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Am J Physiol Renal Physiol 274: F18-F25, 1998;
0363-6127/98 $5.00
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Vol. 274, Issue 1, F18-F25, January 1998

Evidence suggesting that nitric oxide mediates iron-induced toxicity in cultured proximal tubule cells

Liguang Chen, Bao-Hong Zhang, and David C. H. Harris

Department of Renal Medicine and Storr Liver Unit, University of Sydney at Westmead Hospital, Westmead, New South Wales 2145, Australia

The potential role of nitric oxide (NO) in iron-induced toxicity was studied in proximal tubule cells in primary culture. NO production (NO<SUP>−</SUP><SUB>2</SUB>/NO<SUP>−</SUP><SUB>3</SUB>) was significantly increased in iron-treated compared with control cells (3.43 ± 0.08 vs. 1.56 ± 0.08 nmol/dish, P < 0.01). NO synthase (NOS) activity was also induced by iron treatment (16.2 ± 2.0 vs. 0.4 ± 0.2 nmol of [3H]citrulline/mg protein, P < 0.01). L-Arginine, a substrate for NOS, augmented iron-induced NO production and cell damage [lactate dehydrogenase (LDH) leakage], whereas aminoguanidine, an inhibitor of NOS, reduced iron-induced NO production and LDH leakage. Sodium nitroprusside, an exogenous NO donor, induced LDH leakage in a dose-dependent manner, but no effect on lipid peroxidation {malondialdehyde bis[dimethyl acetal] (MDA) production} was observed. Superoxide dismutase and catalase decreased iron-induced MDA production but did not affect LDH leakage or NO production. Dimethylpyrroline N-oxide and desferal prevented MDA production, LDH leakage, and NO production. We concluded that NO is one of the mediators of iron-induced toxicity in proximal tubule cells. NO-induced toxicity is not dependent on lipid peroxidation. This may explain the variable effect of different antioxidants on cell damage and lipid peroxidation in iron-induced cytotoxicity.

iron; cytotoxicity; lipid peroxidation


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