Relation between Mitochondrial Thiols and Thioredoxin System in Some Cancers
Journal Title: INTERNATIONAL JOURNAL OF RECENT TRENDS IN SCIENCE AND TECHNOLOGY - Year 2014, Vol 9, Issue 2
Abstract
Mitochondria are the site for generation of highly reactive oxygen and nitrogen species. These bring about oxidation and nitration of various biomolecules in the vicinity thus affecting their functions. Mitochondrial thiols involved in many important functions may thus be affected. Thioredoxin and Thioredoxin reductase, function to restore modified proteins. Many pathological conditions like cancer are associated with increased production of reactive species generating oxidative stress. The prevalence of breast cancer and that of prostrate and oral cancer including cheek and tongue is increasing. Objectives: The present study was carried out to find out levels of mitochondrial total and membrane protein thiols. Plasma NOx, nitrothiol and nitrotyrosine levels were measured to know the role of NO• and Thioredoxin and Thioredoxin reductase levels were measured as antioxidant defense proteins. Material and methods: Mitochondria were isolated from tissues of patients of breast, prostate, cheek and tongue cancer and non-malignant tissues. Mitochondria were lysed and lysate was used for estimation of Trx, TR, nitrothiols, total and membrane thiol concentrations. The cell lysate was used for estimation of nitrotyrosine. NOx levels were estimated in plasma samples. Observation: It was observed that levels of plasma NOx, were not altered significantly and nitrothiol and nitrotyrosine were not detected. However levels of mitochondrial total and membrane protein thiols were significantly decreased (p<0.05).While levels of Thioredoxin and Thioredoxin reductase were increased significantly (p<0.05). Conclusion: It can be concluded that decrease in mitochondrial thiols causes increase in Thioredoxin and Thioredoxin reductase in cancers under present study which may be independent of NOx, nitrothiol and nitrotyrosine.
Authors and Affiliations
Joshi P. N , Joshi N. G , Bulakh P. M
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