Glutathione concentration in oral cancer tissues

Wong, Dsh; Hsiao, Ying-Lyung; Poon, Chiu-Kwan; Kwan, Po-Cheung; Chao, Shou-Yee; Chou, Su‐Tze; Yang, Chung‐Shi

doi:10.1016/0304-3835(94)90191-0

Cited by 69 publications

(39 citation statements)

References 16 publications

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“…Glutathione, an important substrate for glutathione peroxidase has been documented to have regulatory effects in cell proliferation [34]. Over-expression of glutathione has been reported in malignant tumors [35], and high levels of glutathione were observed in various tumor tissues and cell lines [35,36]. However, there are very few reports on glutathione concentration in experimental oral carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of 4-Nitroquinoline-1-Oxide-Induced Oral Carcinogenesis by Plant Products.

Manoharan

Ramachandran

et al. 1996

J. Clin. Biochem. Nutr.

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SummaryThe modifying effects of naturally occurring plant products such as neem leaf and turmeric extracts on 4-nitroquinoline-l-oxide (4NQO)-induced oral carcinoma were investigated in male Wistar strain rats. All the animals painted with 4NQ0 on their cheek mucosa for 20 weeks developed oral neoplasms identified histologically as squamous cell carcinoma. The oral tumor tissue showed a decrease in lipid peroxidation with concomitant changes in antioxidant activity. In groups of animals painted with 4NQ0 and simultaneous oral administration of neem leaf and turmeric extract, respectively, no tumors were observed; and the lipid peroxidation and antioxidant levels showed a pattern similar to that of untreated controls. Thus, the anticarcinogenic effect of neem leaf and turmeric extract appears to be related to their antioxidant function.We envisage that measurement of lipid peroxidation and antioxidant status with histological changes could be used to biomonitor tumor progression and evaluate the therapeutic response.

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Section: Discussionmentioning

confidence: 99%

Inhibition of 4-Nitroquinoline-1-Oxide-Induced Oral Carcinogenesis by Plant Products.

Manoharan

Ramachandran

et al. 1996

J. Clin. Biochem. Nutr.

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“…Oxidative stress causes profound alterations of various biological structures, including cellular membranes, lipids, proteins and nucleic acids. Oxidative stress is considered to be involved in ageing (14)(15)(16)(17)(18)(19)(20) Redox status expressed as GSH:GSSG ratio as a marker for oxidative stress in paediatric tumour patients (36)(37)(38)(39)(40)(41)(42)(43)(44). There is an increasingly growing interest in identifying biomarkers for diseases, in which oxidative stress is involved (45).…”

Section: Introductionmentioning

confidence: 99%

Redox status expressed as GSH:GSSG ratio as a marker for oxidative stress in paediatric tumour patients

et al. 2012

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Abstract.Oxidative stress causes profound alterations of various biological structures, including cellular membranes, lipids, proteins and nucleic acids, and it is involved in numerous malignancies. Reduced glutathione (GSH) is considered to be one of the most important scavengers of reactive oxygen species (ROS), and its ratio with oxidised glutathione (GSSG) may be used as a marker of oxidative stress. The main aim of this study was to determine GSH:GSSG ratio in the blood serum of paediatric cancer patients to use this ratio as a potential marker of oxidative stress. The whole procedure was optimised and the recoveries for both substances were greater than 80% under the optimised conditions. We analysed a group of paediatric patients (n=116) with various types of cancer, including neuroblastoma, anaplastic ependymoma, germ cell tumour, genital tract tumour, lymphadenopathy, rhabdomyosarcoma, nephroblastoma, Ewing's sarcoma, osteosarcoma, Hodgkin's lymphoma, medulloblastoma and retinoblastoma. We simultaneously determined the levels of reduced and oxidised glutathione, and thus, its ratio in the blood serum of the patients. The highest ratio was observed in retinoblastoma patients and the lowest in anaplastic ependymoma. We were able to distinguish between the diagnoses based on the results of the obtained GSH:GSSG ratio.

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“…22 In clinical studies, GSH levels were approximately 4-fold greater in oral tumor tissue than that in the surrounding ''normal'' epithelium. [23][24][25][26] In one study, increased tumor GSH levels correlated with the stage of the disease. 25 Also, increased GSH levels have been reported in cheek pouch tumors in the DMBA-induced hamster model.…”

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confidence: 99%

Enhanced levels of glutathione and protein glutathiolation in rat tongue epithelium during 4‐NQO‐induced carcinogenesis

Huang¹,

Komninou²,

Kleinman³

et al. 2007

Intl Journal of Cancer

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High glutathione (GSH) levels are commonly found in oral tumors and are thought to play an important role in tumorigenesis. While posttranslational binding of GSH to cellular proteins (protein glutathiolation) has recently been recognized as an important redoxsensitive regulatory mechanism, no data currently exist on this process during carcinogenesis. Our goal was to determine the effects of 4-nitroquinoline-N-oxide (4-NQO)-induced carcinogenesis on tongue levels of protein-bound and free GSH and related thiols in the rat. Male F-344 rats (6 weeks of age) were administered either 4-NQO (20 ppm) in drinking water or tap water alone (controls) for 8 weeks. Twenty-four weeks after cessation of 4-NQO, squamous cell carcinomas of the tongue were observed in all rats. The levels of both free and bound GSH in tumors, as well as in adjacent tissues, were 2-to 3-fold greater than in tongue epithelium from control rats (p < 0.05). Prior to tumor formation, at 8 weeks after cessation of 4-NQO, hyperplasia, dysplasia and carcinoma in situ were observed in 100%, 25% and 12.5% of 4-NQOtreated rats, respectively. At this early stage of carcinogenesis, levels of free and bound GSH were increased 50% compared with tongue tissues from control rats (p < 0.05). Glutathione disulfide (GSSG) levels were also 2-fold greater in tongue tissues from 4-NQO treated vs. control rats (p < 0.05). Altogether, these results suggest that protein glutathiolation, together with GSH and GSSG levels, are induced during oral carcinogenesis in the rat possibly as a result of enhanced levels of oxidative stress. ' 2006 Wiley-Liss, Inc.

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Glutathione concentration in oral cancer tissues

Cited by 69 publications

References 16 publications

Inhibition of 4-Nitroquinoline-1-Oxide-Induced Oral Carcinogenesis by Plant Products.

Inhibition of 4-Nitroquinoline-1-Oxide-Induced Oral Carcinogenesis by Plant Products.

Redox status expressed as GSH:GSSG ratio as a marker for oxidative stress in paediatric tumour patients

Enhanced levels of glutathione and protein glutathiolation in rat tongue epithelium during 4‐NQO‐induced carcinogenesis

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