Antioxidants treatment

The effect of prolonged antioxidant therapy in relation to normal physiological processes (for example, redox cycling, cell-cell signalling, transcription factor activation) must be assessed. It is conceivable that the overload of one antioxidant by dietary supplementation (for example, a-tocopherol) may shift the levels of other antioxidants (for example, by decreasing ascorbate and /3-carotene concentrations), with unknown consequences. To assess the potential for lipid-soluble antioxidant treatment in inflammatory diseases such as RA, further investigations into these questions will be needed. 

There have been more than 20 studies relating to the prevention of atherosclerosis by antioxidants. In vitro, several studies have shown that antioxidant treatment (e.g. vitamin E) inhibits both oxidation and the formation of cytotoxic LDL (Steinbrecher etal., 1984 Par-thasarathy etal., 1986 Esterbauer etal., 1987). In vivo, vitamin E supplementation prevents LDL oxidation in... 

It is important that future studies of antioxidant treatment in patients with specific disorders should be well designed (randomized, double-blind, placebo-controlled) prospective studies that utilize the most up-to-date methodology to assess free-radical activity. 

Morel, D.W. and Chisolm, G.M. (1989). Antioxidant treatment of diabetic rats inhibits lipoprotein oxidation and cytotoxicity. J. Lipid Res. 30, 1827-1834. 

J6. Jebsen, S., Herlevsen, P., Knudsen, P Bud, M. I and Klausen, N. O., Antioxidant treatment with A/-acetylcysteine during adult respiratory distress syndrome A prospective randomized, placebo-controlled study. Cril. Care Med. 20,918-923 (1992). 

As in the case of other cardiovascular diseases, the possibility of antioxidant treatment of diabetes mellitus has been studied in both animal models and diabetic patients. The treatment of streptozotocin-induced diabetic rats with a-lipoic acid reduced superoxide production by aorta and superoxide and peroxynitrite formation by arterioles providing circulation to the region of the sciatic nerve, suppressed lipid peroxidation in serum, and improved lens glutathione level [131]. In contrast, hydroxyethyl starch desferrioxamine had no effect on the markers of oxidative stress in diabetic rats. Lipoic acid also suppressed hyperglycemia and mitochondrial superoxide generation in hearts of glucose-treated rats [132],... 

Thus, the above consideration of earlier studies dedicated to the study of antioxidants as potential drugs for cancer treatment did not show any significant favorable effects of antioxidant treatment. It could be the consequence of a double role of prooxidants and antioxidants because both of them are capable of inhibiting and promoting cancer development. However, the studies of antioxidants for cancer treatment have not been stopped, and to the present day about 10,000 references are cited by Medline on this subject. Of course, it is impossible to discuss all these studies in this book therefore, we will consider here only the several latest ones. 

It is of special interest that rheumatoid arthritis is one of the first examples of the extensive antioxidant treatment of human patients. In previous years the most recommended pharmaceutical antioxidant agent has been SOD. In 1986, Wilsman [245] reviewed the results of 10 years of presumably successful clinical experience with CuZnSOD treatment of inflammatory disorders including RA. Niwa et al. [246] recommended the application of liposomal... 

Vitamin E and idebenone are also potential antioxidant treatments for Alzheimer s disease as they prevent cell death caused by glutamate and amyloid (i-protcin. Clinical trials with L-deprenyl and vitamin E are currently evaluating their ability to slow the progression of Alzheimer s disease. 

Geva, E., Bartoov, B., Zabludovsky, N., Lessing, J.B., Lemer-Geva, L., and Amit, A. 1996. The effect of antioxidant treatment on human spermatozoa and fertilization rate in an in vitro fertilization... 

One of the major problems is the lack of a standard test to determine the OS. Despite the fact that they are not very precise, they still are the only possible tools to determine if an antioxidant treatment can be effective or not. Nobody would use an antihypertensive drug in case of a normal blood pressure. The same should be for antioxidant supplements, no matter which way they are combined. 

Coppey, L. J., Gellett, J. S., Davidson, E. P., Dunlap, J. A., Lund, D. D., and Yorek, M. A. 2001. Effect of antioxidant treatment of streptozotocin-induced diabetic rats on endoneurial blood flow, motor nerve conduction velocity, and vascular reactivity of epineurial arterioles of the sciatic nerve. Diabetes 50 1927-1937. 

Sack, C.A., Socci, D.J., Crandall, B.M., Arendash, G.W. (1996). Antioxidant treatment with phenyl-alpha-tert-butylnitrone (PBN) improves the cognitive performance and survival of aging rats. Neurosci. Lett. 205 181-4. 

T. Blackwell, T. Blackwell, E. Holden, B. Christman and J. Christman, In Vivo Antioxidant Treatment Suppresses Nuclear Factor-kB Activation and Neutrophilic Lung Inflammation, J Immunol 157 (1996) 1630-1637. 

Orrell RW, Lane RJM, Ross M (2005) Antioxidant treatment for amyotrophic lateral sclerosis/motor neuron disease. The Cochrane Database for Systematic Reviews, Volume 4, The Cochrane Collaboration. 

Halliwell B. 2001. Role of free radicals in the neurodegenerative diseases Therapeutic implications for antioxidant treatment. Drugs Aging 18 685-716. 

While a striking departure in its own right, this new story leads to a conclusion that dovetails with a great deal of recent medical research, in particular the complexities associated with antioxidant treatments. The continuous strain between external and internal oxygen levels lies at the root of many human ailments — a strain that is ultimately worked out in the antioxidant balance of individual cells. The retention of a primordial antioxidant balance is analogous to the salt composition of fluids in the... 

Young, V.W., Perry, T.L. and Krisman, A.A. (1986) Depletion of glutathione in brainstem of mice caused by N-methyl-4-phenyl-l,2,3,6-tetrahydropyridine is prevented by antioxidant treatment. Neurosci, Lett. 63 56-60. 

Oxidative stress, rather than being the primary cause of disease, is more often a secondary complication in many disorders. Oxidative stress diseases include inflammatoiy bowel diseases, retinal ischemia, cardiovascular disease and restenosis, AIDS, ARDS, and neurodegenerative diseases such as stroke. Parkin-son s disease, and Alzheimer s disease. Such indications may prove amenable to antioxidant treatment because there is a clear involvement of oxidative injury in these disorders. 

Frlich, 1. and Riederer, P. (1995). Free radical mechanisms in dementia of Alzheimer type and the potential for antioxidative treatment. Drug Res. 45,443—449. 

Hart, RE., Lodi, R., Rajagopalan, B., Bradley, J.L., Crilley, J. G.,Turner, C., Blamire, A.M., Manners, D., Styles, R, Schapira, A.H., and Cooper, J.M., Antioxidant treatment of patients with Friedreich ataxia four-year follow-up. Arch Neurol 62 (4), 621-626, 2005. 

Using an experimental restenosis animal model of dietary-induced hypercholesterolemia combined with balloon injury of abdominal aortas, we demonstrated in this series of studies that antioxidants from the traditional herb medicines, magnolol (36), SM (37), and EGb (38), could attenuate the intimal response to balloon injury in cholesterol-fed rabbits by inhibiting intimal hyperplasia in abdominal aortas. In addition, these antioxidant treatments also markedly decreased atherosclerotic lesion areas in thoracic aortas without endothelial denudation. 

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