Review of the mechanism of cell death resulting from streptozotocin challenge in experimental animals, its practical use
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REVIEW ARTICLE
Open Access
Review of the mechanism of cell death resulting from streptozotocin challenge in experimental animals, its practical use and potential risk to humans Chinedum Ogbonnaya Eleazu1*, Kate Chinedum Eleazu2, Sonia Chukwuma1 and Udeme Nelson Essien2
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. Keywords: Streptozotocin, Animals, Diabetes, Humans, Cell death
Introduction Streptozotocin (STZ) (2-deoxy-2-(3-methyl-3-nitrosourea)1-D-glucopyranose) is a naturally occurring compound, produced by the soil bacterium streptomyces achromogenes, that exhibits broad spectrum of antibacterial properties [1]. It is a mixture of α- and β-stereoisomers that appear as pale yellow or off-white crystalline powder. In terms of solubility, it is very soluble in water, ketones and lower alcohols, but slightly soluble in polar organic solvents [2]. Streptozotocin has a molecular formula of C8H15N3O7, molecular weight of 265 g/mol and the structure is composed of nitrosourea moiety with a methyl group attached at one end and a glucose molecule at the other end [1]. STZ is a cytotoxic glucose analogue. After its discovery, it was being used as a chemotherapeutic alkylating agent in the treatment of metastasizing pancreatic islet cell tumors and other malignancies [3]. In the year 1963, Rakieten and colleagues reported that STZ is diabetogenic [4]. From that time of discovery
* Correspondence: [email protected] 1 Department of Biochemistry, National Root Crops Research Institute, Umudike, Umuahia, Abia State, Nigeria Full list of author information is available at the end of the article
till date, STZ has been one of the chemical agents for the induction of diabetes in experimental animals [5]. Streptozotocin functions as a DNA synthesis inhibitor in both bacterial and mammalian cells [6]. In bacterial cells, a specific interaction with cytosine moieties leads to the degradation of the bacterial DNA [7]. Streptozotocin is cytotoxic to pancreatic β-cells and its effects can be seen within seventy two hours after administration depending on the dose administered [8]. In mammalian cells, the mechanism of action of STZ that results in cell death was not fully identified, though it was thought to be a result of DNA and chromosomal damage brought forth by mechanisms involving free radical generation during STZ metabolism [6]. However, after several years of
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