Synergistic Effect of Tumor Necrosis Factor-Alpha and Hydrogen Peroxide on the Induction of IL-8 Production in Human Intestinal Caco-2 Cells
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It has been suggested that tumor necrosis factor alpha (TNF alpha) acts not only by direct toxicity, but also as a proximal mediator which is able to induce the production of other cytokines, especially interleukin 6 (IL-6) and interleukin 1 beta (IL-1 beta). In order to test the dependence of the release of these two cytokines from leukocytes upon induction by TNF alpha, we stimulated whole blood in vitro with TNF alpha and compared the cytokine levels with those induced by endotoxin. The cytokine release was also determined after stimulation by endotoxin with added TNF alpha and by endotoxin with monoclonal antibodies against TNF alpha (anti-TNF alpha) added in order to reduce TNF alpha. Unstimulated blood samples were used as controls. The plasma levels of both IL-6 and IL-1 beta were significantly higher after stimulation with endotoxin than after stimulation with TNF alpha. TNF alpha did not induce cytokine levels significantly higher than controls. The cytokine levels were the same whether or not anti-TNF alpha was included together with the endotoxin. Plasma from samples with added anti-TNF alpha had no detectable TNF alpha. Our results indicate that the leukocyte-derived production of IL-6 and IL-1 beta in whole blood is stimulated directly by endotoxin and is not mediated by TNF alpha.
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Cylindrospermopsin
Paracellular transport
Transcellular
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Intestinal epithelium
Cyanotoxin
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Zwitterion
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This study examined global oxidative stress (GOS) and antioxidant system and their correlation with disease stage in 19 patients with HD. The results revealed an increase in oxidative stress biomarkers and a reduction in antioxidant systems in HD patients. The effects were more intense in HD1 than in HD2 patients. Additionally, carbonylated proteins and GOS were correlated with disease stage. These findings suggest that oxidative stress plays an important role in the pathogenesis of HD.
Pathogenesis
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Oxidative stress is an imbalance between oxidants and antioxidants in favor of the oxidants, resulting in disruption of redox signaling and control and causing molecular damage. Oxidative stress is related to a variety of diseases, for example, cardiovascular diseases, neurodegenerative diseases, infections, and cancer. It might be that oxidative stress, and, more specifically, reactive oxygen species (ROS), affects longevity in a subtle way through signaling. Possible therapies to reduce oxidative stress in the elderly are nutritional intervention (for example, caloric restriction (CR)) and exercise. Exercise is associated with favorable changes in the expression of antioxidant enzymes and the oxidative stress status in general. A diet with CR also seems to be a promising way to reduce oxidative stress by decreasing oxidant emission and improving antioxidant mechanisms. A better understanding of where the antioxidant mechanisms in the elderly fail could be a big step forward in developing new therapies (such as exercise or diet) that prevent oxidative damage and cellular dysfunction with age.
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xidative stress is defined as ROS in excess of anti-oxidant defense mechanisms. Oxidative stress can result from an excess of ROS, a reduction in antioxi-dants, or both. Damage attributable to oxidative stress is widespread, and oxidative stress is recognized as a prominent feature in numerous disease processes, in-cluding neoplasia and heart disease, as well as trauma and burns.
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