Nephron. Physiology · 2004
Iron dextran causes renal iron deposition but not renal dysfunction in angiotensin II-treated and untreated rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Ishizaka Nobukazu, Saito Kan, Noiri Eisei, Sata Masataka, Mori Ichiro, Ohno Minoru, Nagai Ryozo
Аннотация
BACKGROUND: Angiotensin II infusion into rats causes iron deposition in the kidney, which may augment the pro-proteinuric effects of this octapeptide. We have investigated whether administration of iron mimics the renal damage induced by angiotensin II.
METHODS: Rats were treated with iron dextran at a total dose of 960 mg/kg either with or without angiotensin II treatment at a dose of 0.7 mg/kg/day for 7 days. Protein expression of ferritin and heme oxygenase-1, an oxidative stress-sensitive gene, was determined by Western blot analysis and immunohistochemistry.
RESULTS: Administration of iron dextran did not significantly increase proteinuria or decrease creatinine clearance in the rats with or without angiotensin II treatment. Prussian blue staining showed that iron deposition was observed mainly in the glomerular and medullar regions in the iron dextran-treated rats, but in the tubular epithelial cells in angiotensin II-infused rats. Administration of iron dextran upregulated ferritin, but not heme oxygenase-1.
CONCLUSION: Iron dextran did not enhance or cause the renal dysfunction in the angiotensin II-treated or untreated rats, respectively. The distribution of deposited iron and presumably the type of iron compound administered may be important determinants of the development of renal injury.
METHODS: Rats were treated with iron dextran at a total dose of 960 mg/kg either with or without angiotensin II treatment at a dose of 0.7 mg/kg/day for 7 days. Protein expression of ferritin and heme oxygenase-1, an oxidative stress-sensitive gene, was determined by Western blot analysis and immunohistochemistry.
RESULTS: Administration of iron dextran did not significantly increase proteinuria or decrease creatinine clearance in the rats with or without angiotensin II treatment. Prussian blue staining showed that iron deposition was observed mainly in the glomerular and medullar regions in the iron dextran-treated rats, but in the tubular epithelial cells in angiotensin II-infused rats. Administration of iron dextran upregulated ferritin, but not heme oxygenase-1.
CONCLUSION: Iron dextran did not enhance or cause the renal dysfunction in the angiotensin II-treated or untreated rats, respectively. The distribution of deposited iron and presumably the type of iron compound administered may be important determinants of the development of renal injury.