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      Oxidative Stress and Neurodegenerative Diseases: A Review of Upstream and Downstream Antioxidant Therapeutic Options

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          Abstract

          Free radicals are common outcome of normal aerobic cellular metabolism. In-built antioxidant system of body plays its decisive role in prevention of any loss due to free radicals. However, imbalanced defense mechanism of antioxidants, overproduction or incorporation of free radicals from environment to living system leads to serious penalty leading to neuro-degeneration. Neural cells suffer functional or sensory loss in neurodegenerative diseases. Apart from several other environmental or genetic factors, oxidative stress (OS) leading to free radical attack on neural cells contributes calamitous role to neuro-degeneration. Though, oxygen is imperative for life, imbalanced metabolism and excess reactive oxygen species (ROS) generation end into a range of disorders such as Alzheimer’s disease, Parkinson’s disease, aging and many other neural disorders. Toxicity of free radicals contributes to proteins and DNA injury, inflammation, tissue damage and subsequent cellular apoptosis. Antioxidants are now being looked upon as persuasive therapeutic against solemn neuronal loss, as they have capability to combat by neutralizing free radicals. Diet is major source of antioxidants, as well as medicinal herbs are catching attention to be commercial source of antioxidants at present. Recognition of upstream and downstream antioxidant therapy to oxidative stress has been proved an effective tool in alteration of any neuronal damage as well as free radical scavenging. Antioxidants have a wide scope to sequester metal ions involved in neuronal plaque formation to prevent oxidative stress. In addition, antioxidant therapy is vital in scavenging free radicals and ROS preventing neuronal degeneration in post-oxidative stress scenario.

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          Most cited references 91

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          Hydroperoxide metabolism in mammalian organs.

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            Oxidants, antioxidants, and the degenerative diseases of aging.

            Metabolism, like other aspects of life, involves tradeoffs. Oxidant by-products of normal metabolism cause extensive damage to DNA, protein, and lipid. We argue that this damage (the same as that produced by radiation) is a major contributor to aging and to degenerative diseases of aging such as cancer, cardiovascular disease, immune-system decline, brain dysfunction, and cataracts. Antioxidant defenses against this damage include ascorbate, tocopherol, and carotenoids. Dietary fruits and vegetables are the principal source of ascorbate and carotenoids and are one source of tocopherol. Low dietary intake of fruits and vegetables doubles the risk of most types of cancer as compared to high intake and also markedly increases the risk of heart disease and cataracts. Since only 9% of Americans eat the recommended five servings of fruits and vegetables per day, the opportunity for improving health by improving diet is great.
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              Free radicals, antioxidants, and human disease: curiosity, cause, or consequence?

               B Halliwell (1994)
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                Author and article information

                Journal
                Curr Neuropharmacol
                CN
                Current Neuropharmacology
                Bentham Science Publishers Ltd.
                1570-159X
                1875-6190
                March 2009
                : 7
                : 1
                : 65-74
                Affiliations
                [1 ]Department of Biotechnology, M. J. College, M. J. Road, Jalgaon- 425 001, India;
                [2 ]Centro Interdisciplinare Materiali e Interfacce Nanostrutturati (CIMAINA), Dipartimento di Fisica, Universita di Milano, Via Celoria 16, 20133 Milan, Italy;
                [3 ]Centre for Vascular Disease, University of Ferrara, 41100 Ferrara, Italy
                Author notes
                [* ]Address correspondence to these authors at the Department of Biotechnology, M. J. College, M. J. Road, Jalgaon- 425 001, India; Tel: +91 0257 2234281- 32; Fax: +91 0257 2237363; E-mail: rt_mahajan@rediffmail.com Tel: +91 02582 247702; E-mail: uttarabayani@ 123456yahoo.com
                [#]

                These authors contributed equally to this review.

                Article
                CN-7-65
                10.2174/157015909787602823
                2724665
                19721819
                ©2009 Bentham Science Publishers Ltd.

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.5/) which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

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