Abstract
Oxidative Products of Proteins and Antioxidant Potential of Thiols in Gastric Carcinoma PatientsIt has been suggested that oxidative stress defined as a shift in antioxidant/oxidant balance towards oxidants is associated with the pathogenesis of many diseases, including carcinogenesis. Reactive oxygen species can induce carcinogenesis via injury to macromolecules such as DNA, carbohydrates and proteins. Forty primary gastric carcinoma patients and 40 healthy controls were included in the study. Advanced oxidation protein products, total thiols, total protein, albumin in plasma, % hemolysis in RBC suspension and glutathione in both whole blood and plasma were estimated. Our studies demonstrated a significant increase in advanced oxidation protein products, % hemolysis (p=0.033), A:G ratio (p=0.003) and a highly significant decrease in blood glutathione (p=0.036), total thiols (p=0.001), plasma thiols other than glutathione and total antioxidant activity. The findings suggest that gastric carcinoma is associated with oxygen derived free radicals accumulation, and depletion of total antioxidant activity has lead to oxidative stress and advancement of oxidative-antioxidative disorders followed by progression of gastric cancer.
Highlights
Gastric cancer is a multifactorial disease and has multietiopathogenic factors
There is substantial evidence that oxygen derived free radicals play an important role in the pathogenesis of various tissues
Blood samples were collected from 40 subjects, both male and female diagnosed with gastric carcinoma on clinical basis, who have not undergone surgery, chemotherapy or radiotherapy and age and sex matched 40 healthy individuals devoid of disease conditions like hypertension, diabetes mellitus, epilepsy and psychiatric disorders
Summary
Gastric cancer is a multifactorial disease and has multietiopathogenic factors. It is widely accepted that a major underlying factor of this disorder is the generation of free radicals. The lipoxygenase pathway and the activated inflammatory cells could be involved in the pathogenesis of mucosal damage. In H. pylori infected gastric mucosa and duodenal gastric metaplasia, active inflammation with infiltration of neutrophils in the acute stage of the infection and of macrophages/monocytes, lymphocytes and plasma cells in the chronic stage is observed in the lamina propria of the stomach. These may act as a source of a large quantity of oxygen derived free radicals that could cause cell damage and lead to mucosal injury [1]
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