Signalling apoptosis: a radical approach

Carmody, Ruaidhrı́ J.; Cotter, Thomas G.

doi:10.1179/135100001101536085

Cited by 288 publications

(193 citation statements)

References 156 publications

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“…However, there is increasing evidence supporting the involvement of reactive oxygen species (ROS) and reactive nitrogen species (RNS) (Metodiewa and Koska, 2000;Dawson and Dawson, 2003). Excessive ROS contributes to mitochondrial dysfunction and signals the initiation of cell death (Carmody and Cotter, 2001;Kitazawa et al, 2002). LED treatment significantly reduces ROS and NO generation in KCN, rotenone-or MPP + -poisoned neurons but did not increase normal neuronal ROS or NO levels present study).…”

Section: Discussionmentioning

confidence: 97%

Near-infrared light via light-emitting diode treatment is therapeutic against rotenone- and 1-methyl-4-phenylpyridinium ion-induced neurotoxicity

et al. 2008

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Parkinson's disease is a common progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta. Mitochondrial dysfunction has been strongly implicated in the pathogenesis of Parkinson's disease. Thus, therapeutic approaches that improve mitochondrial function may prove to be beneficial. Previously, we have documented that near-infrared light via light-emitting diode (LED) treatment was therapeutic to neurons functionally inactivated by tetrodotoxin, potassium cyanide (KCN), or methanol intoxication, and LED pretreatment rescued neurons from KCN-induced apoptotic cell death. The current study tested our hypothesis that LED treatment can protect neurons from both rotenone-and MPP + -induced neurotoxicity. Primary cultures of postnatal rat striatal and cortical neurons served as models, and the optimal frequency of LED treatment per day was also determined. Results indicated that LED treatments twice a day significantly increased cellular ATP content, decreased the number of neurons undergoing cell death, and significantly reduced the expressions of reactive oxygen species and reactive nitrogen species in rotenone-or MPP + -exposed neurons as compared to untreated ones. These results strongly suggest that LED treatment may be therapeutic to neurons damaged by neurotoxins linked to Parkinson's disease by energizing the cells and increasing their viability.

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Section: Discussionmentioning

confidence: 97%

Near-infrared light via light-emitting diode treatment is therapeutic against rotenone- and 1-methyl-4-phenylpyridinium ion-induced neurotoxicity

et al. 2008

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“…2 ROS can react with, and so damage, proteins, as well as lipids and carbohydrates. ROS can be generated within the cell as a response to cell stress and may act as secondary messengers 3 to stimulate cell death from apoptosis or necrosis. 4,5 Treatment of cells with many cytotoxic drugs has been shown to result in the production of ROS.…”

Section: Introductionmentioning

confidence: 99%

Carbonylation of glycolytic proteins is a key response to drug-induced oxidative stress and apoptosis

2003

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Recent work has highlighted the importance of protein posttranslational modifications such as phosphorylation (enzymatic) and nitrosylation (nonenzymatic) in the early stages of apoptosis. In this study, we have investigated the levels of protein carbonylation, a nonenzymatic protein modification that occurs in conditions of cellular oxidative stress, during etopside-induced apoptosis of HL60 cells. Within 1 h of VP16 treatment, a number of proteins underwent carbonylation due to oxidative stress. This was inhibited by the antioxidant N-acetyl-L-cysteine. Among the proteins found to be carbonylated were glycolytic enzymes. Subsequently, we found that the rate of glycolysis was significantly reduced, probably due to a carbonylation mediated reduction in enzymatic activity of glycolytic enzymes. Our work demonstrates that protein carbonylation can be rapidly induced through cytotoxic drug treatment and may specifically inhibit the glycolytic pathway. Given the importance of glycolysis as a source of cellular ATP, this has severe implications for cell function.

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“…8 -10 The release of the main mitochondrial proapoptotic protein, cytochrome c, is under the regulation of ROS. 11,12 In addition to the generation of ROS, NO is also generated in anticancer drug-and ␥-ray-treated cancer cells and reaction of ROS with NO is allowed in a favorable circumstance. 13,14 The reactant ONOO Ϫ vigorously damages cells by impairment of proteins and DNA.…”

mentioning

confidence: 99%

Tyrosine‐nitration of caspase 3 and cytochrome c does not suppress apoptosis induction in squamous cell carcinoma cells

Ueta

Kamatani

Yamamoto

et al. 2002

Intl Journal of Cancer

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The influence of tyrosine nitration of cytochrome c and caspase 3 on apoptosis induction was investigated in an established squamous carcinoma cell line, OSC-4. The intracellular NO and O 2 ؊ levels were increased up to about 110 -120% and 140 -180% of the control levels, respectively, after the treatment of OSC-4 cells with 5-FU (100 g/ml), PLM (10 g/ml), CDDP (10 g/ml), or ␥-rays (20 Gy). The treatment of OSC-4 cells with ONOO ؊ (1 mM) and the above anticancer agents induced tyrosine nitration of 14, 32 kDa protein among others and nitration of tyrosine residues of cytochrome c and caspase 3 was identified by the Western blotting of immunoprecipitates obtained by antibodies to these proapoptotic proteins. When cytochrome c and procaspase 3 were treated with ONOO ؊ , tyrosine nitration was increased in a ONOO ؊ -dose dependent manner. Tyrosine nitration of cleaved (17 kDa) Key words: tyrosine-nitration; caspase 3; cytochrome c; apoptosis; squamous cell carcinoma cells; anticancer agentsSuccessful anticancer therapy with chemicals and radiation strongly depends on the strategy for differentiation and apoptosis induction of cancer cells. ROS induce apoptotic signals in cancer cells and apoptosis induction by anticancer drugs and ␥-rays is closely associated with intracellular ROS generation. [1][2][3][4][5][6][7] Apoptotic signals are transduced mainly through 2 pathways, one of which is originates from the mitochondria and the other is the Fas-associated route. 8 -10 The release of the main mitochondrial proapoptotic protein, cytochrome c, is under the regulation of ROS. 11,12 In addition to the generation of ROS, NO is also generated in anticancer drug-and ␥-ray-treated cancer cells and reaction of ROS with NO is allowed in a favorable circumstance. 13,14 The reactant ONOO Ϫ vigorously damages cells by impairment of proteins and DNA. [15][16][17][18][19] Inactivation of the proapoptotic proteins by ONOO Ϫ is therefore probable in chemoradiotherapy of cancers although the apoptosis-inducing activity of ONOO Ϫ has been demonstrated in multiple kinds of cancer cells. 20,21 NO reacts with molecular oxygen (O 2 ), O 2 Ϫ and transitional metals, yielding nitrogen dioxide (NO 2 ), ONOO Ϫ and metalnitrosyl adducts, respectively. 22-24 These reactants are highly reactive and exhibit a variety of physiological activities. 25 In many disorders including inflammatory diseases, the neurotoxicity of stroke, Alzheimer's disease, Parkinson's disease and multiple sclerosis, the highly reactive nitrogen chemicals, especially ONOO Ϫ , are deeply associated with the pathological degeneration of the tissues although the half life of ONOO Ϫ is very short, less than one second in the physiological condition. 26,27 ONOO Ϫ has a potential to cause DNA-strand breaks, lipid peroxidation and diverse modification of cellular molecules such as oxidation of thiol and methionine and nitration of tyrosine and tryptophane. 28 In these modifications, tyrosine nitration has been extensively explored with the aim of analysis of the cytotoxic mec...

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Signalling apoptosis: a radical approach

Cited by 288 publications

References 156 publications

Near-infrared light via light-emitting diode treatment is therapeutic against rotenone- and 1-methyl-4-phenylpyridinium ion-induced neurotoxicity

Near-infrared light via light-emitting diode treatment is therapeutic against rotenone- and 1-methyl-4-phenylpyridinium ion-induced neurotoxicity

Carbonylation of glycolytic proteins is a key response to drug-induced oxidative stress and apoptosis

Tyrosine‐nitration of caspase 3 and cytochrome c does not suppress apoptosis induction in squamous cell carcinoma cells

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