Mechanism for generation of hydrogen peroxide and change of mitochondrial membrane potential during rotenone-induced apoptosis

Life Sciences ◽  
2003 ◽  
Vol 73 (25) ◽  
pp. 3277-3288 ◽  
Author(s):  
Saeko Tada-Oikawa ◽  
Yusuke Hiraku ◽  
Michiko Kawanishi ◽  
Shosuke Kawanishi
Keyword(s):  
Hydrogen Peroxide ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Induced Apoptosis

scholarly journals Generation of hydrogen peroxide precedes loss of mitochondrial membrane potential during DNA alkylation-induced apoptosis

FEBS Letters ◽  
1999 ◽  
Vol 442 (1) ◽  
pp. 65-69 ◽  
Author(s):  
Saeko Tada-Oikawa ◽  
Shinji Oikawa ◽  
Michiko Kawanishi ◽  
Michiyuki Yamada ◽  
Shosuke Kawanishi
Keyword(s):  
Hydrogen Peroxide ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Dna Alkylation ◽  
Induced Apoptosis

Effects of hydrogen peroxide and hypochlorite on membrane potential of mitochondria in situ in rat heart cells

1991 ◽  
Vol 69 (11) ◽  
pp. 1705-1712 ◽  
Author(s):  
Noburu Konno ◽  
K. J. Kako
Keyword(s):  
Hydrogen Peroxide ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Rat Heart ◽  
Mitochondrial Membrane ◽  
Isolated Rat Heart ◽  
Heart Mitochondria ◽  
High Concentrations ◽  
Isolated Rat

Hydrogen peroxide (H2O2) and hypochlorite (HOCl) cause a variety of cellular dysfunctions. In this study we examined the effects of these agents on the electrical potential gradient across the inner membrane of mitochondria in situ in isolated rat heart myocytes. Myocytes were prepared by collagenase digestion and incubated in the presence of H2O2 or HOCl. Transmembrane electrical gradients were measured by distribution of [3H]triphenylmethylphosphonium+, a lipophilic cation. The particulate fraction was separated from the cytosolic compartment first by permeabilization using digitonin, followed by rapid centrifugal sedimentation through a bromododecane layer. We found that the mitochondrial membrane potential (161 ± 7 mV, negative inside) was relatively well maintained under oxidant stress, i.e., the potential was decreased only at high concentrations of HOCl and H2O2 and gradually with time. The membrane potential of isolated rat heart mitochondria was affected similarly by H2O2 and HOCl in a concentration- and time-dependent manner. High concentrations of oxidants also reduced the cellular ATP level but did not significantly change the matrix volume. When the extra-mitochondrial free calcium concentration was increased in permeabilized myocytes, the transmembrane potential was decreased proportionally, and this decrease was potentiated further by H2O2. These results support the view that heart mitochondria are equipped with well-developed defense mechanisms against oxidants, but the action of H2O2 on the transmembrane electrical gradient is exacerbated by an increase in cytosolic calcium. Keywords: ATP, calcium, cardiomyocyte, cell defense, mitochondrial membrane potential, oxidant, triphenylmethylphosphonium.

Bcl-2 protects against FCCP-induced apoptosis and mitochondrial membrane potential depolarization in PC12 cells

1999 ◽  
Vol 1428 (2-3) ◽  
pp. 357-371 ◽  
Author(s):  
Gwenda Dispersyn ◽  
Rony Nuydens ◽  
Rich Connors ◽  
Marcel Borgers ◽  
Hugo Geerts
Keyword(s):  
Membrane Potential ◽  
Pc12 Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Induced Apoptosis

Encircling granulosa cells protects against di-(2-ethylhexyl)phthalate-induced apoptosis in rat oocytes cultured in vitro

Zygote ◽  
2019 ◽  
Vol 27 (4) ◽  
pp. 203-213 ◽  
Author(s):  
Anima Tripathi ◽  
Vivek Pandey ◽  
A.N. Sahu ◽  
Alok K. Singh ◽  
Pawan K. Dubey
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Granulosa Cells ◽  
Mitochondrial Membrane ◽  
Dependent Manner ◽  
Apoptotic Markers ◽  
Induced Apoptosis ◽  
Ethylhexyl Phthalate

SummaryThe present study investigated if the presence of encircling granulosa cells protected against di(2-ethylhexyl)phthalate (DEHP)-induced oxidative stress in rat oocytes cultured in vitro. Denuded oocytes and cumulus–oocyte complexes (COCs) were treated with or without various doses of DEHP (0.0, 25.0, 50.0, 100, 200, 400 and 800 μM) in vitro. Morphological apoptotic changes, levels of oxidative stress and reactive oxygen species (ROS), mitochondrial membrane potential, and expression levels of apoptotic markers (Bcl2, Bax, cytochrome c) were analyzed. Our results showed that DEHP induced morphological apoptotic changes in a dose-dependent manner in denuded oocytes cultured in vitro. The effective dose of DEHP (400 µg) significantly (P>0.05) increased oxidative stress by elevating ROS levels and the mitochondrial membrane potential with higher mRNA expression and protein levels of apoptotic markers (Bax, cytochrome c). Encircling granulosa cells protected oocytes from DEHP-induced morphological changes, increased oxidative stress and ROS levels, as well as increased expression of apoptotic markers. Taken together our data suggested that encircling granulosa cells protected oocytes against DEHP-induced apoptosis and that the presence of granulosa cells could act positively towards the survival of oocytes under in vitro culture conditions and may be helpful during assisted reproductive technique programmes.

scholarly journals Formosanin C-induced apoptosis requires activation of caspase-2 and change of mitochondrial membrane potential

2009 ◽  
Vol 100 (3) ◽  
pp. 503-513 ◽  
Author(s):  
Jenq-Chang Lee ◽  
Chun-Li Su ◽  
Lin-Lin Chen ◽  
Shen-Jeu Won
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Caspase 2 ◽  
Induced Apoptosis

Volatile Anesthetics Induce Caspase-dependent, Mitochondria-mediated Apoptosis in Human T Lymphocytes In Vitro 

2005 ◽  
Vol 102 (6) ◽  
pp. 1147-1157 ◽  
Author(s):  
Torsten Loop ◽  
David Dovi-Akue ◽  
Michael Frick ◽  
Martin Roesslein ◽  
Lotti Egger ◽  
...  
Keyword(s):  
Membrane Potential ◽  
T Lymphocytes ◽  
Cytochrome C ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Volatile Anesthetics ◽  
Human T Lymphocytes ◽  
Induced Apoptosis

Background Volatile anesthetics modulate lymphocyte function during surgery, and this compromises postoperative immune competence. The current work was undertaken to examine whether volatile anesthetics induce apoptosis in human T lymphocytes and what apoptotic signaling pathway might be used. Methods Effects of sevoflurane, isoflurane, and desflurane were studied in primary human CD3 T lymphocytes and Jurkat T cells in vitro. Apoptosis and mitochondrial membrane potential were assessed using flow cytometry after green fluorescent protein-annexin V and DiOC6-fluorochrome staining. Activity and proteolytic processing of caspase 3 was measured by cleaving of the fluorogenic effector caspase substrate Ac-DEVD-AMC and by anti-caspase-3 Western blotting. Release of mitochondrial cytochrome c was studied after cell fractionation using anti-cytochrome c Western blotting and enzyme-linked immunosorbent assays. Results Sevoflurane and isoflurane induced apoptosis in human T lymphocytes in a dose-dependent manner. By contrast, desflurane did not exert any proapoptotic effects. The apoptotic signaling pathway used by sevoflurane involved disruption of the mitochondrial membrane potential and release of cytochrome c from mitochondria to the cytosol. In addition, the authors observed a proteolytic cleavage of the inactive p32 procaspase 3 to the active p17 fragment, increased caspase-3-like activity, and cleavage of the caspase-3 substrate poly-ADP-ribose-polymerase. Sevoflurane-induced apoptosis was blocked by the general caspase inhibitor Z-VAD.fmk. Death signaling was not mediated via the Fas/CD95 receptor pathway because neither anti-Fas/CD95 receptor antagonism nor FADD deficiency or caspase-8 deficiency were able to attenuate sevoflurane-mediated apoptosis. Conclusion Sevoflurane and isoflurane induce apoptosis in T lymphocytes via increased mitochondrial membrane permeability and caspase-3 activation, but independently of death receptor signaling.

Seminal plasma has limited counteracting effects following induction of oxidative stress in donkey spermatozoa

2020 ◽  
Vol 32 (6) ◽  
pp. 619
Author(s):  
Marion Papas ◽  
Jaime Catalan ◽  
Sebastián Bonilla-Correal ◽  
Sabrina Gacem ◽  
Jordi Miró ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Sperm Motility ◽  
Seminal Plasma ◽  
Mitochondrial Membrane ◽  
Skim Milk ◽  
Sperm Parameters ◽  
High Concentration

The aim of this study was to evaluate the response of donkey spermatozoa to oxidative stress induced by hydrogen peroxide, and to determine whether the presence of seminal plasma modulates the sperm response to that stress. Nine ejaculates were collected, extended in skim milk extender and split into two aliquots. Seminal plasma was removed from the first but not second aliquot. Samples were subsequently split into four aliquots supplemented with different concentrations of commercial hydrogen peroxide (0, 100 and 250µM and 50mM). Aliquots were incubated at 37°C under aerobic conditions and several sperm parameters, namely motility, viability, intracellular levels of peroxides and superoxides and mitochondrial membrane potential, were evaluated at 0, 1 and 3h. Exposure to hydrogen peroxide markedly decreased sperm motility but had much less of an effect on sperm viability, mitochondrial membrane potential and intracellular reactive oxygen species levels. A protective effect of seminal plasma against the loss of sperm motility was not apparent, but some kinetic parameters and relative levels of superoxides were better maintained when seminal plasma was present together with high concentration of hydrogen peroxide. In conclusion, oxidative stress induced by hydrogen peroxide reduces donkey sperm motility and has a less apparent effect on other sperm parameters. Finally, seminal plasma is only able to partially ameliorate the detrimental effect of this induced stress.

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