title: Enhanced oxidative stress and leucocyte activation in neoplastic tissues of the colon.
abstract: Excess of intracellular reactive oxygen species results in an environment that may modulate gene expression, or damage cellular molecules. These events are assumed to contribute to the process of carcinogenesis. In the present study, we measured the extent of lipid peroxidation and antioxidative status in colonic tumors and normal colonic mucosa obtained from 25 patients with colorectal carcinoma. Levels of lipid peroxides (PD) and of thiobarbituric acid reactive substances (TBARS) were significantly increased, by 54 and 59%, respectively, in tissue specimens obtained from the colonic tumor as compared with normal colonic mucosa (PD, 2.78+/-0.31 versus 1.81+/-0.29 nmol/mg tissue, TBARS, 0.86+/-0.1 versus 0.54+/-0.08 nmol/mg tissue). Activities of the antioxidant enzymes catalase and glutathione peroxidase (GPx) were also higher (by 67 and 29%, respectively) than in normal mucosa, probably in response to the increased free radical stress occurring in cancerous tissues. Myeloperoxidase (MPO) and adenosine deaminase (ADA) are markers of activated leukocytes and are related to the production of oxygen free radicals by these cells. Their activities were significantly elevated in the neoplastic tissue as compared to the normal tissue (MPO, 7.4+/-1.5 versus 4.1+/-0.95 U/mg tissue, ADA, 4.17+/-0.65 versus 2.99+/-0.80 U/g tissue), suggesting a possible involvement of activated leukocytes in the enhanced oxidative stress in the cancerous tissue. Our results demonstrate an enhanced oxidative stress in the neoplastic tissue. Leukocyte activation was also higher in the carcinogenic tissue, indicating a possible contribution of these cells to a further oxidative stress-derived tissue injury. These observations add to previous studies and may encourage therapeutic trials with antioxidants as a means of preventing colorectal cancer and preventing further tissue injury in the neoplastic tissue and its surroundings.
authors.affiliation: Bnai-Zion Medical Center, Gastroenterology Unit, Haifa, Israel. tova@4utv.col.il
authors.forename: Tova
authors.initials: T
authors.lastname: Rainis
authors.forename: Irit
authors.initials: I
authors.lastname: Maor
authors.forename: Amos
authors.initials: A
authors.lastname: Lanir
authors.forename: Sergay
authors.initials: S
authors.lastname: Shnizer
authors.forename: Alexandra
authors.initials: A
authors.lastname: Lavy
mesh_terms: D000243:Adenosine Deaminase / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D003110:Colonic Neoplasms / Q000378:metabolism*; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D007962:Leukocytes / Q000378:metabolism*; D015227:Lipid Peroxidation; D008054:Lipid Peroxides / Q000378:metabolism; D018384:Oxidative Stress; D009195:Peroxidase / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D008054:Lipid Peroxides; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D002374:Catalase; D009195:Peroxidase; D005979:Glutathione Peroxidase; D000243:Adenosine Deaminase