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Effects of Gentamicin on Iron and Copper Contents of Kidney Tissue
Author(s) -
İlker Durak,
Mustafa Kavutçu,
Orhan Canbolat,
Serdar Öztürk,
S. Ulutepe,
Ismail Hakki Gökhun
Publication year - 1995
Publication title -
˜the œnephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000188626
Subject(s) - icon , medicine , subject (documents) , library science , gentamicin , chemistry , computer science , biochemistry , programming language , antibiotics
Dr. Ilker Durak, Biyokimya A.B.D. (Dekanlik Binasi), Ankara Universitesi Tip Fakultesi, 06 100 Sihhiye-Ankara (Turkey) Table 1. Element contents of kidney tissues (μg/g protein) from gentamicin-treated and control guinea pigs Iron (p > O.05) Copper (p > 0.05) Control group (n= 10) 330.7 ± 80.9 119.1 ± 57.8 Gentamicin group (n = 10) 334.0 ± 67.7 114.6 ± 39.7 Statistical significance was evaluated with the Student t test. Dear Sir, Gentamicin is an aminoglycoside antibiotic, which is widely used in the treatment of gramnegative infections. There are however several reports indicating that gentamicin is nephrotoxic [1,2]. Mechanisms relating to its nephrotoxicity have not yet been fully clarified. Several researchers suggest that toxicity mainly arises from increased lipid peroxidation due to changed free radical metabolism [2-5]. Concerning this subject, Walker and Shah [2] suggested that deferoxamine, an iron chelator, prevented gentamicin-induced renal failure. They concluded that the primary radical responsible for the gentamicin-induced lipid peroxidation was the hydroxyl radical (OH), which was formed from the superoxide radical and hydrogen peroxide by the Haber-Weiss reaction. In this kind of reaction, the primary catalyst is iron. For this reasons, researchers proposed that tissue iron concentrations might be of importance in the hydroxyl radical formation process [2]. They assume that reactive oxygen metabolites might play a role in the release of iron from ferritin into tissue and an additional possible source of iron for the generation of hydroxyl radical might be the enhanced uptake of iron by tissue. In fact, altered trace metal metabolism with increased concentrations of iron in kidney have previously been reported in some diseases [6]. However, it has been pointed out that the precise source of iron and how it gets mobilized to participate in the generation of hydroxyl radical in gentamicininduced acute renal failure remains unknown. In our opinion, one must first elucidate the tissue iron status in such a state before making hypothetical evaluations. To test this hypothesis, we treated 10 guinea pigs (2 months old, weight 450 g approximately) with gentamicin (200 mg/kg/day) for 10 days. As control group we used another 10 guinea pigs injected with only physiologic serum solution during this period. Then

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