Permeabilization of the inner mitochondrial membrane by Ca2+ ions is stimulated by t-butyl hydroperoxide and mediated by reactive oxygen species generated by mitochondria

1995 ◽  
Vol 18 (3) ◽  
pp. 479-486 ◽  
Author(s):  
Roger F. Castilho ◽  
Alicia J. Kowaltowski ◽  
AndréR. Meinicke ◽  
Etelvino J.H. Bechara ◽  
Aníbal E. Vercesi
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Membrane ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Inner Mitochondrial Membrane ◽  
Butyl Hydroperoxide

Reserpine Induces Apoptosis and Cell Cycle Arrest in Hormone Independent Prostate Cancer Cells through Mitochondrial Membrane Potential Failure

2019 ◽  
Vol 18 (9) ◽  
pp. 1313-1322 ◽  
Author(s):  
Manjula Devi Ramamoorthy ◽  
Ashok Kumar ◽  
Mahesh Ayyavu ◽  
Kannan Narayanan Dhiraviam
Keyword(s):  
Prostate Cancer ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Membrane Potential ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Prostate Cancer Cells

Background: Reserpine, an indole alkaloid commonly used for hypertension, is found in the roots of Rauwolfia serpentina. Although the root extract has been used for the treatment of cancer, the molecular mechanism of its anti-cancer activity on hormonal independent prostate cancer remains elusive. Methods: we evaluated the cytotoxicity of reserpine and other indole alkaloids, yohimbine and ajmaline on Prostate Cancer cells (PC3) using MTT assay. We investigated the mechanism of apoptosis using a combination of techniques including acridine orange/ethidium bromide staining, high content imaging of Annexin V-FITC staining, flow cytometric quantification of the mitochondrial membrane potential and Reactive Oxygen Species (ROS) and cell cycle analysis. Results: Our results indicate that reserpine inhibits DNA synthesis by arresting the cells at the G2 phase and showed all standard sequential features of apoptosis including, destabilization of mitochondrial membrane potential, reduced production of reactive oxygen species and DNA ladder formation. Our in silico analysis further confirmed that indeed reserpine docks to the catalytic cleft of anti-apoptotic proteins substantiating our results. Conclusion: Collectively, our findings suggest that reserpine can be a novel therapeutic agent for the treatment of androgen-independent prostate cancer.

scholarly journals The toxic effect of Vu-Defr, a defensin from Vigna unguiculata seeds, on Leishmania amazonensis is associated with reactive oxygen species production, mitochondrial dysfunction, and plasma membrane perturbation

2018 ◽  
Vol 64 (7) ◽  
pp. 455-464 ◽  
Author(s):  
Géssika Silva Souza ◽  
Lais Pessanha de Carvalho ◽  
Edésio José Tenório de Melo ◽  
Valdirene Moreira Gomes ◽  
André de Oliveira Carvalho
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Membrane ◽  
Biological Activities ◽  
Reactive Oxygen ◽  
Leishmania Amazonensis ◽  
New Drugs ◽  
Oxygen Species ◽  
Membrane Perturbation ◽  
Plant Defensins

Plant defensins are plant antimicrobial peptides that present diverse biological activities in vitro, including the elimination of Leishmania amazonensis. Plant defensins are considered promising candidates for the development of new drugs. This protozoan genus has great epidemiological importance and the mechanism behind the protozoan death by defensins is unknown, thus, we chose L. amazonensis for this study. The aim of the work was to analyze the possible toxic mechanisms of Vu-Defr against L. amazonensis. For analyses, the antimicrobial assay was repeated as previously described, and after 24 h, an aliquot of the culture was tested for viability, membrane perturbation, mitochondrial membrane potential, reactive oxygen species (ROS) and nitric oxide (NO) inductions. The results of these analyses indicated that after interaction with L. amazonensis, the Vu-Defr causes elimination of promastigotes from culture, membrane perturbation, mitochondrial membrane collapse, and ROS induction. Our analysis demonstrated that NO is not produced after Vu-Defr and L. amazonensis interaction. In conclusion, our work strives to help to fill the gap relating to effects caused by plant defensins on protozoan and thus better understand the mechanism of action of this peptide against L. amazonensis.

scholarly journals High glucose promotes apoptosis and autophagy of MC3T3-E1 osteoblasts

2020 ◽  
Author(s):  
Pei Zhang ◽  
Jing Liao ◽  
Xiaoju Wang ◽  
Zhengping Feng
Keyword(s):  
Reactive Oxygen Species ◽  
High Glucose ◽  
Mitochondrial Membrane ◽  
Metabolic Diseases ◽  
Reactive Oxygen ◽  
Intracellular Reactive Oxygen Species ◽  
Control Group ◽  
Oxygen Species ◽  
Glucose Fluctuation ◽  
High Glucose Group

IntroductionDiabetes and osteoporosis are common metabolic diseases. Abnormal high glucose can lead to the apoptosis of osteoblasts. Autophagy is a highly conserved cellular process that degrades proteins or organelles. In the present study, we comparatively analyzed the effects of high glucose and glucose fluctuation on apoptosis and autophagy of MC3T3-E1 osteoblasts.Material and methodsMC3T3-E1 cells were respectively treated with different concentrations of D-glucose: 5.5 mM for the control group, 25 mM for the high glucose group and 5.5/25 mM for the glucose fluctuation group.ResultsHigh glucose and glucose fluctuation decreased MC3T3-E1 proliferation and activated autophagy. Also, high glucose and glucose fluctuation might induce the production of reactive oxygen species, decline the mitochondrial membrane potential and trigger apoptosis. The differences in the glucose fluctuation treatment group were more significant. Moreover, N-acetylcysteine, an antioxidant reagent, dramatically eliminated the intracellular reactive oxygen species induced by high glucose and glucose fluctuation, and significantly inhibited the autophagy and apoptosis in MC3T3-E1 osteoblasts. Furthermore, treatment with chloroquine, an inhibitor of autophagy, significantly increased the apoptosis of MC3T3-E1 osteoblasts.ConclusionsHigh glucose, especially high glucose fluctuation, inhibits proliferation and promotes apoptosis and autophagy of MC3T3-E1 osteoblasts. This may occur through inducing oxidative stress and mitochondrial damage in the osteoblasts.

scholarly journals Prohibitin-1 maintains the angiogenic capacity of endothelial cells by regulating mitochondrial function and senescence

2008 ◽  
Vol 180 (1) ◽  
pp. 101-112 ◽  
Author(s):  
Michael Schleicher ◽  
Benjamin R. Shepherd ◽  
Yajaira Suarez ◽  
Carlos Fernandez-Hernando ◽  
Jun Yu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Mitochondrial Function ◽  
Vascular System ◽  
Reactive Oxygen ◽  
Direct Consequence ◽  
Oxygen Species ◽  
Inner Mitochondrial Membrane ◽  
Prohibitin 1

Prohibitin 1 (PHB1) is a highly conserved protein that is mainly localized to the inner mitochondrial membrane and has been implicated in regulating mitochondrial function in yeast. Because mitochondria are emerging as an important regulator of vascular homeostasis, we examined PHB1 function in endothelial cells. PHB1 is highly expressed in the vascular system and knockdown of PHB1 in endothelial cells increases mitochondrial production of reactive oxygen species via inhibition of complex I, which results in cellular senescence. As a direct consequence, both Akt and Rac1 are hyperactivated, leading to cytoskeletal rearrangements and decreased endothelial cell motility, e.g., migration and tube formation. This is also reflected in an in vivo angiogenesis assay, where silencing of PHB1 blocks the formation of functional blood vessels. Collectively, our results provide evidence that PHB1 is important for mitochondrial function and prevents reactive oxygen species–induced senescence and thereby maintains the angiogenic capacity of endothelial cells.

Allelopathic effects of weed spp on the root border cells of Fagopyrum tataricum (L.) Gaertn

2021 ◽  
Vol 52 (1) ◽  
pp. 85-102
Author(s):  
Y.Y. Xie ◽  
L.X. Yao ◽  
S. Wei ◽  
S.H. He ◽  
L. Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Mitochondrial Membrane ◽  
Reactive Oxygen ◽  
Aqueous Extracts ◽  
Oxygen Species ◽  
Weed Species ◽  
Fagopyrum Tataricum ◽  
Bidens Pilosa ◽  
Allelopathic Effects

We studied the allelopathic effects of aqueous extracts of Galinsoga parviflora Cav., Chenopodium ambrosioides L., and Bidens pilosa L. weed species on the developmental characteristics of Tartary buckwheat RBCs. The increase in the concentration of aqueous extracts, there was increase in apoptosis rate and mucigel thickness of the RBCs, level of intracellular reactive oxygen species and nitric oxide, but decreased the mitochondrial membrane potential (P <0.05). The allelopathic effects of aqueous extracts of donor weed species on RBCs followed the order: C. ambrosioides > B. pilosa > G. parviflora. The increased levels of reactive oxygen species, nitric oxide and the reduced potential of mitochondrial membrane, further disrupted the homeostasis and normal metabolism of cells, thereby inducing the cell death. Among the three weed species, C. ambrosioides had the most significant impact

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