Oxidative stress delayed

The above data demonstrate an important, possibly even critical role of oxidative stress in AD pathogenesis. Therefore, it is reasonable to suggest that antioxidant administration could be useful for the treatment of AD patients. Grundman [320] recently summarized the results of clinical trial, in which vitamin E was administrated to AD patients with moderately severe disease. It has been concluded that the treatment with vitamin E may delay and slow disease progress in these patients. 

Inflamed tissue associated with an oxidative stress as a consequence of a disbalance in the pro-oxidant/antioxidant homeostasis in chronic wounds is thought to drive a deleterious sequence of events that finally results in the non-healing state [29]. Experimental studies showed that wounds of delayed healing type are accompanied... 

Delayed re-epithelialisation and persistent epithelial defects are typical features of chronic ulcers which hardly heal [31, 37], It has been proposed that excessive and uncontrolled proteolytic activity is an important pathogenesis factor for chronic wounds [44]. Proteolysis is caused mainly by the oxidative stress accompanying an... 

Press, C. and Milbrandt, J. (2008) Nmnat delays axonal degeneration caused by mitochondrial and oxidative stress. J Neurosci 28, 4861 4871. 

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... 

The mechanism of action of sulfur mustard is multifaceted and complex, and has been reviewed in some detail by Papirmeister et al. (1991), Hurst and Smith (2008), and Smith et al. (2008). Efforts to understand the mechanisms of sulfur mustard toxicity are ongoing. Basically, sulfur mustard disrupts the interface of the epidermis and basement membrane causing blistering between the epidermis and dermis. Both immediate (immediate cell membrane damage) and delayed phases (secondary effects resulting from inflammatory responses, DNA damage, vascular leakage) have been described for sulfur mustard-induced dermal effects (Somani and Babu, 1989). Many of the toxic effects of sulfur mustard can be attributed to oxidative stress. 

The model of carbon monoxide toxicity proposed by Kao and Nanagas (2006) combines the cascade of changes resulting from three primary events - binding to HB, direct cellular injury, and increased NO activity. CO is not a radical but many of the injuries produced by it are those that are caused by oxidative stress, which is secondary to hypoxia. In the model of Kao and Nanagas (2006), the oxidant is NO, which contributes to oxidative damage to the brain and produces the clinical syndrome of delayed neurologic sequelae (Thom et al, 1997). 

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