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      Review of the mechanism of cell death resulting from streptozotocin challenge in experimental animals, its practical use and potential risk to humans

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          Abstract

          Streptozotocin (STZ) (2-deoxy-2-({[methyl(nitroso)amino]carbonyl}amino)-β-D-glucopyranose) is a naturally occurring diabetogenic compound, produced by the soil bacterium streptomyces achromogenes, that exhibits broad spectrum of antibacterial properties. Streptozotocin functions as a DNA synthesis inhibitor in both bacterial and mammalian cells. In mammalian cells, the actual mechanism and metabolic targets of STZ toxicity that results in cell death is not known. This review identifies four key areas that explain the mechanism of the cytotoxicity of STZ in mammalian cell lines, investigates the practical aspects of using STZ in experimental animals and the potential risks of its exposure to human health.

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          Radicals and oxidative stress in diabetes.

          C. West (2000)
          Recent evidence is reviewed indicating increased oxidative damage in Type 1 and Type 2 diabetes mellitus as well as deficits in antioxidant defence enzymes and vitamins. Mechanisms are considered whereby hyperglycaemia can increase oxidative stress, and change the redox potential of glutathione and whereby reactive oxygen species can cause hyperglycaemia. It is argued that oxygen, antioxidant defences, and cellular redox status should now be regarded as central players in diabetes and the metabolic syndrome.
          Article 0 comments Cited 141 times – based on 0 reviews     Review now
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            Invited review: Effects of acute exercise and exercise training on insulin resistance.

            E Henriksen (2002)
            Insulin resistance of skeletal muscle glucose transport is a key defect in the development of impaired glucose tolerance and Type 2 diabetes. It is well established that both an acute bout of exercise and chronic endurance exercise training can have beneficial effects on insulin action in insulin-resistant states. This review summarizes the present state of knowledge regarding these effects in the obese Zucker rat, a widely used rodent model of obesity-associated insulin resistance, and in insulin-resistant humans with impaired glucose tolerance or Type 2 diabetes. A single bout of prolonged aerobic exercise (30-60 min at approximately 60-70% of maximal oxygen consumption) can significantly lower plasma glucose levels, owing to normal contraction-induced stimulation of GLUT-4 glucose transporter translocation and glucose transport activity in insulin-resistant skeletal muscle. However, little is currently known about the effects of acute exercise on muscle insulin signaling in the postexercise state in insulin-resistant individuals. A well-established adaptive response to exercise training in conditions of insulin resistance is improved glucose tolerance and enhanced skeletal muscle insulin sensitivity of glucose transport. This training-induced enhancement of insulin action is associated with upregulation of specific components of the glucose transport system in insulin-resistant muscle and includes increased protein expression of GLUT-4 and insulin receptor substrate-1. It is clear that further investigations are needed to further elucidate the specific molecular mechanisms underlying the beneficial effects of acute exercise and exercise training on the glucose transport system in insulin-resistant mammalian skeletal muscle.
            Article 0 comments Cited 92 times – based on 0 reviews     Review now
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              Autoxidative glycosylation and possible involvement of peroxides and free radicals in LDL modification by glucose.

              Jamie Hunt, Mary S Wolff, Anthony Smith (1990)
              It has been postulated that the etiology of the complications of diabetes involves oxidative stress, perhaps as a result of hyperglycemia. Consistent with this hypothesis, it has been shown that glucose, under physiological conditions, produces oxidants that possess reactivity similar to the hydroxyl free radical. These oxidants hydroxylate benzoic acid, fragment protein, and induce peroxidation in phosphatidylcholine liposomes and low-density lipoprotein (LDL) when LDL is incubated with hyperglycemic levels of glucose in vitro. These reactions are accelerated by transition metals and inhibited by a metal-chelating agent. The atherosclerotic potential of LDL in diabetes mellitus is often discussed in terms of protein glycosylation, which may affect cellular interactions. Our studies demonstrate, however, that peroxidative reactions also accompany LDL glycosylation in vitro. Peroxidative modification of LDL has also been implicated in LDL atherogenicity. Our studies indicate that glycosylation and peroxidation occur concomitantly in LDL modified by glucose in vitro and may both contribute to the behavioral changes of this lipoprotein.
              Article 0 comments Cited 62 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Chinedum Ogbonnaya Eleazu
                Kate Chinedum Eleazu
                Sonia Chukwuma
                Udeme Nelson Essien
                Journal
                Journal ID (nlm-ta): J Diabetes Metab Disord
                Journal ID (iso-abbrev): J Diabetes Metab Disord
                Title: Journal of Diabetes and Metabolic Disorders
                Publisher: BioMed Central
                ISSN (Electronic): 2251-6581
                Publication date Collection: 2013
                Publication date (Electronic): 23 December 2013
                Volume: 12
                Page: 60
                Affiliations
                [1 ]Department of Biochemistry, National Root Crops Research Institute, Umudike, Umuahia, Abia State, Nigeria
                [2 ]Department of Biochemistry, Michael Okpara University of Agriculture, Umudike, Umuahia, Abia State, Nigeria
                Article
                Publisher ID: 2251-6581-12-60
                DOI: 10.1186/2251-6581-12-60
                PMC ID: 3933000
                PubMed ID: 24364898
                SO-VID: 99fb1519-1645-4d0e-b842-af579e44cc5e
                Copyright © Copyright © 2013 Eleazu et al.; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 16 September 2013
                Date accepted : 5 November 2013
                Categories
                Subject: Review Article

                Keywords: streptozotocin,animals,diabetes,humans,cell death
                Data availability:
                Keywords: streptozotocin, animals, diabetes, humans, cell death

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