scholarly journals Calphostin C-mediated translocation and integration of Bax into mitochondria induces cytochrome c release before mitochondrial dysfunction

2000 ◽  
Vol 7 (6) ◽  
pp. 511-520 ◽  
Author(s):  
H Ikemoto ◽  
E Tani ◽  
I Ozaki ◽  
H Kitagawa ◽  
N Arita
Keyword(s):  
Cytochrome C ◽  
Mitochondrial Dysfunction ◽  
Cytochrome C Release ◽  
Calphostin C

Ischemic Preconditioning Is Capable of Inducing Mitochondrial Tolerance in the Rat Brain

2002 ◽  
Vol 97 (4) ◽  
pp. 896-901 ◽  
Author(s):  
Ren-Zhi Zhan ◽  
Hideyoshi Fujihara ◽  
Hiroshi Baba ◽  
Tomohiro Yamakura ◽  
Koki Shimoji
Keyword(s):  
Cerebral Ischemia ◽  
Cytochrome C ◽  
Mitochondrial Dysfunction ◽  
Ischemic Preconditioning ◽  
Neuronal Death ◽  
Brain Mitochondria ◽  
Sham Operation ◽  
Cytochrome C Release ◽  
Hippocampal Ca1 ◽  
Ischemic Episode

Background Preconditioning to ischemia is a phenomenon whereby a brief episode of sublethal ischemia and other nonlethal stressors produce protection against a subsequent detrimental ischemic insult. As mitochondrial dysfunction is related to necrotic and apoptotic neuronal death after cerebral ischemia, the authors examined if ischemic preconditioning is capable of inducing mitochondrial tolerance. Methods Forebrain ischemia was induced by bilateral common carotid artery occlusion with simultaneous hypotension for 8 min in Wistar rats (275-300 g). A 3-min ischemic episode performed 48 h before the 8-min ischemia was used for preconditioning. The extents of hippocampal CA1 neuronal damage were evaluated 7 days after reperfusion by neuro-specific nuclear protein immunostaining. Brain mitochondria were isolated 48 h after animals were subjected to the sham operation or the 3-min conditioning ischemia. Loss of cytochrome c from mitochondria after cerebral ischemia in vivo and after exposure of brain mitochondria to calcium in vitro was used as an indication of mitochondrial dysfunction. Results Results showed that ischemic preconditioning induced by a 3-min ischemic episode dramatically reduced the loss of hippocampal CA1 neurons resulting from a subsequent 8-min ischemia 7 days after reperfusion, and this protection was associated with a preservation of mitochondrial cytochrome c as examined after early reperfusion. Exposure of isolated brain mitochondria to calcium produced a dose-dependent increase in cytochrome c release either at 30 degrees C or at 37 degrees C. Compared with those animals receiving only sham operation, cytochrome c release caused by 100 microm calcium was significantly reduced in conditioned animals. Conclusion Regarding the importance of mitochondrial dysfunction in mediating ischemic neuronal death, the above results indicate that mitochondria may serve as end-effecting organelles to ischemic preconditioning.

scholarly journals Melatonin Protects Tobacco Suspension Cells against Pb-Induced Mitochondrial Dysfunction

2021 ◽  
Vol 22 (24) ◽  
pp. 13368
Author(s):  
Agnieszka Kobylińska ◽  
Małgorzata Maria Posmyk
Keyword(s):  
Cytochrome C ◽  
Mitochondrial Dysfunction ◽  
Plant Tolerance ◽  
Suspension Cells ◽  
Cytochrome C Release ◽  
Bright Yellow ◽  
Nicotiana Tabacum L ◽  
Tobacco Suspension Cells ◽  
Defence Strategies

Recent studies have shown that melatonin is an important molecule in plant physiology. It seems that the most important is that melatonin effectively eliminates oxidative stress (direct and indirect antioxidant) and switches on different defence strategies (preventive and interventive actions) during environmental stresses. In the presented report, exogenous melatonin potential to protect Nicotiana tabacum L. line Bright Yellow 2 (BY-2) exposed to lead against death was examined. Analyses of cell proliferation and viability, the level of intracellular calcium, changes in mitochondrial membrane potential (ΔΨm) as well as possible translocation of cytochrome c from mitochondria to cytosol and subsequent caspase-like proteolytic activity were conducted. Our results indicate that pretreatment BY-2 with melatonin protected tobacco cells against mitochondrial dysfunction and caspase-like activation caused by lead. The findings suggest the possible role of this indoleamine in the molecular mechanism of mitochondria, safeguarding against potential collapse and cytochrome c release. Thus, it seems that applied melatonin acted as an effective factor, promoting survival and increasing plant tolerance to lead.

scholarly journals Organic Dust Exposure Induces Stress Response and Mitochondrial Dysfunction in Monocytic Cells

2020 ◽  
Author(s):  
Sanjana Mahadev-Bhat ◽  
Denusha Shrestha ◽  
Nyzil Massey ◽  
Locke A. Karriker ◽  
Anumantha G. Kanthasamy ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Cell Viability ◽  
Mitochondrial Dysfunction ◽  
Inflammatory Responses ◽  
Ethyl Pyruvate ◽  
Dust Exposure ◽  
Organic Dust ◽  
Cytochrome C Release ◽  
Monocytic Cell ◽  
Functional Changes

AbstractExposure to airborne organic dust (OD), rich in microbial pathogen-associated molecular patterns, has been shown to induce inflammatory responses in the lung resulting in changes in airway structure and function. A common manifestation in lung inflammation is the occurrence of altered mitochondrial structure and bioenergetics, consequently regulating mitochondrial ROS (mROS) and creating a vicious cycle of mitochondrial dysfunction.The role of mitochondrial dysfunction in airway diseases such as COPD and asthma is well known. However, whether OD exposure induces mitochondrial dysfunction largely remains unknown. Therefore, in this study, we tested a hypothesis that OD exposure induces mitochondrial stress using a human monocytic cell line (THP-1). We examined the mechanisms of organic dust extract (ODE) exposure-induced mitochondrial structural and functional changes in THP-1 cells.In addition, the effect of co-exposure to ethyl pyruvate (EP), a known anti-inflammatory agent, or mitoapocynin (MA), a mitochondria targeting NOX2 inhibitor was examined. Transmission electron microscopy images showed significant changes in cellular and organelle morphology upon ODE exposure. ODE exposure with and without EP co-treatment increased the mtDNA leakage into the cytosol. Next, ODE exposure increased the PINK1 and Parkin expression, cytoplasmic cytochrome c levels and reduced mitochondrial mass and cell viability, indicating mitophagy. MA treatment was partially protective by decreasing Parkin expression, mtDNA and cytochrome c release and increasing cell viability.

Mitochondrial dysfunction and transactivation of p53-dependent apoptotic genes in BaP-treated human fetal lung fibroblasts

2011 ◽  
Vol 30 (12) ◽  
pp. 1904-1913 ◽  
Author(s):  
Guangtao Yang ◽  
Ying Jiang ◽  
Kaimin Rao ◽  
Xi Chen ◽  
Qian Wang ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Mitochondrial Dysfunction ◽  
Fetal Lung ◽  
Lung Fibroblasts ◽  
Ros Generation ◽  
Cytochrome C Release ◽  
Total Antioxidant ◽  
Apoptotic Genes ◽  
Human Fetal Lung ◽  
Time Point

Benzo(a)pyrene (BaP) has been shown to be an inducer of apoptosis. However, mechanisms involved in BaP-induced mitochondrial dysfunction are not well-known. In this study, human fetal lung fibroblasts cells were treated with BaP (8, 16, 32, 64 and 128 μM) for 4 and 12 h. Cell viability, intracellular level of reactive oxygen species (ROS), total antioxidant capacity (T-AOC), mitochondrial membrane potential (Δ Ψm) and cytochrome c release were determined. Changes in transcriptional levels of p53-dependent apoptotic genes ( p53, APAF1, CASPASE3, CASPASE9, NOXA and PUMA) were measured. At time point of 4 h, BaP induced the intracellular ROS generation in 64 ( p < .05) and 128 μM BaP groups ( p < .01) but decreased the T-AOC activities in 32, 64 ( p < .05 for both) and 128 μM BaP groups ( p < .01). At time point of 12 h, Δ Ψm significantly decreased in ≥32 μM BaP groups ( p < .05 for all). Amount of mitochondrial cytochrome c significantly increased in 128 μM BaP group ( p < .01). Transcriptional levels of CASPASE3, CASPASE9, APAF1 and PUMA were up-regulated in all BaP groups ( p < .05 for all) and in ≥32 μM groups for NOXA ( p < .05). But only in 16 μM BaP group a relatively little expression of p53 mRNA was observed ( p < .05). The results indicate that in the earlier period BaP promoted the generation of excessive ROS and subsequently the mitochondrial depolarization, whereas transactivations of the p53-dependent apoptotic genes were significantly induced at the later period.

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