Hydrogen peroxide induces apoptosis in HeLa cells through mitochondrial pathway

Singh, Mayank; Sharma, Himani; Singh, Neeta

doi:10.1016/j.mito.2007.07.003

Cited by 160 publications

(128 citation statements)

References 29 publications

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“…This suggested that • OH-induced cytochrome c release and ROS generation in fish erythrocytes. This is consistent with the report that H 2 O 2 induces cytochrome c release in HeLa cells [36] and ROS production in rat neuronal cells [78]. The cytochrome c release and ROS generation may be related to mitochondrion in fish erythrocytes.…”

Section: • Oh-induced Apoptosis In Fish Erythrocytessupporting

confidence: 93%

“…These displayed that the • OH-induced caspase-3 activation was caspase-8 and caspase-9 dependent in fish erythrocytes. This was consistent with the reports that H 2 O 2 induces the mitochondria cytochrome c release that initiates the activation of caspase-9 with subsequent caspases-3 in HeLa cells [36]. Although no reports have been published on that caspase-8 activation is death receptors (CD95) dependent in fish erythrocytes, it is speculated that • OH may activate caspase-8 by triggering CD95.…”

Section: • Oh-induced Apoptosis In Fish Erythrocytessupporting

confidence: 91%

“…CD95) with subsequent caspase-8 activation, and stimulate the release of mitochondrial cytochrome c with subsequent caspase-9 activation [35], both caspases converge finally at the activation of effector caspases (e.g. caspase-3) that results in nucleus DNA fragmentation (a biomarker of apoptosis) in mammal nucleated cells [36][37][38]. It has been reported that the mechanisms of antioxidant defences in fish cells are similar to those in mammal nucleated cells [39][40][41].…”

Section: Introductionmentioning

confidence: 99%

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The metabolites of glutamine prevent hydroxyl radical-induced apoptosis through inhibiting mitochondria and calcium ion involved pathways in fish erythrocytes

Jiang

Liu

et al. 2016

Free Radical Biology and Medicine

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a b s t r a c tThe present study explored the apoptosis pathways in hydroxyl radicals ( • OH)-induced carp erythrocytes. Carp erythrocytes were treated with the caspase inhibitors in physiological carp saline (PCS) or Ca 2 þ -free PCS in the presence of 40 μM FeSO 4 /20 μM H 2 O 2 . The results showed that the generation of reactive oxygen species (ROS), the release of cytochrome c and DNA fragmentation were caspase-dependent, and Ca 2 þ was involved in calpain activation and phosphatidylserine (PS) exposure in • OH-induced carp erythrocytes. Moreover, the results suggested that caspases were involved in PS exposure, and Ca 2 þ was involved in DNA fragmentation in • OH-induced fish erythrocytes. These results demonstrated that there might be two apoptosis pathways in fish erythrocytes, one is the caspase and cytochrome c-dependent apoptosis that is similar to that in mammal nucleated cells, the other is the Ca 2 þ -involved apoptosis that was similar to that in mammal non-nucleated erythrocytes. So, fish erythrocytes may be used as a model for studying oxidative stress and apoptosis in mammal cells. Furthermore, the present study investigated the effects of glutamine (Gln)'s metabolites [alanine (Ala), citrulline (Cit), proline (Pro) and their combination (Ala 10 Pro 4 Cit 1 )] on the pathways of apoptosis in fish erythrocytes. The results displayed that Ala, Cit, Pro and Ala 10 Pro 4 Cit 1 effectively suppressed ROS generation, cytochrome c release, activation of caspase-3, caspase-8 and caspase-9 at the physiological concentrations, prevented Ca 2 þ influx, calpain activation, PS exposure, DNA fragmentation and the degradation of the cytoskeleton and oxidation of membrane and hemoglobin (Hb) and increased activity of anti-hydroxyl radical (AHR) in • OH-induced carp erythrocytes. Ala 10 Pro 4 Cit 1 produced a synergistic effect of inhibited oxidative stress and apoptosis in fish erythrocytes. These results demonstrated that Ala, Cit, Pro and their combination can protect mammal erythrocytes and nucleated cells against oxidative stress and apoptosis. The studies supported the use of Gln, Ala, Cit and Pro as oxidative stress and apoptosis inhibitors in mammal cells and the hypothesis that the inhibited effects of Gln on oxidative stress and apoptosis are at least partly dependent on that of its metabolites in mammalian.

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Section: • Oh-induced Apoptosis In Fish Erythrocytessupporting

confidence: 93%

Section: • Oh-induced Apoptosis In Fish Erythrocytessupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

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The metabolites of glutamine prevent hydroxyl radical-induced apoptosis through inhibiting mitochondria and calcium ion involved pathways in fish erythrocytes

Jiang

Liu

et al. 2016

Free Radical Biology and Medicine

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“…Increased production of mitochondrial H 2 O 2 is a classical signal of mitochondrial dysfunction and an essential mediator of cell death (Singh, Sharma & Singh, 2007). H 2 O 2 is a membrane permeable second messenger, as well as a potent precursor of other ROS generation (Turrens, 2003).…”

Section: Resultsmentioning

confidence: 99%

Carbonic anhydrase inhibition selectively prevents amyloid β neurovascular mitochondrial toxicity

et al. 2018

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SummaryMounting evidence suggests that mitochondrial dysfunction plays a causal role in the etiology and progression of Alzheimer's disease (AD). We recently showed that the carbonic anhydrase inhibitor (CAI) methazolamide (MTZ) prevents amyloid β (Aβ)‐mediated onset of apoptosis in the mouse brain. In this study, we used MTZ and, for the first time, the analog CAI acetazolamide (ATZ) in neuronal and cerebral vascular cells challenged with Aβ, to clarify their protective effects and mitochondrial molecular mechanism of action. The CAIs selectively inhibited mitochondrial dysfunction pathways induced by Aβ, without affecting metabolic function. ATZ was effective at concentrations 10 times lower than MTZ. Both MTZ and ATZ prevented mitochondrial membrane depolarization and H2O2 generation, with no effects on intracellular pH or ATP production. Importantly, the drugs did not primarily affect calcium homeostasis. This work suggests a new role for carbonic anhydrases (CAs) in the Aβ‐induced mitochondrial toxicity associated with AD and cerebral amyloid angiopathy (CAA), and paves the way to AD clinical trials for CAIs, FDA‐approved drugs with a well‐known profile of brain delivery.

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“…Accordingly it has been shown that ROS production can be an efficient activator of p73 expression [35]. On the other hand, different point mutations in the p53 gene have been evidenced in Jurkat cells, mostly at the C-terminal A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 16 basic domain [30], which is required for the activation of the p21 Waf1/Cip1 gene, for cell cycle arrest and for apoptosis [36].…”

Section: Discussionmentioning

confidence: 99%

Induction of apoptosis by thymoquinone in lymphoblastic leukemia Jurkat cells is mediated by a p73-dependent pathway which targets the epigenetic integrator UHRF1

Alhosin

Abusnina

Achour

et al. 2010

Biochemical Pharmacology

129

112

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The salvage anti-tumoral pathway which implicates the p53-related p73 gene is not yet fully characterized. We therefore attempted to identify the up-and down-stream events involved in the activation of the p73-dependent pro-apoptotic pathway, by focusing on the anti-apoptotic and epigenetic integrator UHRF1 which is essential for cell cycle progression. For this purpose, we analyzed the effects of a known anti-neoplastic drug, thymoquinone (TQ), on the p53-deficient acute lymphoblastic leukemia (ALL) Jurkat cell line. Our results showed that TQ inhibits the proliferation of Jurkat cells and induces G1 cell cycle arrest in a dose-dependent manner. Moreover, TQ treatment triggers programmed cell death, production of reactive oxygen species (ROS) and alteration of the mitochondrial membrane potential (m). TQ-induced apoptosis, confirmed by the presence of hypodiploid G0/G1 cells, is associated with a rapid and sharp re-expression of p73 and dose-dependent changes of the levels of caspase-3 cleaved subunits. These modifications are accompanied by a dramatic down-regulation of UHRF1 and two of its main partners, namely DNMT1 and HDAC1, which are all involved in the epigenetic code regulation. Knockdown of p73 expression restores UHRF1 expression, reactivates cell cycle progression and inhibits TQ-induced apoptosis. Altogether our results showed that TQ mediates its growth inhibitory effects on ALL p53-mutated cells via the activation of a p73-dependent mitochondrial and cell cycle checkpoint signaling pathway which subsequently targets UHRF1.

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Hydrogen peroxide induces apoptosis in HeLa cells through mitochondrial pathway

Cited by 160 publications

References 29 publications

The metabolites of glutamine prevent hydroxyl radical-induced apoptosis through inhibiting mitochondria and calcium ion involved pathways in fish erythrocytes

The metabolites of glutamine prevent hydroxyl radical-induced apoptosis through inhibiting mitochondria and calcium ion involved pathways in fish erythrocytes

Carbonic anhydrase inhibition selectively prevents amyloid β neurovascular mitochondrial toxicity

Induction of apoptosis by thymoquinone in lymphoblastic leukemia Jurkat cells is mediated by a p73-dependent pathway which targets the epigenetic integrator UHRF1

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