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Aromatic hydroxylation in animal models of diabetes mellitus
Author(s) -
Lubec Barbara,
Hermon Michael,
Hoeger Harald,
Lubec Gert
Publication year - 1998
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.12.14.1581
Subject(s) - streptozotocin , diabetes mellitus , hydroxylation , medicine , lipid peroxidation , oxidative stress , endocrinology , malondialdehyde , chemistry , biochemistry , enzyme
Although the involvement of oxidative stress is well documented in the diabetic state, the individual active oxygen species generated have not been demonstrated in animal models of diabetes currently used. Since streptozotocin‐induced diabetes mellitus in animals still serves as an animal model of diabetes mellitus, but streptozotocin induces diabetes and generates oxidative stress per se, we decided to study whether aromatic hydroxylation reflecting hydroxyl radical attack was found in three animal models of diabetes mellitus without streptozotocin induction or in streptozotocin‐induced diabetes only. For this purpose, we compared lipid peroxidation, aromatic hydroxylation of phenylalanine, glycoxidation in genetically determined diabetic mouse strains db/db and kk, and the diabetic BB rat to these parameters in the streptozotocin‐treated rat. Kidney malondialdehyde concentrations, reflecting lipid peroxidation, pentosidine, and N ε ‐caboxymethyllysine concentrations, reflecting glycoxidation, were significantly elevated in all diabetic groups as compared to their nondiabetic mates. Aromatic hydroxylation was significantly elevated in the streptozotocin‐induced diabetic state exclusively. We conclude that biochemical, pathophysiological, and treatment studies in the streptozotocin model of diabetes mellitus may be confounded by the presence of products, reactions, and tissue damage generated by aromatic hydroxylation reflecting hydroxyl radical attack. We suggest it is not the diabetic state but streptozotocin that generates the hydroxyl radical, as reflected by aromatic hydroxylation in this model.—Lubec, B., Hermon, M., Hoeger, H., Lubec, G. Aromatic hydroxylation in animal models of diabetes mellitus. FASEB J. 12, 1581–1587 (1998)