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      Oxidative stress in the pathogenesis of diabetic neuropathy.

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          Abstract

          Oxidative stress results from a cell or tissue failing to detoxify the free radicals that are produced during metabolic activity. Diabetes is characterized by chronic hyperglycemia that produces dysregulation of cellular metabolism. This review explores the concept that diabetes overloads glucose metabolic pathways, resulting in excess free radical production and oxidative stress. Evidence is presented to support the idea that both chronic and acute hyperglycemia cause oxidative stress in the peripheral nervous system that can promote the development of diabetic neuropathy. Proteins that are damaged by oxidative stress have decreased biological activity leading to loss of energy metabolism, cell signaling, transport, and, ultimately, to cell death. Examination of the data from animal and cell culture models of diabetes, as well as clinical trials of antioxidants, strongly implicates hyperglycemia-induced oxidative stress in diabetic neuropathy. We conclude that striving for superior antioxidative therapies remains essential for the prevention of neuropathy in diabetic patients.

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          Author and article information

          Journal
          Endocr Rev
          Endocrine reviews
          The Endocrine Society
          0163-769X
          0163-769X
          Aug 2004
          : 25
          : 4
          Affiliations
          [1 ] Department of Neurology, University of Michigan, Room 4414, Kresge III, 200 Zina Pitcher Place, Ann Arbor 48109, USA. andreav@umich.edu
          Article
          25/4/612
          10.1210/er.2003-0019
          15294884
          94428774-9000-4452-9c96-94046ec66bd8
          History

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