Oxidative stress and apoptosis

doi:10.1016/S0928-4680(00)00053-5

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Oxidative stress and apoptosis

Journal Article•DOI•

Oxidative stress and apoptosis

Krishnaswamy Kannan¹, Sushil K. Jain¹•Institutions (1)

Louisiana State University¹

01 Sep 2000-Pathophysiology (Elsevier)-Vol. 7, Iss: 3, pp 153-163

TL;DR: Increasing evidences provide support that oxidative stress and apoptosis are closely linked physiological phenomena and are implicated in pathophysiology of some of the chronic diseases including AIDS, autoimmunity, cancer, diabetes mellitus, Alzheimer's and Parkinson's and ischemia of heart and brain.

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About: This article is published in Pathophysiology.The article was published on 2000-09-01. It has received 1013 citations till now. The article focuses on the topics: Intrinsic apoptosis & Apoptosome.

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Journal Article•DOI•

Oxidative stress and apoptosis: Impact on cancer therapy

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Tomris Ozben¹•Institutions (1)

Akdeniz University¹

01 Sep 2007-Journal of Pharmaceutical Sciences

TL;DR: This review will address some of the current paradigms of oxidative stress, and antioxidants on apoptosis, and discuss the potential mechanisms by which oxidants can regulate apoptotic pathways and new developments in eliminating cancer cells by selectively inducing apoptosis.

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655 citations

Journal Article•DOI•

Oxidative stress in autism

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Abha Chauhan, Ved Chauhan

01 Aug 2006-Pathophysiology

TL;DR: Increases in oxidative stress with membrane lipid abnormalities, inflammation, aberrant immune response, impaired energy metabolism and excitotoxicity, leading to clinical symptoms and pathogenesis of autism is proposed.

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569 citations

Journal Article•DOI•

Oxidative stress, cell cycle, and neurodegeneration

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Jeff Klein, Susan L. Ackerman

15 Mar 2003-Journal of Clinical Investigation

TL;DR: This work will discuss recent findings regarding the influence of oxidative stress on neurodegeneration and possible connections between oxidative stress and unscheduled cell cycle reentry, the understanding of which could lead to new strategies in the development of therapeutic agents for Neurodegenerative disorders.

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Abstract: While numerous studies have examined the existence of increased reactive oxygen species (ROS) in later-onset neurodegenerative disorders, the mechanism by which neurons die under conditions of oxidative stress remains largely unknown. Fairly recent evidence has suggested that one mechanism linked to the death of terminally differentiated neurons is aberrant reentry into the cell cycle. This phenomenon has been reported in Alzheimer disease (AD) patients (1), Down syndrome patients (2), and several mouse neurodegenerative models (3–5). We will discuss recent findings regarding the influence of oxidative stress on neurodegeneration and possible connections between oxidative stress and unscheduled cell cycle reentry, the understanding of which could lead to new strategies in the development of therapeutic agents for neurodegenerative disorders.

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502 citations

Cites background from "Oxidative stress and apoptosis"

...Indeed, ROS have been implicated in cell signaling, specifically through mitogens (6, 70, 71)....
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...Unchecked, excessive ROS can lead to the destruction of cellular components including lipids, protein, and DNA, and ultimately cell death via apoptosis or necrosis (6)....
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Journal Article•

The histone deacetylase inhibitor MS-275 promotes differentiation or apoptosis in human leukemia cells through a process regulated by generation of reactive oxygen species and induction of p21CIP1/WAF1 1.

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Roberto R. Rosato¹, Jorge A. Almenara¹, Steven Grant¹•Institutions (1)

VCU Medical Center¹

01 Jul 2003-Cancer Research

TL;DR: It is demonstrated that MS-275 exerts dose-dependent effects in human leukemia cells, i.e., p21(CIP1/WAF1)-dependent growth arrest and differentiation at low drug concentrations and a marked induction of ROS, mitochondrial damage, caspase activation, and apoptosis at higher concentrations.

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Abstract: Effects of the histone deacetylase (HDAC) inhibitor MS-275 have been examined in human leukemia and lymphoma cells (U937, HL-60, K562, and Jurkat) as well as in primary acute myelogenous leukemia blasts in relation to differentiation and apoptosis. MS-275 displayed dose-dependent effects in each of the cell lines. When administered at a low concentration (e.g., 1 micro M), MS-275 exhibited potent antiproliferative activity, inducing p21(CIP1/WAF1)-mediated growth arrest and expression of differentiation markers (CD11b) in U937 cells. These events were accompanied by an increase in hypophosphorylated retinoblastoma protein and down-regulation of cell cycle-related proteins including cyclin D1. However, at higher concentrations (e.g., 5 micro M), MS-275 potently induced cell death, triggering apoptosis in approximately 70% of cells at 48 h. In contrast to other HDAC inhibitors such as apicidin, the extrinsic, receptor-mediated pathway played a minimal role in MS-275 lethality. However, MS-275 potently induced a very early (e.g., within 2 h) increase in reactive oxygen species (ROS), followed by the loss of mitochondrial membrane potential (Delta psi(m)) and cytosolic release of cytochrome c. These events culminated in activation of the caspase cascade, manifested by poly(ADP-ribose) polymerase, p21(CIP1/WAF1), p27(KIP), Bcl-2, and retinoblastoma protein degradation. MS-275 exposure also resulted in diminished expression of cyclin D1 and the antiapoptotic proteins Mcl-1 and XIAP. Administration of the free radical scavenger L-N-acetylcysteine blocked MS-275-mediated mitochondrial injury and apoptosis, suggesting a primary role for ROS generation in MS-275-associated lethality. Lastly, U937 cells stably expressing a p21(CIP1/WAF1) antisense construct were significantly more sensitive to MS-275-mediated apoptosis than controls, but they were impaired in their differentiation response. Together, these findings demonstrate that MS-275 exerts dose-dependent effects in human leukemia cells, i.e., p21(CIP1/WAF1)-dependent growth arrest and differentiation at low drug concentrations and a marked induction of ROS, mitochondrial damage, caspase activation, and apoptosis at higher concentrations.

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463 citations

Cites background from "Oxidative stress and apoptosis"

...mitochondrial function under conditions of oxidative stress is an important contributor to the apoptotic response ( 41 , 48, 49)....
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Journal Article•DOI•

Proline suppresses apoptosis in the fungal pathogen Colletotrichum trifolii.

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Changbin Chen¹, Martin B. Dickman•Institutions (1)

University of Nebraska–Lincoln¹

01 Mar 2005-Proceedings of the National Academy of Sciences of the United States of America

TL;DR: The ability of proline to scavenge intracellular ROS and inhibit ROS-mediated apoptosis may be an important and broad-based function of this amino acid in responding to cellular stress, in addition to its well established role as an osmolyte.

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Abstract: The role of reactive oxygen species (ROS) in cell communication, control of gene expression, and oxygen sensing is well established. Inappropriate regulation of ROS levels can damage cells, resulting in a diseased state. In Colletotrichum trifolii, a fungal pathogen of alfalfa, the mutationally activated oncogenic fungal Ras (DARas) elevates levels of ROS, causing abnormal fungal growth and development and eventual apoptotic-like cell death but only when grown under nutrient-limiting conditions. Remarkably, restoration to the wild-type phenotype requires only proline. Here, we describe a generally unrecognized function of proline: its ability to function as a potent antioxidant and inhibitor of programmed cell death. Addition of proline to DARas mutant cells effectively quenched ROS levels and prevented cell death. Treating cells with inhibitors of ROS production yielded similar results. In addition, proline protected wild-type C. trifolii cells against various lethal stresses, including UV light, salt, heat, and hydrogen peroxide. These observations appear to be general because proline also protected yeast cells from lethal levels of the ROS-generating herbicide methyl viologen (paraquat), suggesting a common protective role for proline in response to oxidative stress. The ability of proline to scavenge intracellular ROS and inhibit ROS-mediated apoptosis may be an important and broad-based function of this amino acid in responding to cellular stress, in addition to its well established role as an osmolyte.

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455 citations

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References

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Book•

Free radicals in biology and medicine

[...]

Barry Halliwell, John M.C. Gutteridge

13 Jun 1985

TL;DR: 1. Oxygen is a toxic gas - an introduction to oxygen toxicity and reactive species, and the chemistry of free radicals and related 'reactive species'

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Abstract: 1. Oxygen is a toxic gas - an introductionto oxygen toxicity and reactive species 2. The chemistry of free radicals and related 'reactive species' 3. Antioxidant defences Endogenous and Diet Derived 4. Cellular responses to oxidative stress: adaptation, damage, repair, senescence and death 5. Measurement of reactive species 6. Reactive species can pose special problems needing special solutions. Some examples. 7. Reactive species can be useful some more examples 8. Reactive species can be poisonous: their role in toxicology 9. Reactive species and disease: fact, fiction or filibuster? 10. Ageing, nutrition, disease, and therapy: A role for antioxidants?

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21,528 citations

"Oxidative stress and apoptosis" refers background in this paper

...Oxidative stress can occur under conditions when oxygen radicals production is greater than the detoxification capacity of the cell [47,48]....
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...Among the more susceptible targets are polyunsaturated fatty acids [48,63–65]....
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...[48] B Halliwell, J....
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Journal Article•DOI•

Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics.

[...]

J. F. R. Kerr, Andrew H. Wyllie, A. R. Currie

01 Aug 1972-British Journal of Cancer

TL;DR: Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development, and participates in at least some types of therapeutically induced tumour regression.

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Abstract: The term apoptosis is proposed for a hitherto little recognized mechanism of controlled cell deletion, which appears to play a complementary but opposite role to mitosis in the regulation of animal cell populations. Its morphological features suggest that it is an active, inherently programmed phenomenon, and it has been shown that it can be initiated or inhibited by a variety of environmental stimuli, both physiological and pathological.The structural changes take place in two discrete stages. The first comprises nuclear and cytoplasmic condensation and breaking up of the cell into a number of membrane-bound, ultrastructurally well-preserved fragments. In the second stage these apoptotic bodies are shed from epithelial-lined surfaces or are taken up by other cells, where they undergo a series of changes resembling in vitro autolysis within phagosomes, and are rapidly degraded by lysosomal enzymes derived from the ingesting cells.Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development. It occurs spontaneously in untreated malignant neoplasms, and participates in at least some types of therapeutically induced tumour regression. It is implicated in both physiological involution and atrophy of various tissues and organs. It can also be triggered by noxious agents, both in the embryo and adult animal.

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15,416 citations

"Oxidative stress and apoptosis" refers background in this paper

...Ischemic heart disease, AIDS and neurodegenerative diseases such as Alzheimer’s, and Parkinson’s are the best examples of too much apoptosis [2–6]....
[...]
...Apoptotic cells are efficiently cleared in vivo by antigen processing cells within 2–4 h [1,3,5]....
[...]
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...These observations raise the intriguing possibility of the coexistence of multiple signaling pathways that converge upstream of a common mechanism of events, predisposing the cell to apoptosis [1–5]....
[...]

Journal Article•DOI•

Mitochondria and apoptosis

[...]

Douglas R. Green¹, John C. Reed¹•Institutions (1)

La Jolla Institute for Allergy and Immunology¹

28 Aug 1998-Science

TL;DR: A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins.

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Abstract: A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins. The different signals that converge on mitochondria to trigger or inhibit these events and their downstream effects delineate several major pathways in physiological cell death.

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8,757 citations

"Oxidative stress and apoptosis" refers background in this paper

...[11] D....
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...Permeability transition is also associated with the release of apoptotic inducing factor (AIF), which has recently been identified and characterized [11,53,54]....
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...Another crucial step in the early changes in mitochondria is alteration of mitochondrial transmembrane potential (DCm) [9–13]....
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...release of cytochrome C, which, along with dATP and APAF-1, facilitates the activation of pro-caspase 9 to its active form of caspase 9 [11,108,109]....
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...Several studies have shown that the global shutdown of mitochondrial function under conditions of oxidative stress could contribute to apoptosis [9–13]....
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Journal Article•DOI•

Caspases: Enemies Within

[...]

Nancy A. Thornberry¹, Yuri Lazebnik²•Institutions (2)

Merck & Co.¹, Cold Spring Harbor Laboratory²

28 Aug 1998-Science

TL;DR: This work has shown that understanding caspase regulation is intimately linked to the ability to rationally manipulate apoptosis for therapeutic gain.

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Abstract: Apoptosis, an evolutionarily conserved form of cell suicide, requires specialized machinery. The central component of this machinery is a proteolytic system involving a family of proteases called caspases. These enzymes participate in a cascade that is triggered in response to proapoptotic signals and culminates in cleavage of a set of proteins, resulting in disassembly of the cell. Understanding caspase regulation is intimately linked to the ability to rationally manipulate apoptosis for therapeutic gain.

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6,924 citations

"Oxidative stress and apoptosis" refers background in this paper

...Another major player in cell death by apoptosis is a class of enzymes called ‘caspases’, which are cysteinedependent enzymes and are sensitive to the redox status of the cell [8,30,35,36]....
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...These enzymes cut off the cell–cell contact to the surrounding cells, disorganize the cytoskeleton, shut down DNA replication and repair, interrupt splicing, destroy DNA, disrupt the nuclear structure, induce biochemical changes on the cell surface for easy recognition by phagocytes, and finally disintegrate the cell to vesicular bodies [35,37–42]....
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...[35] N....
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...The homologue to Ced4 in human has been identified to be APAF-1 (apoptotic protease-activating factor-1) [35]....
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...The Ced9 gene negatively regulates the Ced3 and Ced4 genes [1,35,97–99]....
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Journal Article•DOI•

Apoptosis in the pathogenesis and treatment of disease

[...]

Craig B. Thompson¹•Institutions (1)

Howard Hughes Medical Institute¹

10 Mar 1995-Science

TL;DR: In multicellular organisms, homeostasis is maintained through a balance between cell proliferation and cell death, and recent evidence suggests that alterations in cell survival contribute to the pathogenesis of a number of human diseases.

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Abstract: In multicellular organisms, homeostasis is maintained through a balance between cell proliferation and cell death. Although much is known about the control of cell proliferation, less is known about the control of cell death. Physiologic cell death occurs primarily through an evolutionarily conserved form of cell suicide termed apoptosis. The decision of a cell to undergo apoptosis can be influenced by a wide variety of regulatory stimuli. Recent evidence suggests that alterations in cell survival contribute to the pathogenesis of a number of human diseases, including cancer, viral infections, autoimmune diseases, neurodegenerative disorders, and AIDS (acquired immunodeficiency syndrome). Treatments designed to specifically alter the apoptotic threshold may have the potential to change the natural progression of some of these diseases.

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6,462 citations

"Oxidative stress and apoptosis" refers background in this paper

...Ischemic heart disease, AIDS and neurodegenerative diseases such as Alzheimer’s, and Parkinson’s are the best examples of too much apoptosis [2–6]....
[...]
...For example, adriamycin is known to chelate iron and generate ROS that result in apoptosis of cancer cells [1–3,80]....
[...]
...These observations raise the intriguing possibility of the coexistence of multiple signaling pathways that converge upstream of a common mechanism of events, predisposing the cell to apoptosis [1–5]....
[...]
...[2] C....
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