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(Reference retrieved automatically from SciELO through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

5-Aminolevulinic acid and the hepatic oxidative stress in the early phase of experimental hexachlorobenzene intoxication

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Author(s):
Tânia Cristina Higashi Sawada [1] ; Vanessa Vitoriano da Silva [2] ; Sonia Barros [3] ; Cristina Dislich Röpke [4] ; Silvia Berlanga de Moraes Barros [5]
Total Authors: 5
Affiliation:
[1] Universidade de São Paulo. Faculdade de Ciências Farmacêuticas. Departamento de Análises Clínicas e Toxicológicas
[2] Universidade de São Paulo. Faculdade de Ciências Farmacêuticas. Departamento de Análises Clínicas e Toxicológicas
[3] Universidade de São Paulo. Faculdade de Ciências Farmacêuticas. Departamento de Análises Clínicas e Toxicológicas
[4] Universidade de São Paulo. Faculdade de Ciências Farmacêuticas. Departamento de Análises Clínicas e Toxicológicas
[5] Universidade de São Paulo. Faculdade de Ciências Farmacêuticas. Departamento de Análises Clínicas e Toxicológicas
Total Affiliations: 5
Document type: Journal article
Source: Revista Brasileira de Ciências Farmacêuticas; v. 40, n. 2, p. 203-208, 2004-06-00.
Abstract

This work evaluated the levels of 5-aminolevulinic acid (ALA) in the liver of rats exposed to different doses of HCB (25,50, and 100 mg/kg b.w. for 4 weeks) and correlated them with lipid peroxidation parameters. Levels of ALA were determined by high-pressure liquid chromatography after derivatization with acetylacetone and formaldehyde, followed by fluorescence detection. The methodology was carefully validated, nonetheless hepatic levels of ALA in all animals treated or not were below the detection limit of the method (2.27mg of ALA/g liver). On the other hand, lipid peroxidation, evaluated as thiobarbituric acid reactants production and chemiluminescence was found significantly increased in the livers of all treated rats, in comparison with control values (p<0.05). These results suggest that the hepatic oxidative stress observed in animals following HCB treatment may not necessarily be associated with increased levels of ALA in the liver. Another possibility is that increased levels of ALA in the liver, even below the detection limit of the method are sufficient to induce hepatic oxidative stress. (AU)