Therapies anti-oxidants

Halliwell, B. and Gutteridge, J.M.C. (1984). Lipid peroxidation, oxygen radicals, cell damage and anti-oxidant therapy. Lancet i, 1396-1398. 

Analysis of antioxidants (antioxidant status) for characterization of the anti-oxidative homeostasis in organisms by selective measurement of the ACP can be very meaningful for efficient supervision of antioxidant therapy as well. 

Stephens N (1997). Anti-oxidant therapy for ischemic heart disease where do we stand Lancet 349 1710-1711... 

Kilner RG, D Souza RJ, Oliveira DB, MacPhee IA,Turner DR, Eastwood JB. Acute renal failure from intoxication by Cortinarius orellanus recovery using anti-oxidant therapy and steroids. Nephrol Dial Transplant 1999 14 2779-2780... 

Kendall MJ, Nuttall SL Anti-oxidant therapy for the treatment of coronary artery disease. Expert Opin... 

The major limitation of nitrate therapy is the development of tolerance with continuous use. The loss of anti-anginal effects may occur within the first 24 hours of continuous nitrate therapy. While the cause of tolerance is unclear, several mechanisms have been proposed. These include depletion of the sulfhydryl groups necessary for the conversion of nitrates to nitric oxide, activation of neurohormonal systems, increased intravascular volume, and generation of free radicals that degrade nitric oxide. The most effective method to avoid tolerance and maintain the anti-anginal efficacy of nitrates is to allow a daily nitrate-free interval of at least 8 to 12 hours. Nitrates do not provide protection from ischemia during the nitrate-free period. Therefore, the nitrate-free... 

A common metabolite found in the urine and plasma of patients treated with gold drugs is [Au(CN)2], an ion which readily enters cells and can inhibit the oxidative burst of white blood cells. It may therefore be an active metabolite of gold drugs. It also exhibits anticancer and anti-HIV activity. The high Au contents of red blood cells of smokers receiving gold therapy has been attributed to the inhalation of HCN in smoke (420). 

In conclusion as for the role of A3 receptors in the inhibition of TNF-a production in macrophages discrepant results have been obtained and not only due to the different species considered. For example some studies attributed reduction of TNF-a to A3 receptors either in human and mouse species (Sajjadi et al. 1996 McWhinney et al. 1996), whilst other found this effect to be mediated essentially by A2A and in minor part by A2B without the involvement of the A3 receptors again in both human and mouse species (Zhang et al. 2005 Kreckler et al. 2006). Therefore it is difficult in this case to verify the relevance of the A3 receptor-induced cellular response when other adenosine subtypes like A2A and A2B are also activated. As for the effects exerted by the A3 subtype in human monocytes and macrophages it is possible to find support for an anti-inflammatory role for this receptor as attested by reduction of tissue factor, oxidative burst and perhaps TNF-a release. Also the recent discovery of an increase in MMP9 supports a role for A3 agonists in the therapy of myocardial infarction (Velot et al. 2008) (Fig. 12.4). 

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