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.

Chemopreventive Effect of Different Ratios of Fish Oil and Corn Oil in Experimental Colon Carcinogenesis

“…The level of GSH and GSH dependent enzymes were raised along with the increase in the apoptosis. Increase in the activities of SOD and CAT in the carcinogen treated animals have also been reported by other workers [52,53]. An increased expression of GSH, GPx and GST in the neoplastic cell confers a selective growth advantage against onslaught of oxidative stress and allows these cells to propagate and proliferate [54].…”

Influence of Alcohol Consumption on Oxidative Stress and Antioxidant Status in Cancer Patients - Case-control Study from Western Nepal

“…The raised TBARS indicates the weak antioxidant defense system against raised OS. There were numerous reports indicating raised OS in cancer patients due to alcohol consumption (Terry et al, 2001;Poschl and Seitz, 2004;Rainis et al, 2007;Ha et al, 2010;Manjunath et al, 2010). Not only the commercial alcohol but also the combination of alcohol and commercial alcohol consumption plays an important role in increased OS and further in cancer development.…”

Free Radicals: Properties, Sources, Targets, and Their Implication in Various Diseases

“…Since the intestinal mucosa is constantly confronting with diet and bacterial-derived oxidants and carcinogens, an unrestrained production of free radicals, redox imbalance, and DNA damage occurs, finally leads to an altered intestinal metabolic homeostasis with cancer as an endpoint [133]. The human colorectal tumors have increased levels of nitric oxide (NO) [132], 8-oxodG in DNA [133], and lipid peroxides [134]. Suzuki et al 2004 [135] have reported increased serum levels of oxidized low density lipoprotein in patients with CRC compared to healthy individuals.…”