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      Heme Metabolism and Lipid Peroxidation in Rat Kidney Hexachlorobenzene–Induced Porphyria: A Compartmentalized Study of Biochemical Pathogenic Mechanisms

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          Abstract

          In the present study, the effects of hexachlorobenzene (HCB) on lipid peroxidation and heme metabolism in the different constitutive suborgans of the kidney were determined. For this purpose, conjugated diene and malondialdehyde levels, as lipid peroxidation parameters, and porphyrin accumulation, uroporphyrinogen decarboxylase activity, and its inhibitor formation, as measures of heme metabolism, were determined in renal cortex, medulla, and papilla. Adult Wistar rats were treated with HCB during 1, 2, 3, or 4 weeks. A significant increase in cortical conjugated dienes was observed from the 1st week of treatment. The malondialdehyde levels rose by 47, 34, and 28% after 2, 3, and 4 weeks of intoxication, respectively. The porphyrin content showed a tenfold increase after 4 weeks of treatment, and the uroporphyrinogen decarboxylase activity was reduced by 26 and 58% with respect to control values after 3 and 4 weeks of treatment, respectively. The results demonstrate a direct correlation between the oxidative environment and the effect elicited by the drug on heme metabolism in the renal cortex. In contrast, in papilla and medulla, where the antioxidant systems were higher, HCB showed no porphyrinogenic effect.

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          Most cited references 4

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          Studies on the active centre of rat liver porphyrinogen carboxylyase in vivo effect of hexachlorobenzene

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            Oxidation of uroporphyrinogens by hydroxyl radicals Evidence for nonporphyrin products as potential inhibitors of uroporphyrinogen decar☐ylase

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              Urinary porphyrins as biological indicators of oxidative stress in the kidney

              Reduced porphyrins (hexahydroporphyrins, porphyrinogens) are readily oxidized in vitro by free radicals which are known to mediate oxidative stress in tissue cells. To determine if increased urinary porphyrin concentrations may reflect oxidative stress to the kidney in vivo, we measured the urinary porphyrin content of rats treated with mercury as methyl mercury hydroxide (MMH) or cephaloridine, both nephrotoxic, oxidative stress-inducing agents. Rats exposed to MMH at 5 ppm in the drinking water for 4 weeks showed a 4-fold increase in 24-hr total urinary porphyrin content and a 1.3-fold increase in urinary malondialdehyde (MDA), an established measure of oxidative stress in vivo. Treatment with cephaloridine alone (10-500 mg/kg, i.p.) produced a dose-related increase in urinary MDA and total porphyrin levels up to 1.6 and 7 times control values, respectively. Injection of MMH-treated rats with cephaloridine (500 mg/kg) caused a synergistic (20-fold) increase in urinary porphyrin levels, but an additive (1.9-fold) increase in the MDA concentration. Studies in vitro demonstrated that cephaloridine stimulated the iron-catalyzed H2O2-dependent oxidation of porphyrinogens to porphyrins in the absence of either microsomes or mitochondria. Additionally, porphyrinogens were oxidized to porphyrins in an iron-dependent microsomal lipid peroxidation system. Moreover, porphyrinogens served as an effective antioxidant (EC50 approximately 1-2 microM) to lipid peroxidation. These results demonstrate that MMH and cephaloridine synergistically, as well as individually, promote increased oxidation of reduced porphyrins in the kidney and that this action may be mechanistically linked to oxidative stress elicited by these chemicals. Increased urinary porphyrin levels may, therefore, represent a sensitive indicator of oxidative stress in the kidney in vivo.
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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                1420-4096
                1423-0143
                2000
                2000
                15 October 1999
                : 23
                : 1
                : 20-26
                Affiliations
                aDepartamento de Ciencias Biológicas, Cátedra de Biología Celular e Histología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, IQUIFIB–CONICET, y bDepartamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina
                Article
                25950 Kidney Blood Press Res 2000;23:20–26
                10.1159/000025950
                10567850
                © 1999 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 3, Tables: 2, References: 22, Pages: 7
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/25950
                Categories
                Original Paper

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