Reactive oxygen effects

Azelaic acid is effective on P. acnes suppression, even if less than benzoyl peroxide. The anti-inflammatory effect of azelaic acid seems to be related to a decreased production of reactive oxygen species by neutrophils. Azelaic acid may also regulate the ductal cell keratinization, reducing the number of comedones, ft is not sebosuppressive. 

The reactive species might be V(OH)2l, produced in a similar manner to the analogous species in the oxidation of bromide ion, which could undergo one-equivalent breakdown to V(IV) and atomic iodine. Ramsey et al postulate transfer of OH to iodide ion, but the intermediacy of-12 is referred to in a later study of the oxygen effect to account for the relation ... 

LIN J K s, LEE F, HUANG Y T, LiN-SHiAU s Y (1995) Signal transduction and oncogene expression mediated by reactive oxygen species. In Proceedings of the International Symposium on Natural Antioxidants - Molecular Mechanisms and Health Effects. Eds Packer, L, Traber, M G, Xin, W Champaign, I L, USA AOCS Press, 303-19. 

The protective effects of carotenoids against chronic diseases appear to be correlated to their antioxidant capacities. Indeed, oxidative stress and reactive oxygen species (ROS) formation are at the basis of oxidative processes occurring in cardiovascular incidents, cancers, and ocular diseases. Carotenoids are then able to scavenge free radicals such as singlet molecular oxygen ( O2) and peroxyl radicals particularly, and protect cellular systems from oxidation. 

A molecule that has a prooxidant effect can be dehned as a molecule that can react with reactive oxygen species (ROS) to form compounds more deleterious to biomolecules than the ROS alone. Possible prooxidant activity of carotenoids was for the first time mentioned by Burton and Ingold. Since then, many other examples of loss of antioxidant activity or prooxidant activity have been illustrated and reviewed in the literature. Increasing oxygen partial pressure (PO2) and/or carotenoid concentration can convert a carotenoid from antioxidant to prooxidant. Thus, depending on the environment, the same molecule can exert either antioxidant or prooxidant activity. ... 

At the present time it is difficult to single out any one factor that could be held ultimately responsible for cell death after cerebral ischaemia. Recent studies, however, have provided us with sufficient evidence to conclude that free radical damage is at least one component in a chain of events that leads to cell death in ischaemia/reperfiision injury. As noted earlier in this review, much of the evidence for free radicals in the brain and the sources of free radicals come from studies in animals subjected to cerebral ischaemia. Perhaps the best evidence for a role for free radicals or reactive oxygen species in cerebral ischaemia is derived from studies that demonstrate protective effects of antioxidants. Antioxidants and inhibitors of lipid peroxidation have been shown to have profound protective effects in models of cerebral ischaemia. Details of some of these studies will be mentioned later. Several reviews have been written on the role of oxygen radicals in cerebral ischaemia (Braughler and HaU, 1989 Hall and Btaughler, 1989 Kontos, 1989 Floyd, 1990 Nelson ef /., 1992 Panetta and Clemens, 1993). 

Haydek, J., Parveen, S., List, T., Doria, M. and Keshvarian, A. (1991). Reactive oxygen metabolites in experimental colitis the effect of catalase. Gastroenterology, 100, A585. 

Manna, C. et al. (1997). The protective effect of the olive oil polyphenol (3,4-dihydroxyphenyl)-ethanol counteracts reactive oxygen metabolite-induced cytotoxicity in Caco-2 cells. J. Nutr. 127(2) 286-292. 

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