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Antioxidant enzymes response

In plants, phenolic metabolites can stimulate cellular protective response coupled to antioxidant function in the presence of biotic and abiotic stress (Briskin 2000). Among abiotic stress, UV light induces phenolic phytochemicals through the phenylpropanoid and flavonoid glycoside pathways as a protective of metabolic response (Logemann et al. 2000). This UV inducible phenolic phytochemical response can help to counter intracellular ROS produced in response to UV. This UV-inducible phenolic response ean be coupled to antioxidant enzyme response (Rao 1996) to attenuate damage from UV radiation. [Pg.101]

Randhir, R., Vattem, D., and Shetty, K. 2005. Antioxidant enzyme response studies in H202-stressed porcine muscle tissue following treatment with oregano phenolic extracts. Process Biochemistry, 40(6), 2123—2134. [Pg.299]

A major contribution of the free-radical scavenging activity in blood plasma is attributable to the macro-molecular proteins (Wayner et al., 1985) of which albumin is a primary component and trapping agertt (Holt et al., 1984). Serum sulphydryl levels, primarily albumin-related, are decreased in subjects with rheumatoid complicated coalworkers pneumoconiosis, indicative of exacerbated inflammatory R.OM production (Thomas and Evans, 1975). Experimental asbestos inhalation in rats leads to an adaptive but evidendy insufficient response by an increase in endogenous antioxidant enzymes (Janssen etal., 1990). Protection of the vascular endothelium against iron-mediated ROM generation and injury is afforded by the iron sequestiant protein ferritin (Balia et al., 1992). [Pg.254]

Breinholt, V., S. T. Lauridsen, B. Daneshvar, and J. Jakobsen. 2000. Dose-response effects of lycopene on selected drug-metabolizing and antioxidant enzymes in the rat. Cancer Lett 154(2) 201-210. [Pg.430]

Researchers focused on the metabolically competent human hepatoma cell line HepG2 as a model of human liver. HepG2 cells are a well-known hepatoma cell line that retains many of the morphological characteristics of liver parenchymal cells. This model is often used as a useful tool for HRA/ERA-oriented chemical risk assessment due to the expression of antioxidant and xenobiotic metabolizing enzymes (in particular phase I and phase II enzymes responsible for the bioactivation/detoxification of various xenobiotics) that can be induced or inhibited by dietary and non-dietary agents [28-30]. [Pg.178]

Fig. 27.5 Level of tissue antioxidant enzymes SOD, CAT and GPX in control (normal) and chronic leg ulcer patients before and after LLLT among total, low and high response groups... Fig. 27.5 Level of tissue antioxidant enzymes SOD, CAT and GPX in control (normal) and chronic leg ulcer patients before and after LLLT among total, low and high response groups...
Throughout evolution, plants and animals have been constantly exposed to oxidative stress, high response, organisms have evolved to acquire, synthesize, store, and use antioxidant chemicals and proteins. For example, humans synthesize the antioxidant enzymes Cu-Zn superoxide dismu-tase (SOD), Mn-SOD, glutathione peroxidase, and catalase, and they can incorporate dietary antioxidants such as plant phenolics, vitamin C, and vitamin E into their tissues. [Pg.403]

Increase in TAC is not always a good prognostic it may simply indicate an initial response to oxidative stress, as with concentrations of individual antioxidants and activities of antioxidant enzymes, or when it is due to disturbances in uric acid metabolism. Because uric acid is the main determinant of TAC of blood plasma, TAC increases in situations when the concentration of urate is increased, for example, in metabolic disorders and kidney failure. TAC is increased in urine from renal transplant recipients with delayed graft function (SI6). Ischemia of small intestine leads to an increase in TAC of rat blood serum, which is maximal (almost twofold) immediately after termination of 45-min ischemia (S22). TAC of blood plasma of rats poisoned with a high dose of carbon tetrachloride (1200 mg/kg, intraperitoneal injection, measurement 16 hr after injection) was significantly (over twofold) increased (Kl). These apparently paradoxical effects can be explained, however, by release of antioxidants from cells undergoing necrosis. Increase in TAC after intensive physical exercise also may be a marker of tissue... [Pg.271]

They play an important role in maturation and differentiation of B and T lymphocytes, NK cells, macrophages, and cytokines they release Decrease amount of lymphocytes T helpers, have anti-inflammatory action, diminish allergenic responses of delayed type, depress mitogenic response of T cells, increase level of antioxidative enzymes, decrease number of free radicals... [Pg.54]

Understandably, there are examples of oxygen-tolerant cell lines which have much higher levels of constitutive antioxidant enzymes than normal [249]. The ability of other cells to protect themselves by means of antioxidant enzymes is limited by their biosynthetic response to oxidative stress. In vitro exposure to paraquat induces an increase in SOD and catalase activities in human and hamster fibroblasts [250,251]. In cultured HeLa cells, a chronic exposure to paraquat induces a simultaneous increase in Mn- and Cu/Zn-SOD activities in surviving cells [252], Interestingly, such cells have apparently acquired resistance to paraquat, and their higher level of SOD activities persists for many months following the exposure to paraquat. In Chinese hamster fibroblasts, a chronic exposure to H2O2 results in a 5-40-fold increase in catalase activity [253], which... [Pg.52]


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