Oxidative stress is generated via the mitochondrial respiratory chain during plant cell apoptosis

Weir, Iona E.; Pham, Nhu-An; Hedley, David W.

doi:10.1002/cyto.a.10054

Cited by 22 publications

(21 citation statements)

References 30 publications

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“…Many strategies aimed at slowing down the aging process or preventing cancer are based on protection of DNA from oxidative damage, primarily by scavenging the endogenous oxidants. While approaches to measure the presence of oxidants within the cell have been developed, 10,11 the possibilities for detecting DSBs generated by endogenous oxidants are limited. DNA damage assessment by the comet methodology 12 is rather cumbersome, lacks the desired sensitivity and cannot provide information on the relationship between DNA damage and the cell cycle phase in which the damage occurred.…”

mentioning

confidence: 99%

Constitutive Histone H2AX Phosphorylation and ATM Activation, the Reporters of DNA Damage by Endogenous Oxidants

Tanaka

Halicka²,

Huang³

et al. 2006

Cell Cycle

190

197

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DNA in live cells undergoes continuous oxidative damage caused by metabolically generated endogenous as well as external oxidants and oxidant-inducers. The cumulative oxidative DNA damage is considered the key factor in aging and senescence while the effectiveness of anti-aging agents is often assessed by their ability to reduce such damage. Oxidative DNA damage also preconditions cells to neoplastic transformation. Sensitive reporters of DNA damage, particularly the induction of DNA double-strand breaks (DSBs), are activation of ATM, through its phosphorylation on Ser 1981, and phosphorylation of histone H2AX on Ser 139; the phosphorylated form of H2AX has been named γH2AX. We review the observations that constitutive ATM activation (CAA) and H2AX phosphorylation (CHP) take place in normal cells as well in the cells of tumor lines untreated by exogenous genotoxic agents. We postulate that CAA and CHP, which have been measured by multiparameter cytometry in relation to the cell cycle phase, are triggered by oxidative DNA damage. This review also presents the findings on differences in CAA and CHP in various cell lines as well as on the effects of several agents and growth conditions that modulate the extent of these histone and ATM modifications. Specifically, described are effects of the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC), and the glutathione synthetase inhibitor buthionine sulfoximine (BSO) as well as suppression of cell metabolism by growth at higher cell density or in the presence of the glucose antimetabolite 2-deoxy-D-glucose. Collectively, the reviewed data indicate that multiparameter cytometric measurement of the level of CHP and/or CAA allows one to estimate the extent of ongoing oxidative DNA damage and to measure the DNA protective-effects of antioxidants or agents that reduce or amplify generation of endogenous ROS. Keywordsaging; senescence; DNA replication; DNA double-strand breaks; cell cycle; free radicals; reactive oxygen species (ROS); reactive oxygen intermediates (ROIs); anti-oxidants; oxidative stress DNA DAMAGE BY ENDOGENOUS OXIDANTSBeing continuously exposed to oxidants produced during metabolic activity and to external oxidants or oxidant-inducers, DNA within cells undergoes oxidative damage. Estimates of the extent of endogenous DNA damage vary widely. [1][2][3][4][5] 5 Recombinatorial repair (also known as template-assisted repair or homologous recombination repair) and nonhomologous DNA-end joining (NHEJ) are two major pathways for repair of DSBs. The NHEJ pathway is error-prone, often resulting in deletion of a few base pairs. 6,7 This leads to accumulation of DNA damage with each sequential cell cycle, which is considered to be the primary cause of cell aging and senescence. 4,8,9 The cumulative DNA damage also promotes development of preneoplastic changes. Many strategies aimed at slowing down the aging process or preventing cancer are based on protection of DNA from oxidative damage, primarily by scavenging the endogenous oxidants. While appr...

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mentioning

confidence: 99%

Constitutive Histone H2AX Phosphorylation and ATM Activation, the Reporters of DNA Damage by Endogenous Oxidants

Tanaka

Halicka²,

Huang³

et al. 2006

Cell Cycle

190

197

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“…Inhibition of complex IV should not promote superoxide generation by Q o because the back-up of the high potential chain should inhibit QH 2 oxidation (Crofts 2004). That a threshold level of mitochondrial generated ROS may be important for cell death induction is broadly consistent with studies that have shown a very early and localized increase in mitochondrial ROS (Naton et al 1996;Yao et al 2002;Weir et al 2003;Yao and Greenberg 2006). In some studies, this ROS burst was shown to coincide with (and was likely the result of) a hyperpolarization of the inner mitochondrial membrane (Naton et al 1996;Weir et al 2003).…”

Section: A Specific Restriction Of Electron Flow At Complex III Can Amentioning

confidence: 59%

Interactions between mitochondrial electron transport, reactive oxygen species, and the susceptibility of Nicotiana tabacum cells to programmed cell death

Robson

Zhao

Vanlerberghe

2008

Botany

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We investigated the impact of steady-state cellular reactive oxygen species (ROS) level on subsequent susceptibility to cell death induction by signaling molecules or respiratory inhibitors. We utilized Nicotiana tabacum L. ('Petit Havana SR1') suspension cell lines differing in steady-state ROS level owing to either genetic manipulation of the mitochondrial electron transport chain or manipulation of growth conditions. In either case, higher steady-state ROS level increased susceptibility to the signaling molecules salicylic acid and nitric oxide, suggesting that these molecules can engage a ''steady-state ROS-primed cell death pathway''. We found that susceptibility to the complex III inhibitor antimycin A (AA) was also dependent upon steady-state ROS level and that this susceptibility was independent of that afforded by the inhibition of energy metabolism by AA. AA was unique in this respect, since susceptibility to two other electron transport chain inhibitors appeared strictly dependent upon their ability to inhibit energy metabolism. The results indicate that complex III may have a particular capacity to engage the steady-state ROS-primed cell death pathway (similarly to salicylic acid and nitric oxide) and may relate to the ability of this complex to generate superoxide. We also examined changes in cellular ROS post-treatment with the signaling molecules and respiratory inhibitors. In this case, the more susceptible cells (i.e., those that had experienced higher steady-state ROS levels) exhibited post-treatment declines in cellular ROS level, whereas the less susceptible cells were able to better maintain or increase their ROS post-treatment. This differential response may be an important determinant of cell fate.Résumé : Les auteurs ont examiné l'impact des espèces d'oxygène cellulaires réactives (ROS) à l'état constant sur la susceptibilité subséquente à l'induction de la mortalité cellulaire, par des molécules de signalisation ou des inhibiteurs cellulaires. Ils ont utilisé des lignées de suspension cellulaire du Nicotiana tabacum L. ('Petit Havane SR1'), de différents degrés de ROS à l'état constant, provenant soit de manipulations génétiques de la chaîne de transport des électrons mitochondriaux, ou soit par manipulation des conditions de croissance. Dans chaque cas, un degré supérieur de ROS à l'état constant augmente la susceptibilité aux molécules de signalisation comme l'acide sallicylique ou l'oxyde d'azote, ce qui suggère que ces molécules peuvent ouvrir un sentier de mortalité cellulaire, enclenché par le ROS à l'état constant. On constate que la susceptibilité au complexe III de l'antimycine A inhibitrice (AA) dépend également du degré de ROS à l'état constant et que cette susceptibilité est indépendante de celle provenant de l'inhibition du métabolisme énergétique par AA. Dans ce cas, l'AA est unique puisque la susceptibilité aux deux autres inhibiteurs de la chaîne de transport des électrons apparaît strictement dépendante de la capacité à inhiber le métabolisme énergétique. Les résultats in...

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“…One possible explanation for this observation could be formation of intracellular coordination complex of malic acid with nickel ions (46, 49 -53), which reduces free ion activity and thereby modulates ROS. In a previous study, malic acid reduced ROS in the early steps of apoptosis induction in protoplasts (19).…”

Section: Discussionmentioning

confidence: 74%

Transient Influx of Nickel in Root Mitochondria Modulates Organic Acid and Reactive Oxygen Species Production in Nickel Hyperaccumulator Alyssum murale

Agrawal

Czymmek

Sparks

et al. 2013

Journal of Biological Chemistry

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Oxidative stress is generated via the mitochondrial respiratory chain during plant cell apoptosis

Cited by 22 publications

References 30 publications

Constitutive Histone H2AX Phosphorylation and ATM Activation, the Reporters of DNA Damage by Endogenous Oxidants

Constitutive Histone H2AX Phosphorylation and ATM Activation, the Reporters of DNA Damage by Endogenous Oxidants

Interactions between mitochondrial electron transport, reactive oxygen species, and the susceptibility of Nicotiana tabacum cells to programmed cell death

Transient Influx of Nickel in Root Mitochondria Modulates Organic Acid and Reactive Oxygen Species Production in Nickel Hyperaccumulator Alyssum murale

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