Oxidative Stress and Cytokines in the Pathogenesis of Pancreatic Cancer
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Pancreatic cancer is one of the most aggressive, drug-resistant and lethal types of cancer with poor prognosis. Various factors including reactive oxygen species, cytokines, growth factors, and extracellular matrix proteins are reported to be involved in the development of pancreatic cancer. However, the pathogenesis of pancreatic cancer has not been completely elucidated. Oxidative stress has been shown to contribute to the development of pancreatic cancer. Evidences supporting the role of reactive oxygen species and cytokines as a risk for pancreatic cancer and the concept of antioxidant supplementation as a preventive approach for pancreatic cancer have been proposed. Here, we review the literature on oxidative stress, cytokine expression, inflammatory signaling, and natural antioxidant supplementation in relation to pancreatic cancer.Keywords:
Pathogenesis
Proinflammatory cytokine
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Reactive nitrogen species
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Oxidative stress is caused by a shift in the balance between highly reactive molecules, such as reactive oxygen species, and antioxidant body’s defense system. Reactive oxygen species play a pivotal role in the human body and are produced by a living organism as a result of normal cellular metabolism and environmental factors, such as pollutants and cigarette smoke. However, their high activity might have important biological consequences. ROS can be considered as a significant mediator of damage to major biomolecules and cell structures. It is also well documented that oxidative stress takes part in a growing number of pathological states and diseases, especially when inflammation is prominent. Aerobic organisms have developed an antioxidant system and are effective in opposing the effect of ROS. These antioxidants can be divided into the following: enzymatic and non-enzymatic. In pathological conditions the antioxidant system may be overwhelmed, which leads to oxidative stress. The purpose of this mini-review is to introduce the important findings concerning the ROS and salivary antioxidants (Dent.
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Oxidative stress can be defined as a rise of oxidative potential or decrease of antioxidant status. Oxidative stress is caused by reactive oxygen species (ROS) which are produced by one-electron reduction of oxygen in the electron transport chain, as well as many other reactions. Effects of ROS can result in cellular membrane damage, structural and functional changes in enzymatic and non-enzymatic proteins, and damage to the DNA structure. Excessive generation of free radicals, decrease of enzymatic antioxidant activity, and/or reducing agents are considered as the main causes of oxidative stress. Since the brain contains a large amount of polyunsaturated fatty acids, consumes up to 20% of oxygen used by the whole body, and shows low antioxidant activity, it seems to be especially vulnerable to oxidative stress. Numerous data show the significant role of oxidative stress in pathogenesis of many neurodegenerative diseases.
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Oxidative stress indicates an imbalance state between production of reactive oxygen species (ROS) and antioxidant defenses. It occurs when excessive production of ROS overwhelms the one of antioxidant defense system or when there is a significant decrease or lack in production of antioxidant defenses. Recently, it has attracted more and more researchers' attention as one cause of many diseases. In obstetrics, many researches suggested that oxidative stress is associated with normal and abnormal pregnancies. In this article, we reviewed relationship between oxidative stress and pregnancy.[
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Tumor progression
CA19-9
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Oxidative stress results from a prooxidant-antioxidant imbalance, leading to cellular damage. It is mediated by free radicals, such as reactive oxygen species or reactive nitrogen species, that are generated during physiological aerobic metabolism and pathological inflammatory processes. Skin serves as a protective organ that plays an important role in defending both external and internal toxic stimuli and maintaining homeostasis. It is becoming increasingly evident that oxidative stress is involved in numerous skin diseases and that antioxidative strategies can serve as effective and easy methods for improving these conditions. Herein, we review dysregulated antioxidant systems and antioxidative therapeutic strategies in dermatology.
Reactive nitrogen species
Homeostasis
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The generation of oxygen radicals and their derivatives, known as reactive oxygen species, (ROS) is a part of the signaling process in higher plants at lower concentrations, but at higher concentrations, those ROS cause oxidative stress. Salinity-induced osmotic stress and ionic stress trigger the overproduction of ROS and, ultimately, result in oxidative damage to cell organelles and membrane components, and at severe levels, they cause cell and plant death. The antioxidant defense system protects the plant from salt-induced oxidative damage by detoxifying the ROS and also by maintaining the balance of ROS generation under salt stress. Different plant hormones and genes are also associated with the signaling and antioxidant defense system to protect plants when they are exposed to salt stress. Salt-induced ROS overgeneration is one of the major reasons for hampering the morpho-physiological and biochemical activities of plants which can be largely restored through enhancing the antioxidant defense system that detoxifies ROS. In this review, we discuss the salt-induced generation of ROS, oxidative stress and antioxidant defense of plants under salinity.
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Medical microbiology
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Oxidative stress, in recent times, appears to be a major underlying risk factor in the occurrence of major diseases such as cardiovascular diseases (CVD) and inflammatory diseases. During oxidative stress, an overall dysfunction of the balance between the production of reactive oxygen species (ROS) and the antioxidant defence mechanism occurs and a shift is obtained in favour of ROS production. Consequently, this may cause severe molecular, cellular and histological damage of the heart and vascular membranes in both animal and human living system which may lead to more serious complications. Previous studies proposed that reactive oxygen species represent at a molecular basis a key aspect in the pathogenesis of endothelial dysfunction and atherosclerosis which in fact constitute major underlying pathologies of most CVD. In this review, we discuss the role of reactive oxygen species in the pathogenesis of cardiovascular disease.
Key words: Cardiovascular disease, reactive oxygen species, inflammation.
Pathogenesis
Endothelial Dysfunction
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Generation of reactive oxygen species (ROS) is a normal process. Under physiological conditions, these deleterious species are mostly removed by the cellular antioxidant systems, which include antioxidant vitamins, protein and non-protein thiols, and antioxidant enzymes. An acute bout of exercise at sufficient intensity has been shown to stimulate activities of antioxidant enzymes. This could be considered as a defensive mechanism of the cell under oxidative stress. However, we still have insufficient knowledge about the interaction between exercise and antioxidants, which are important in assessing the adequacy of protection against oxidative damage and about the necessity of dietary manipulation and/or supplementation. This review concerns effects of acute exercise on various oxidative stress parameters and antioxidant defense system.
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