Antioxidant enzyme levels in oral squamous cell carcinoma and normal human oral epithelium

Yang, Jin‐Ming; Lam, Ernest W.N.; Hammad, Huda M.; Oberley, Terry D.; Oberley, Larry W.

doi:10.1034/j.1600-0714.2002.310202.x

Cited by 78 publications

(55 citation statements)

References 17 publications

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“…The rationale to use this combination is supported by 3 lines of evidences: first, because of their lack of antioxidant defenses, cancer cells are more sensitive towards an oxidative injury [4][5][6] ; second, ascorbate seems to be preferentially taken up by cancer cells, due to their overexpression of GLUT receptors 34 ; and third, cancer cells show an almost universal glycolytic phenotype, required to survive and to invade cells/tissues of their neighborhood. 3,35,36 …”

Section: Discussionmentioning

confidence: 99%

“…3 In addition to this high energetic dependence, cancer cells generally exhibit a poor antioxidant status. [4][5][6] Therefore, we developed a novel strategy consisting of the generation of an oxidative stress by the use of a combination of sodium ascorbate (vitamin C) and menadione (vitamin K 3 ). 7 In this strategy, a redox cycle is initiated by electron transfer from ascorbate (AscH 2 ) to quinone (Q) as shown in the next equations:…”

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confidence: 99%

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Role of glycolysis inhibition and poly(ADP‐ribose) polymerase activation in necrotic‐like cell death caused by ascorbate/menadione‐induced oxidative stress in K562 human chronic myelogenous leukemic cells

Verrax

Vanbever

Stockis

et al. 2006

Intl Journal of Cancer

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Among different features of cancer cells, two of them have retained our interest: their nearly universal glycolytic phenotype and their sensitivity towards an oxidative stress. Therefore, we took advantage of these features to develop an experimental approach by selectively exposing cancer cells to an oxidant insult induced by the combination of menadione (vitamin K 3 ) and ascorbate (vitamin C). Ascorbate enhances the menadione redox cycling, increases the formation of reactive oxygen species and kills K562 cells as shown by more than 65% of LDH leakage after 24 hr of incubation. Since both lactate formation and ATP content are depressed by about 80% following ascorbate/menadione exposure, we suggest that the major intracellular event involved in such a cytotoxicity is related to the impairment of glycolysis. Indeed, NAD 1 is rapidly and severely depleted, a fact most probably related to a strong Poly(ADP-ribose) polymerase (PARP) activation, as shown by the high amount of poly-ADP-ribosylated proteins. The addition of N-acetylcysteine (NAC) restores most of the ATP content and the production of lactate as well. The PARP inhibitor dihydroxyisoquinoline (DiQ) was able to partially restore both parameters as well as cell death induced by ascorbate/menadione. These results suggest that the PARP activation induced by the oxidative stress is a major but not the only intracellular event involved in cell death by ascorbate/menadione. Due to the high energetic dependence of cancer cells on glycolysis, the impairment of such an essential pathway may explain the effectiveness of this combination to kill cancer cells. ' 2006 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Role of glycolysis inhibition and poly(ADP‐ribose) polymerase activation in necrotic‐like cell death caused by ascorbate/menadione‐induced oxidative stress in K562 human chronic myelogenous leukemic cells

Verrax

Vanbever

Stockis

et al. 2006

Intl Journal of Cancer

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“…Carcinogenesis is generally divided into three stages: initiation, promotion and progression. ROS are postulated to be involved in these processes, especially in the stages of initiation and promotion (11). ROS are low molecular weight metabolites sufficiently reactive to damage essential biological molecules, including nucleic acids (10).…”

Section: Introductionmentioning

confidence: 99%

Implications of antioxidant enzymes in human gastric neoplasms

Monari¹

2009

Int J Mol Med

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Abstract. The present study is the first to evaluate the expression and activity of MnSOD, Cu/ZnSOD and catalase in human gastric samples, since ROS play a significant role in the pathogenesis of different forms of malignancy inducing mutations and various diseases such as gastric cancer. Biopsies and surgical samples from 53 patients (male/female 22/31, mean age 56.5±15.8 years) consisted of 15 healthy, 12 autoimmune atrophic gastritis, 10 Helicobacter pylori (HP) infection, 8 HP-negative chronic gastritis (CG) and 8 adenocarcinoma cases. Enzyme activity and expression were evaluated by spectrophotometry and immunoblotting after specific extraction in phosphate buffer. We found that MnSOD activity was increased in adenocarcinoma, CG and HP tissues (p<0.05-0.001), while Cu/ZnSOD was significantly lower in adenocarcinoma and HP tissues (p<0.001) when compared to the healthy control. MnSOD and Cu/ZnSOD were expressed to a significantly higher degree in adenocarcinoma and HP tissues (p<0.05 and <0.001 respectively) and to a significantly lower degree in CG tissues with respect to the healthy patients (p<0.05 and <0.001). A significant decrease in CAT activity in adenocarcinoma and HP tissues was observed (p<0.01 and <0.05). Gastric human neoplasms showed significant changes in antioxidant enzymes, that represent the first line in antioxidant protection against radical attack. The difficulties in correlating the antioxidant enzyme with the neoplasms was related to the complexity of the biochemical pathways that regulate the cellular redox balance. Our results are important in enhancing the understanding of the role that these enzymes play in the promotion/ suppression of the carcinogenesis cascade in human gastric mucosa.

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“…Herbs, such as bilberry, turmeric (curcumin), grape seed or pine bark extracts, and ginkgo can also provide powerful antioxidant protection for the body. Melatonin is a hormone secreted by pineal gland and proves to be powerful antioxidant and free radical scavenger (Yang et al,2002 andKoc et al, 2003).…”

Section: Antioxidantsmentioning

confidence: 99%

Lipid Peroxidation End-Products as a Key of Oxidative Stress: Effect of Antioxidant on Their Production and Transfer of Free Radicals

El-Aal¹

2012

Lipid Peroxidation

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Antioxidant enzyme levels in oral squamous cell carcinoma and normal human oral epithelium

Cited by 78 publications

References 17 publications

Role of glycolysis inhibition and poly(ADP‐ribose) polymerase activation in necrotic‐like cell death caused by ascorbate/menadione‐induced oxidative stress in K562 human chronic myelogenous leukemic cells

Role of glycolysis inhibition and poly(ADP‐ribose) polymerase activation in necrotic‐like cell death caused by ascorbate/menadione‐induced oxidative stress in K562 human chronic myelogenous leukemic cells

Implications of antioxidant enzymes in human gastric neoplasms

Lipid Peroxidation End-Products as a Key of Oxidative Stress: Effect of Antioxidant on Their Production and Transfer of Free Radicals

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