Aclonifen causes developmental abnormalities in zebrafish embryos through mitochondrial dysfunction and oxidative stress

2021 ◽  
Vol 771 ◽  
pp. 145445
Author(s):  
Jin-Young Lee ◽  
Hahyun Park ◽  
Whasun Lim ◽  
Gwonhwa Song
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Zebrafish Embryos ◽  
Developmental Abnormalities ◽  
And Oxidative Stress

scholarly journals Autophagy mitigates ethanol-induced mitochondrial dysfunction and oxidative stress in esophageal keratinocytes

PLoS ONE ◽  
2020 ◽  
Vol 15 (9) ◽  
pp. e0239625
Author(s):  
Prasanna M. Chandramouleeswaran ◽  
Manti Guha ◽  
Masataka Shimonosono ◽  
Kelly A. Whelan ◽  
Hisatsugu Maekawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
And Oxidative Stress

scholarly journals Roots and stems of Kadsura coccinea extract induced developmental toxicity in zebrafish embryos/larvae through apoptosis and oxidative stress

2020 ◽  
Vol 58 (1) ◽  
pp. 1294-1301
Author(s):  
Zhongshang Xia ◽  
Erwei Hao ◽  
Zhangmei Chen ◽  
Mingzhe Zhang ◽  
Yanting Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Developmental Toxicity ◽  
Zebrafish Embryos ◽  
Kadsura Coccinea ◽  
And Oxidative Stress

scholarly journals One Week of CDAHFD Induces Steatohepatitis and Mitochondrial Dysfunction with Oxidative Stress in Liver

2021 ◽  
Vol 22 (11) ◽  
pp. 5851
Author(s):  
Takehito Sugasawa ◽  
Seiko Ono ◽  
Masato Yonamine ◽  
Shin-ichiro Fujita ◽  
Yuki Matsumoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Early Stage ◽  
Droplet Deposition ◽  
Nonalcoholic Fatty Liver ◽  
Stress Markers ◽  
Mitochondrial Dna Copy Number ◽  
Short Period ◽  
And Oxidative Stress

The prevalence of nonalcoholic fatty liver disease (NAFLD) has been rapidly increasing worldwide. A choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) has been used to create a mouse model of nonalcoholic steatohepatitis (NASH). There are some reports on the effects on mice of being fed a CDAHFD for long periods of 1 to 3 months. However, the effect of this diet over a short period is unknown. Therefore, we examined the effect of 1-week CDAHFD feeding on the mouse liver. Feeding a CDAHFD diet for only 1-week induced lipid droplet deposition in the liver with increasing activity of liver-derived enzymes in the plasma. On the other hand, it did not induce fibrosis or cirrhosis. Additionally, it was demonstrated that CDAHFD significantly impaired mitochondrial respiration with severe oxidative stress to the liver, which is associated with a decreasing mitochondrial DNA copy number and complex proteins. In the gene expression analysis of the liver, inflammatory and oxidative stress markers were significantly increased by CDAHFD. These results demonstrated that 1 week of feeding CDAHFD to mice induces steatohepatitis with mitochondrial dysfunction and severe oxidative stress, without fibrosis, which can partially mimic the early stage of NASH in humans.

scholarly journals Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 229
Author(s):  
JunHyuk Woo ◽  
Hyesun Cho ◽  
YunHee Seol ◽  
Soon Ho Kim ◽  
Chanhyeok Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Computational Models ◽  
Neuronal Damage ◽  
Living Organism ◽  
The Body ◽  
Mitochondrial Functions ◽  
A Cell ◽  
The Brain ◽  
And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

Isoliquiritigenin triggers developmental toxicity and oxidative stress–mediated apoptosis in zebrafish embryos/larvae via Nrf2-HO1/JNK-ERK/mitochondrion pathway

Chemosphere ◽  
2020 ◽  
Vol 246 ◽  
pp. 125727 ◽  
Author(s):  
Zhenzhen Song ◽  
Yun Zhang ◽  
Huazheng Zhang ◽  
R. Samuel Rajendran ◽  
Rongchun Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Developmental Toxicity ◽  
Zebrafish Embryos ◽  
And Oxidative Stress

trans,trans-2,4-decadienal induces mitochondrial dysfunction and oxidative stress

2008 ◽  
Vol 40 (2) ◽  
pp. 103-109 ◽  
Author(s):  
Carlos A. O. Sigolo ◽  
Paolo Di Mascio ◽  
Alicia J. Kowaltowski ◽  
Camila C. M. Garcia ◽  
Marisa H. G. Medeiros
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
And Oxidative Stress

scholarly journals Relationship Between Oxidative Stress, ER Stress, and Inflammation in Type 2 Diabetes: The Battle Continues

2019 ◽  
Vol 8 (9) ◽  
pp. 1385 ◽  
Author(s):  
Burgos-Morón ◽  
Abad-Jiménez ◽  
Marañón ◽  
Iannantuoni ◽  
Escribano-López ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Current Knowledge ◽  
Β Cells ◽  
The Relationship ◽  
And Oxidative Stress

Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAMs) means that the ROS generated in mitochondria promote ER stress. Therefore, a state of stress and mitochondrial dysfunction are consequences of this vicious cycle. The implication of mitochondria in insulin release and the exposure of pancreatic β-cells to hyperglycemia make them especially susceptible to oxidative stress and mitochondrial dysfunction. In fact, crosstalk between both mechanisms is related with alterations in glucose homeostasis and can lead to the diabetes-associated insulin-resistance status. In the present review, we discuss the current knowledge of the relationship between oxidative stress, mitochondria, ER stress, inflammation, and lipotoxicity in T2D.

G6PD, bond by miR-24, regulates mitochondrial dysfunction and oxidative stress in phenylephrine-induced hypertrophic cardiomyocytes

Life Sciences ◽  
2020 ◽  
Vol 260 ◽  
pp. 118378
Author(s):  
Bing Li ◽  
Xiaotong Wang ◽  
Ming Yu ◽  
Ping Yang ◽  
Wei Wang
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
And Oxidative Stress
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