Combined effects of temperature and copper ion concentration on the superoxide dismutase activity in Crassostrea ariakensis

Background: Cardiac hypertrophy involves marked wall thickening or chamber enlargement. If sustained, this condition will lead to dysfunctional mitochondria and oxidative stress. Mitochondria have ATP-sensitive K+ channels (mitoKATP) in the inner membrane that modulate the redox status of the cell. Objective: We investigated the in vivo effects of mitoKATP opening on oxidative stress in isoproterenol- induced cardiac hypertrophy. Methods: Cardiac hypertrophy was induced in Swiss mice treated intraperitoneally with isoproterenol (ISO - 30 mg/kg/day) for 8 days. From day 4, diazoxide (DZX - 5 mg/kg/day) was used in order to open mitoKATP (a clinically relevant therapy scheme) and 5-hydroxydecanoate (5HD - 5 mg/kg/day) or glibenclamide (GLI - 3 mg/kg/day) were used as mitoKATP blockers. Results: Isoproterenol-treated mice had elevated heart weight/tibia length ratios (HW/TL). Additionally, hypertrophic hearts had elevated levels of carbonylated proteins and Thiobarbituric Acid Reactive Substances (TBARS), markers of protein and lipid oxidation. In contrast, mitoKATP opening with DZX avoided ISO effects on gross hypertrophic markers (HW/TL), carbonylated proteins and TBARS, in a manner reversed by 5HD and GLI. Moreover, DZX improved mitochondrial superoxide dismutase activity. This effect was also blocked by 5HD and GLI. Additionally, ex vivo treatment of isoproterenol- induced hypertrophic cardiac tissue with DZX decreased H2O2 production in a manner sensitive to 5HD, indicating that this drug also acutely avoids oxidative stress. Conclusion: Our results suggest that diazoxide blocks oxidative stress and reverses cardiac hypertrophy. This pharmacological intervention could be a potential therapeutic strategy to prevent oxidative stress associated with cardiac hypertrophy.

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Complexation of Mn(II) by Rigid Pyclen Diacetates: Equilibrium, Kinetic, Relaxometric, Density Functional Theory, and Superoxide Dismutase Activity Studies

Inorganic Chemistry ◽

10.1021/acs.inorgchem.0c03276 ◽

2020 ◽

Author(s):

Zoltán Garda ◽

Enikő Molnár ◽

Nadège Hamon ◽

José Luis Barriada ◽

David Esteban-Gómez ◽

...

Keyword(s):

Density Functional Theory ◽

Superoxide Dismutase ◽

Density Functional ◽

Superoxide Dismutase Activity ◽

Functional Theory

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Commonalities between Copper Neurotoxicity and Alzheimer’s Disease

Toxics ◽

10.3390/toxics9010004 ◽

2021 ◽

Vol 9 (1) ◽

pp. 4

Author(s):

Roshni Patel ◽

Michael Aschner

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Structural Changes ◽

Copper Ion ◽

Plaque Formation ◽

Ion Concentration ◽

Medical Community ◽

Disease Etiology ◽

Parent Protein ◽

Lead Zinc

Alzheimer’s disease, a highly prevalent form of dementia, targets neuron function beginning from the hippocampal region and expanding outwards. Alzheimer’s disease is caused by elevated levels of heavy metals, such as lead, zinc, and copper. Copper is found in many areas of daily life, raising a concern as to how this metal and Alzheimer’s disease are related. Previous studies have not identified the common pathways between excess copper and Alzheimer’s disease etiology. Our review corroborates that both copper and Alzheimer’s disease target the hippocampus, cerebral cortex, cerebellum, and brainstem, affecting motor skills and critical thinking. Additionally, Aβ plaque formation was analyzed beginning from synthesis at the APP parent protein site until Aβ plaque formation was completed. Structural changes were also noted. Further analysis revealed a relationship between amyloid-beta plaques and copper ion concentration. As copper ion levels increased, it bound to the Aβ monomer, expediting the plaque formation process, and furthering neurodegeneration. These conclusions can be utilized in the medical community to further research on the etiology of Alzheimer’s disease and its relationships to copper and other metal-induced neurotoxicity.

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Combined effects of temperature and salt solution on swelling of GMZ01 bentonite–sand mixtures

Bulletin of Engineering Geology and the Environment ◽

10.1007/s10064-021-02342-y ◽

2021 ◽

Author(s):

Guo-sheng Xiang ◽

Wei-min Ye ◽

Yinkang Zhou ◽

Fazal E. Jalal

Keyword(s):

Salt Solution ◽

Combined Effects ◽

Gmz01 Bentonite ◽

Effects Of Temperature

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Two New Compounds From the Heartwood of Dalbergia melanoxylon and Their Protective Effect on Hypoxia/Reoxygenation Injury in H9c2

Natural Product Communications ◽

10.1177/1934578x20987776 ◽

2021 ◽

Vol 16 (1) ◽

pp. 1934578X2098777

Author(s):

Yang Liu ◽

Ni Zhang ◽

Jun-wei He ◽

Lan-ying Chen ◽

Li Yang ◽

...

Keyword(s):

Superoxide Dismutase ◽

Lactate Dehydrogenase ◽

Protective Effect ◽

Superoxide Dismutase Activity ◽

Spectral Evidence ◽

Reoxygenation Injury ◽

Dalbergia Melanoxylon ◽

New Compounds ◽

Hypoxia Reoxygenation

A new neoflavonoid, named as (7 R)-(-)-3′,5-dihydroxy-4′,2,4-trimethoxy-dalbergiquinol (1) and a new phenanthrenedione, named as 3′,7-dihydroxy-3,6- dimethoxy-9-phenyl-1,4-phenanthrenedione (2), together with 4 known compounds, 5- O-methyldalbergiphenol (3), 3′,7-dihydroxy-4′,3,6-trimethoxy-9-phenyl-1,4-phenanthrenedione (4), (+)-obtusafuran (5), and melanoxin (6) were isolated from the heartwood of Dalbergia melanoxylon. Their structures were elucidated on the basis of chemical and spectral evidence, as well as by comparison with literature data. Moreover, compound 1 showed a protective effect on hypoxia/reoxygenation injury in H9c2 at 10.0 μM by decreasing lactate dehydrogenase and malondialdehyde activity and enhancing superoxide dismutase activity.

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Combined Effects of Temperature and Toxic Algal Abundance on Paralytic Shellfish Toxic Accumulation, Tissue Distribution and Elimination Dynamics in Mussels Mytilus coruscus

Toxins ◽

10.3390/toxins13060425 ◽

2021 ◽

Vol 13 (6) ◽

pp. 425

Author(s):

Yunyu Tang ◽

Haiyan Zhang ◽

Yu Wang ◽

Chengqi Fan ◽

Xiaosheng Shen

Keyword(s):

Tissue Distribution ◽

Combined Effects ◽

Mytilus Coruscus ◽

Paralytic Shellfish Toxins ◽

Rapid Elimination ◽

Simulated Environment ◽

Paralytic Shellfish ◽

Algal Abundance ◽

Effects Of Temperature ◽

The Impact

This study assessed the impact of increasing seawater surface temperature (SST) and toxic algal abundance (TAA) on the accumulation, tissue distribution and elimination dynamics of paralytic shellfish toxins (PSTs) in mussels. Mytilus coruscus were fed with the PSTs-producing dinoflagellate A. catenella under four simulated environment conditions. The maximum PSTs concentration was determined to be 3548 µg STX eq.kg−1, which was four times higher than the EU regulatory limit. The increasing SST caused a significant decline in PSTs levels in mussels with rapid elimination rates, whereas high TAA increased the PSTs concentration. As a result, the PSTs toxicity levels decreased under the combined condition. Additionally, toxin burdens were assessed within shellfish tissues, with the highest levels quantified in the hepatopancreas. It is noteworthy that the toxin burden shifted towards the mantle from gill, muscle and gonad at the 17th day. Moreover, variability of PSTs was measured, and was associated with changes in each environmental factor. Hence, this study primarily illustrates the combined effects of SST and TAA on PSTs toxicity, showing that increasing environmental temperature is of benefit to lower PSTs toxicity with rapid elimination rates.

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