Family history and gastric carcinoma: The role of glutathione peroxidase

Citation
Ai. Fiaschi et al., Family history and gastric carcinoma: The role of glutathione peroxidase, CURR THER R, 61(11), 2000, pp. 807-816
Citations number
35
Categorie Soggetti
Pharmacology,"Pharmacology & Toxicology
Journal title
CURRENT THERAPEUTIC RESEARCH-CLINICAL AND EXPERIMENTAL
ISSN journal
0011393X → ACNP
Volume
61
Issue
11
Year of publication
2000
Pages
807 - 816
Database
ISI
SICI code
0011-393X(200011)61:11<807:FHAGCT>2.0.ZU;2-1
Abstract
Background: The risk of gastric carcinoma is increased in persons with a po sitive family history of the disease, Previous findings suggest that free r adicals are involved in both the initiation and promotion of carcinogenesis . Objective: The aim of this study was to assess whether alterations in the a ntioxidant defense system of gastric mucosal cells in patients with gastric carcinoma are related to a positive family history. Methods: Glutathione peroxidase activity, oxidized glutathione, total gluta thione, and malondialdehyde levels were assayed in patients with gastric ca rcinoma with and without a family history of the disease. A control group c onsisted of healthy volunteers. Results: The study enrolled 65 patients with gastric carcinoma: 35 with and 30 without a family history of the disease, as well as 30 control subjects . The level of glutathione peroxidase activity in tu mor-free tissue sample s from patients with a family history of gastric carcinoma was higher than in samples from those without such family history. Glutathione peroxidase a ctivity was also significantly higher in neoplastic than in tumor-free tiss ue. There was no significant difference in glutathione peroxidase activity between neoplastic tissue samples taken from patients with and without a po sitive family history. Conclusions: The results appear to support the existence of an enzymatic im balance caused by cellular initiation in patients with a family history of gastric carcinoma. This imbalance may lead to an altered response to free r adical oxygen species and a consequent progressive increase in biologic dam age.