽  
Aquatic Organisms ◽  
Potential Hazard ◽  
Oxygen Species ◽  
Nano Tio2 ◽  
Physiological Regulation ◽  
Toxic Injury ◽  
Transfer Channel ◽  
Atpase Inhibition

This study examines the potential hazard of an individual nanomaterial on the Cu biotoxicity to aquatic organisms.Daphnia magnain the absence or presence of nano-TiO2was exposed to Cu. Maintaining nano-TiO2at a safe concentration cannot eliminate its potential hazard. The biomarkers superoxide dismutase, catalase, and Na+/K+-ATPase inD. magnawere measured. Cu in the presence of nano-TiO2induced higher levels of oxidative stress and physiological damage because of the sorption of Cu. Nano-TiO2also caused Na+/K+-ATPase inhibition possibly by impeding the Na+/K+transfer channel. The correlations among the biomarkers, mortality, and accumulation further showed that the overloading reactive oxygen species generation caused by nano-TiO2contributed to deeper oxidative stress and physiological regulation, thereby causing greater toxic injury.

Molecular cloning and responsive expression to injury stimulus of a defender against cell death 1 (DAD1) gene from bay scallops Argopecten irradians

2007 ◽  
Vol 35 (2) ◽  
pp. 125-132 ◽  
Author(s):  
Ling Zhu ◽  
Linsheng Song ◽  
Huan Zhang ◽  
Jianmin Zhao ◽  
Chenghua Li ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Cloning ◽  
Argopecten Irradians ◽  
Bay Scallops

scholarly journals Changes in oxidation-antioxidation function on the thymus of chickens infected with reticuloendotheliosis virus

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Dahan Yang ◽  
Chenhui Zhao ◽  
Meixi Zhang ◽  
Shujun Zhang ◽  
Jie Zhai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Control Group ◽  
Reticuloendotheliosis Virus ◽  
Antioxidative Function ◽  
Group I ◽  
Antioxidant Function ◽  
Thymus Atrophy ◽  
The Status ◽  
Specific Pathogen

Abstract Background Reticuloendotheliosis virus (REV) is a retrovirus that causes severe immunosuppression in poultry. Animals grow slowly under conditions of oxidative stress. In addition, long-term oxidative stress can impair immune function, as well as accelerate aging and death. This study aimed to elucidate the pathogenesis of REV from the perspective of changes in oxidative-antioxidative function following REV infection. Methods A total of 80 one-day-old specific pathogen free (SPF) chickens were randomly divided into a control group (Group C) and an REV-infected group (Group I). The chickens in Group I received intraperitoneal injections of REV with 104.62/0.1 mL TCID50. Thymus was collected on day 1, 3, 7, 14, 21, 28, 35, and 49 for histopathology and assessed the status of oxidative stress. Results In chickens infected with REV, the levels of H2O2 and MDA in the thymus increased, the levels of TAC, SOD, CAT, and GPx1 decreased, and there was a reduction in CAT and Gpx1 mRNA expression compared with the control group. The thymus index was also significantly reduced. Morphological analysis showed that REV infection caused an increase in the thymic reticular endothelial cells, inflammatory cell infiltration, mitochondrial swelling, and nuclear damage. Conclusions These results indicate that an increase in oxidative stress enhanced lipid peroxidation, markedly decreased antioxidant function, caused thymus atrophy, and immunosuppression in REV-infected chickens.

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