Oxidative injury antioxidants

Of the various HSP, heme oxygenase-1, HO-1, by generating the vasoactive molecule carbon monoxide and the potent antioxidant bilirubin, represents a novel protective system potentially active against brain oxidative injury (Rossler et al.,... 

Mahadik S. P. and Scheffer R. E. (1996). Oxidative injury and potential use of antioxidants in schizophrenia. Prostaglandins Leukot. Essent. Fatty Acids 55 45-54. 

Asai et al. (1999) determined that phospholipid hydroperoxides (PLOOH) are key products for oxidative injury in membranous phospholipid layers in the plasma, red blood cells (RBC), and liver of mice. The formation and accumulation of PLOOH have been confirmed in several cellular disorders, various diseases, and in aging. A lower PLOOH level was found in RBC of the spice-extract-fed mice (65 to 74% of the nonsupplemented control mice). The liver lipid peroxidizability induced with Fe2+/ascorbic acid was effectively suppressed in mice by dietary supplementation with the turmeric and capsicum extracts. Although no difference in the plasma lipids was observed, the liver triacylglycerol concentration of the turmeric-extract-fed mice was markedly reduced to half of the level in the control mice. These findings suggest that these spice extracts could act antioxidatively in vivo by food supplementation, and that the turmeric extract has the ability to prevent the deposition of triacylglycerols in the liver. 

M. L. Barnard, R. R. Baker, and S. Matalon, Mitigation of oxidant injury to lung microvasculature by intratracheal instillation of antioxidant enzymes, Am. J. Physiol. 265 L340 (1993). 

To prevent this sun-induced cascade of oxidative injuries, topical preparations containing antioxidants have been developed in the past several decades. Initially, such antioxidants were added as stabilizers to various dermatologic and cosmetic preparations. In particular, lipophilic Vitamin E has been the favorite as a stabilizing agent. However, following oxidation, Vitamin E is degraded into particularly harmful prooxidative metabolites.177... 

Lesnefsky, E.J. Tissue iron overload and mechanisms ofiron-catalyzed oxidative injury. In Free Radicals in Diagnostic Medicine. A Systems Approach to Laboratory Technology, Clinical Correlations, and Antioxidant Therapy, Advances in Experimental Medicine and Biology Armstrong, D., Ed. Plenum Press New York, 1994 366, 129-146. 

Sepsis is also associated with increased reactive oxygen species. Antioxidants and superoxide scavengers have been suggested to attenuate the renal dysfunction of sepsis [91,92]. Recent studies have further indicated that peroxynitrite, the product of the reaction between NO and superoxide, may be responsible for the renal oxidant injury associated with endotoxemia [93]. 

Quinlan T, Spivak S, and Mossman BT (1994) Regulation of antioxidant enzymes in lung after oxidant injury. Environmental Health Perspectives 103(Suppl. 2) 79-87. 

Acalypha wilkesiana van macafeana hort. Din et al. [236] studied the properties of Acalypha wilkesiana var. macafeana hort, used to heal wounds in Malaysian traditional medicine. Acalypha wilkesiana ar. macafeana hort. protected human hepatocellular liver carcinoma (HepG2) cells exposed to tert-butylhydroperoxide, and protected cells against oxidative injuries, showing potent antioxidant and cytoprotective activities. These effects might be exerted bygeraniin [236],... 

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