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Glutathione peroxidase exposure

Other examples of possible damaging effects of radio frequency MFs on humans are the MF effects on cellular phones. Moustafa et al. [216] suggested that acute exposure to the MFs of commercially available cellular phones for 1, 2, or 4 h significantly increased plasma lipid peroxidation and decreased the activities of SOD and glutathione peroxidase in erythrocytes. [Pg.713]

C. carpio 10 during exposure for 96 h, significant alterations were recorded in lipid peroxidation rate, hemoglobin concentration, and erythrocyte antioxidant enzymes, that is, catalase, superoxide dismutase, and glutathione peroxidase activities 20... [Pg.1172]

In addition to catalase, the enzymes glutathione peroxidase and superoxide dismutase are important elements in the cellular defenses against free radical oxygen. Cytoplasmic activity of glutathione peroxidase was decreased in rats by 14 and 28 days of exposure to doses of 500-2,000 mg/kg/day DEHP (Elliott and Elcombe 1987 Perera et al. 1986) and superoxide dismutase activity was decreased by a 28 day exposure of rats to 1,000 and 2,000 mg/kg/day (Elliott and Elcombe 1987). Glutathione... [Pg.87]

Rasmussen, T.R., S.K.Kjaergaard, U.Tarp, and O.F.Pedersen. 1992. Delayed effects of N02 exposure on alveolar permeability and glutathione peroxidase in healthy humans. Am. [Pg.267]

Recent studies have shown that cyanide also inhibits the antioxidant defense enzymes (such as catalase, superoxide dismutase, and glutathione peroxidase) and stimulates neurotransmitter release. These effects of cyanide may also contribute to its acute toxicity. The prolonged energy deficit and the consequent loss of ionic homeostasis, which may result in activation of calcium signaling cascade and eventually cell injury, contribute to cyanide toxicity resulting from subacute exposure or in the postintoxication sequela. [Pg.699]

With selenium or Vitamin E deficient diets, repeated exposure to silver (76 ppm in the drinking water for 52 days) in rats elicited hepatic necrosis and ultra-structural changes in the liver indicative of oxidative damage. This toxicity may be related to a silver-induced selenium deficiency and impairment of synthesis of the enzyme glutathione peroxidase. Dietary supplementation with selenium or Vitamin E prevented such changes. Mice exposed to silver nitrate in the drinking water for 4 months exhibited... [Pg.2408]

The data indicate that zinc-induced metallothionein binds mercury in the renal cortex and shifts the distribution of mercury from its site of toxicity at the epithelial cells of the proximal tubules. Thus, the renal content of mercury is increased, yet less is available to cause toxicity. In contrast, the renal toxicity of mercuric chloride is exacerbated in zinc-deficient animals (Fukino et al. 1992). In the zinc-deficient state, less mercury accumulates in the kidneys, but the toxicity is greater. The mechanism of the protection appears to involve more than simply a redistribution of renal mercury, because in the absence of mercury exposure, zinc deficiency increases renal oxidative stress (increased lipid peroxidation, decreased reduced ascorbate). When mercury exposure occurs, the oxidative stress is compounded (increased lipid peroxidation and decreased glutathione and glutathione peroxidase). Thus, zinc appears to affect the biochemical protective mechanisms in the kidneys as well. [Pg.355]

The co-administration of M. oleifera seed powder with arsenic protects animals from arsenic induced oxidative stress and reduce body arsenic burden (49). Exposure of rats to arsenie (2.5 mg/kg, intraperitoneally for 6 weeks) increases the levels of tissue reaetive oxygen species (ROS), metallothionein (MT) and thiobarbitnrie aeid reaetive substance (TEARS) and is accompanied by a decrease in the aetivities in the antioxidant enzymes such as superoxide dismutase (SOD), eatalase and glutathione peroxidase (GPx). Also, Arsenic exposed mice exhibits hver injury as reflected by reduced acid phosphatase (AGP), alkaline phosphatase (ALP) and aspartate aminotransferase (AST) activities and altered heme synthesis pathway as shown by inhibited blood 8-aminolevulinic acid dehydratase (5-ALAD) activity. Co-administration of M. oleifera seed powder (250 and 500 mg/kg, orally) with arsenie significantly increases the activities of SOD, catalase, GPx with elevation in redueed GSH level in tissues (liver, kidney and brain). These ehanges are accompanied by approximately 57%, 64% and 17% decrease in blood ROS, liver metallothionein (MT) and lipid peroxidation respectively in animal eo-administered with M. oleifera and arsenic. There is a reduced uptake of arsenie in soft tissues (55% in blood, 65% in liver, 54% in kidneys and 34% in brain) following eo-administration of M. oleifera seed powder (particularly at the dose of 500 mg/kg). This points to the fact that administration of M. oleifera seed powder could be beneficial during chelation therapy with a thiol chelator (26). [Pg.453]

Coriandrum sativum L. Conundrum sativum L. (coriander) belongs to the Apiaceae family and is cultivated worldwide for its nutritional value and medicinal properties (relief of pain, anxiety, flatulence, loss of appetite, and convulsions). The effects of inhaled coriander volatile oil (1-3 %) extracted from Coriandrum sativum var. microcarpum on spatial memory performance were assessed in an Ap2 2 rat model of AD. Exposure to coriander volatile oil improved spatial memory, increased superoxide dismutase (SOD), lactate dehydrogenase (LDH), and decreased glutathione peroxidase (GPX) specific activities along with an elevation of malondial-dehyde (MDA) level [288],... [Pg.416]

The utility of antioxidants in terrestrial animals has received relatively little attention so far. In earthworms, inhibition of CAT and glutathione peroxidase but not SOD have been demonstrated in E.fetida exposed to lead and uranium (Labrot et al., 1996). However, SOD and CAT activity were not induced in E. veneta and E.fetida exposed to Zn, Cu and Hg and the herbicide paraquat (Honsi et al., 1999). Antioxidant enzyme measurement therefore cannot be considered a reliable biomarker of exposure in soil invertebrates. [Pg.177]


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See also in sourсe #XX -- [ Pg.234 ]




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