scholarly journals Betaine Alleviates Heat Stress-Induced Hepatic and Mitochondrial Oxidative Damage in Broilers

2020 ◽  
Author(s):  
Chao Wen ◽  
Zhixian Leng ◽  
Yueping Chen ◽  
Liren Ding ◽  
Tian Wang ◽  
...  
Keyword(s):  
Heat Stress ◽  
Oxidative Damage ◽  
Mitochondrial Oxidative Damage

scholarly journals Mitochondrial Oxidative Damage in Chicken Skeletal Muscle Induced by Acute Heat Stress

2007 ◽  
Vol 44 (4) ◽  
pp. 439-445 ◽  
Author(s):  
Ahmad Mujahid ◽  
Neil R. Pumford ◽  
Walter Bottje ◽  
Kiyotaka Nakagawa ◽  
Teruo Miyazawa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Oxidative Damage ◽  
Acute Heat Stress ◽  
Mitochondrial Oxidative Damage ◽  
Chicken Skeletal Muscle

scholarly journals Acrolein Aggravates Secondary Brain Injury After Intracerebral Hemorrhage Through Drp1-Mediated Mitochondrial Oxidative Damage in Mice

2020 ◽  
Vol 36 (10) ◽  
pp. 1158-1170
Author(s):  
Xun Wu ◽  
Wenxing Cui ◽  
Wei Guo ◽  
Haixiao Liu ◽  
Jianing Luo ◽  
...  
Keyword(s):  
Brain Injury ◽  
Oxidative Damage ◽  
Mitochondrial Membrane ◽  
Molecular Mechanisms ◽  
Mitochondrial Fission ◽  
Secondary Brain Injury ◽  
Functional Deficits ◽  
Highly Active ◽  
Neural Apoptosis ◽  
Mitochondrial Oxidative Damage

Abstract Clinical advances in the treatment of intracranial hemorrhage (ICH) are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain injury. Acrolein is a highly active unsaturated aldehyde which has been implicated in many nervous system diseases. Our results indicated a significant increase in the level of acrolein after ICH in mouse brain. In primary neurons, acrolein induced an increase in mitochondrial fragmentation, loss of mitochondrial membrane potential, generation of reactive oxidative species, and release of mitochondrial cytochrome c. Mechanistically, acrolein facilitated the translocation of dynamin-related protein1 (Drp1) from the cytoplasm onto the mitochondrial membrane and led to excessive mitochondrial fission. Further studies found that treatment with hydralazine (an acrolein scavenger) significantly reversed Drp1 translocation and the morphological damage of mitochondria after ICH. In parallel, the neural apoptosis, brain edema, and neurological functional deficits induced by ICH were also remarkably alleviated. In conclusion, our results identify acrolein as an important contributor to the secondary brain injury following ICH. Meanwhile, we uncovered a novel mechanism by which Drp1-mediated mitochondrial oxidative damage is involved in acrolein-induced brain injury.

scholarly journals Melatonin administration prevents cardiac and diaphragmatic mitochondrial oxidative damage in senescence-accelerated mice

2007 ◽  
Vol 194 (3) ◽  
pp. 637-643 ◽  
Author(s):  
M I Rodriguez ◽  
G Escames ◽  
L C López ◽  
J A García ◽  
F Ortiz ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Chronic Treatment ◽  
Melatonin Treatment ◽  
Mitochondrial Oxidative Stress ◽  
Melatonin Administration ◽  
Age Dependent ◽  
Mitochondrial Oxidative Damage ◽  
Senescence Accelerated Mice ◽  
Ratio Reduction

Cardiac and diaphragmatic mitochondria from male SAMP8 (senescent) and SAMR1 (resistant) mice of 5 or 10 months of age were studied. Levels of lipid peroxidation (LPO), glutathione (GSH), GSH disulfide (GSSG), and GSH peroxidase and GSH reductase (GRd) activities were measured. In addition, the effect of chronic treatment with the antioxidant melatonin from 1 to 10 months of age was evaluated. Cardiac and diaphragmatic mitochondria show an age-dependent increase in LPO levels and a reduction in GSH:GSSG ratios. Chronic treatment with melatonin counteracted the age-dependent LPO increase and GSH:GSSG ratio reduction in these mitochondria. Melatonin also increased GRd activity, an effect that may account for the maintenance of the mitochondrial GSH pool. Total mitochondrial content of GSH increased after melatonin treatment. In general, the effects of age and melatonin treatment were similar in senescence-resistant mice (SAMR1) and SAMP8 cardiac and diaphragmatic mitochondria, suggesting that these mice strains display similar mitochondrial oxidative damage at the age of 10 months. The results also support the efficacy of long-term melatonin treatment in preventing the age-dependent mitochondrial oxidative stress.

Proteomic responses to oxidative damage in meat from ducks exposed to heat stress

2019 ◽  
Vol 295 ◽  
pp. 129-137 ◽  
Author(s):  
Jun He ◽  
Chenlan Xia ◽  
Yuxin He ◽  
Daodong Pan ◽  
Jinxuan Cao ◽  
...  
Keyword(s):  
Heat Stress ◽  
Oxidative Damage ◽  
Proteomic Responses
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