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pubmed-article:3663701pubmed:abstractTextIron and aluminum complexes of nitrilotriacetic acid cause severe nephrotoxicity in Wistar rats. In addition, a high incidence of renal cell carcinoma is seen in ferric nitrilotriacetate-treated animals. The present study was performed to see if lipid peroxidation is involved in ferric nitrilotriacetate toxicity. Ferric nitrilotriacetate had more bleomycin-detectable 'free' iron than any ferric salt, while iron complexed with desferrioxamine or ferric chondroitin sulfate had none. The toxicity of ferric nitrilotriacetate in vivo was more pronounced in vitamin E-deficient rats. A thiobarbituric acid-reactive substance was present in the kidneys of vitamin E-deficient rats in amounts markedly elevated compared to vitamin E-sufficient, or vitamin E-supplemented rats. Non-complexed nitrilotriacetate or aluminum nitrilotriacetate did not produce any thiobarbituric acid-reactive substance in vitamin E-sufficient rats died by the 58th day of administration. We suggest that the iron-stimulated production of free radicals leading to lipid peroxidation is the major cause of ferric nitrilotriacetate-mediated renal toxicity. Vitamin E, a known scavenger of free radicals, is effective in protecting against this iron-induced toxicity.lld:pubmed
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pubmed-article:3663701pubmed:articleTitleNephrotoxicity and its prevention by vitamin E in ferric nitrilotriacetate-promoted lipid peroxidation.lld:pubmed
pubmed-article:3663701pubmed:affiliationDepartment of Pathology, Faculty of Medicine, Kyoto University, Japan.lld:pubmed
pubmed-article:3663701pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:3663701pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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