scholarly journals The effect of postmortem pH decline rate on mitochondrial apoptosis and tenderness of bovine skeletal muscle during aging

2021 ◽  
Author(s):  
Jibing Ma ◽  
Qunli Yu ◽  
Mingshan Han ◽  
Ling Han
Keyword(s):  
Mitochondrial Dysfunction ◽  
Shear Force ◽  
Protein Denaturation ◽  
Mitochondrial Apoptosis ◽  
Bovine Muscle ◽  
Mitochondrial Ros ◽  
Decline Rate ◽  
Slow Group ◽  
Induced Apoptosis ◽  
Bovine Skeletal Muscle

Abstract This study aimed to investigate the effect of postmortem pH decline rate on mitochondrial dysfunction-induced apoptosis and bovine muscle tenderness during aging. Protein denaturation, reactive oxygen species (ROS) levels, mitochondrial apoptosis factors, and shear force were assessed in bovine muscles with different pH decline rates. The results showed that compared to the slow group, fast pH decline in bovine muscle significantly increased sarcoplasmic protein denaturation at 6–12 h and mitochondrial ROS levels at 6–24 h (P<0.05), and in turn significantly accentuated mitochondrial dysfunction and cytochrome c oxidation levels (P<0.05), resulting in caspase-3 activation, apoptosis, and reduced muscle shear force (P<0.05). These results demonstrated that the fast postmortem pH decline enhanced mitochondrial apoptosis and bovine muscle tenderization by inducing ROS accumulation during aging.

scholarly journals Exenatide Attenuates Obesity-Induced Mitochondrial Dysfunction by Activating SIRT1 in Renal Tubular Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Yao Wang ◽  
Wei He ◽  
Wei Wei ◽  
Xiaoxue Mei ◽  
Ming Yang ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Kidney Injury ◽  
Protective Effects ◽  
Mitochondrial Apoptosis ◽  
Renal Tubular Cells ◽  
Mitochondrial Ros ◽  
Glucagon Like Peptide 1 ◽  
Treatment Of Obesity ◽  
Underlying Mechanisms ◽  
Renal Tubular

Saturated free fatty acid (FFA)-induced lipotoxicity plays an important role in obesity-induced kidney injury. Exenatide, a Glucagon-like peptide-1 receptor agonist(GLP-1RA), protects against high-fat diet (HFD)-induced kidney injury. The precise mechanism needs to be further explored. This study investigated whether exenatide protects against FFA-induced tubular epithelial cells (TECs) lipotoxicity and elucidated its underlying mechanisms. Here, we show that exenatide treatment reversed HFD induced TECs injuries, including TECs apoptosis and SIRT1 downregulation. The efficacy of exenatide was better than simvastatin. In palmitate (PA)-stimulated HK2 cells, exenatide treatment reversed the downregulation of SIRT1 and prevented an increase in reactive oxygen species (ROS) production, a decrease in mitochondrial membrane potential, and mitochondrial apoptosis. The renal-protective effects of exenatide on the generation of mitochondrial ROS and mitochondrial apoptosis were blocked by inhibiting SIRT1 activation. Collectively, these findings show that exenatide was superior to simvastatin in the treatment of obesity-TECs injuries, the mechanism is partially through SIRT1 restoration, which directly reverses mitochondrial dysfunction and apoptosis.

scholarly journals Melatonin Protects TEGDMA induced Pre-odontoblasts Mitochondrial Apoptosis via JNK/MAPK Signaling Pathway

2021 ◽  
Author(s):  
Qihao Yu ◽  
Yi Liu ◽  
Konghuai Wang ◽  
Xunben Weng ◽  
Shengbin Huang ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Dental Pulp ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Protective Effects ◽  
Mitochondrial Apoptosis ◽  
Atp Level ◽  
Induced Apoptosis

Abstract Background: Resin monomer induced dental pulp injury presents a mitochondrial dysfunction related pathology. Melatonin has been regarded as a strong mitochondrial protective bioactive compound from pineal gland. However, it remains unknown whether melatonin can prevent dental pulp from resin monomer induced injury. The aim of the study is to investigate the effects of melatonin on TEGDMA, a major component in dental resin, induced mouse pre-odontoblast cell lines (mDPC6T) mitochondrial apoptosis and to verify whether JNK/MAPK signaling pathway mediate the protective effect of melatonin. Methods: We adopted a well-established TEGDMA-induced mDPC6T apoptosis model to investigate the preventive effect of melatonin by detecting cell viability, apoptosis rate, expression of apoptosis related protein, mitochondrial ROS (mtROS) production, mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) level. Inhibitors of MAPKs signaling were used to explore which pathway was participated in TEGDMA induced apoptosis. Finally, we verified the role of JNK/MAPK pathway during the protective effects of melatonin above by the agonist and antagonists of JNK.Results: Melatonin attenuated TEGDMA induced mDPC6T apoptosis via reducing mtROS production, rescuing MMP and ATP level. Meanwhile, the mitochondrial dysfunction and apoptosis was alleviated by the JNK/MAPK inhibitor SP600125 but not the other MAPKs signaling inhibitors. Furthermore, melatonin down-regulated the expression of phosphorylated-JNK, and eliminated the active effects of Anisomycin on JNK/MAPK pathway, which mimicked the effects of the SP600125.Conclusion: Our findings demonstrated that melatonin protected mDPC6T against TEGDMA induced apoptosis via JNK/MAPK signaling and maintenance of mitochondrial function, which presented a novel therapeutic strategy for prevention against resin monomer-induced dental pulp injury.

Nanosized polyamidoamine (PAMAM) dendrimer-induced apoptosis mediated by mitochondrial dysfunction

2009 ◽  
Vol 190 (2) ◽  
pp. 202-207 ◽  
Author(s):  
Jong-Ho Lee ◽  
Kyung Eun Cha ◽  
Min Soo Kim ◽  
Hye Won Hong ◽  
Dong June Chung ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Pamam Dendrimer ◽  
Induced Apoptosis

RETRACTED: 6-OHDA-induced apoptosis and mitochondrial dysfunction are mediated by early modulation of intracellular signals and interaction of Nrf2 and NF-κB factors

Toxicology ◽  
2013 ◽  
Vol 304 ◽  
pp. 109-119 ◽  
Author(s):  
Julio C. Tobón-Velasco ◽  
Jorge H. Limón-Pacheco ◽  
Marisol Orozco-Ibarra ◽  
Marina Macías-Silva ◽  
Genaro Vázquez-Victorio ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Intracellular Signals ◽  
Induced Apoptosis

scholarly journals Effects of Photoperiod Regime on Meat Quality, Oxidative Stability, and Metabolites of Postmortem Broiler Fillet (M. Pectoralis major) Muscles

Foods ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 215 ◽  
Author(s):  
Jacob R. Tuell ◽  
Jun-Young Park ◽  
Weichao Wang ◽  
Bruce Cooper ◽  
Tiago Sobreira ◽  
...  
Keyword(s):  
Oxidative Stability ◽  
Meat Quality ◽  
Shear Force ◽  
Protein Denaturation ◽  
Aromatic Amino Acids ◽  
Pectoralis Major ◽  
Photoperiod Regime ◽  
Weight Yield ◽  
Considerable Impact ◽  
Water Holding

The objective of this study was to evaluate the effects of photoperiod on meat quality, oxidative stability, and metabolites of broiler fillet (M. Pectoralis major) muscles. A total of 432 broilers was split among 4 photoperiod treatments [hours light(L):dark(D)]: 20L:4D, 18L:6D, 16L:8D, and 12L:12D. At 42 days, a total of 48 broilers (12 broilers/treatment) was randomly selected and harvested. At 1 day postmortem, fillet muscles were dissected and displayed for 7 days. No considerable impacts of photoperiods on general carcass and meat quality attributes, such as carcass weight, yield, pH, water-holding capacity, and shear force, were found (p > 0.05). However, color and oxidative stability were influenced by the photoperiod, where muscles from 20L:4D appeared lighter and more discolored, coupled with higher lipid oxidation (p < 0.05) and protein denaturation (p = 0.058) compared to 12L:12D. The UPLC–MS metabolomics identified that 20 metabolites were different between the 20L:4D and 12L:12D groups, and 15 were tentatively identified. In general, lower aromatic amino acids/dipeptides, and higher oxidized glutathione and guanine/methylated guanosine were observed in 20L:4D. These results suggest that a photoperiod would result in no considerable impact on initial meat quality, but extended photoperiods might negatively impact oxidative stability through an alteration of the muscle metabolites.

Mitochondrial dysfunction is an early event in high-NaCl-induced apoptosis of mIMCD3 cells

2002 ◽  
Vol 282 (6) ◽  
pp. F981-F990 ◽  
Author(s):  
Luis Michea ◽  
Christian Combs ◽  
Peter Andrews ◽  
Natalia Dmitrieva ◽  
Maurice B. Burg
Keyword(s):  
Mitochondrial Dysfunction ◽  
Collecting Duct ◽  
Early Event ◽  
Mitochondrial Morphology ◽  
Cytochrome C Release ◽  
Activity Increase ◽  
Transmission Electron ◽  
Mitochondrial Membrane Depolarization ◽  
Medullary Collecting Duct ◽  
Induced Apoptosis

Raising osmolality to 700 mosmol/kgH2O by the addition of NaCl rapidly kills most murine inner renal medullary collecting duct cells (mIMCD3), but they survive at 500 mosmol/kgH2O. At 300 and 500 mosmol/kgH2O, NADH autofluorescence is present in a mitochondria-associated, punctate perinuclear pattern. Within 45 s to 30 min at 700 mosmol/kgH2O, the autofluorescence spreads diffusely throughout the cell. This correlates with mitochondrial membrane depolarization, measured as decreased tetramethylrhodamine methyl ester perchlorate (TMRM) fluorescence. Mitochondrial dysfunction should increase the cellular ADP/ATP ratio. In agreement, this ratio increases within 1–6 h. Mitochondrial morphology (transmission electron microscopy) is unaffected, but nuclear hypercondensation becomes evident. Progressive apoptosis occurs beginning 1 h after osmolality is raised to 700, but not to 500, mosmol/kgH2O. General caspase activity and caspase-9 activity increase only after 6 h at 700 mosmol/kgH2O. The mitochondrial Bcl-2/Bax ratio decreases within 1–3 h, but no cytochrome c release is evident. The mitochondria contain little p53 at any osmolality. Adding urea to 700 mosmol/kgH2O does not change NADH or TMRM fluorescence. We conclude that extreme acute hypertonicity causes a mitochondrial dysfunction involved in the initiation of apoptosis.

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