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Abstract:

δ-aminolevulinic acid (ALA) promotes the generation of reactive oxygen species (ROS). Accumulation of ALA, as occurs in acute intermittent porphyria (AIP), is a potential endogenous source of ROS, which can then exert oxidative damage to cell structures. In this work we investigated the role of pharmacological concentrations of melatonin on the deleterious effect of ALA and its effect on porphyrin biosynthesis. Rat cerebellum incubations were carried out with either ALA (1.0 mM) together with increasing concentrations of melatonin (0.1-2.0 mM) or 2.0 mM melatonin together with varying ALA concentrations (0.05-2.0 mM) for different times (1-4 hr). ALA-induced lipid peroxidation was significantly diminished by melatonin in a concentration-dependent manner. In all conditions 2.0 mM melatonin restored malondialdehyde levels to control values. In incubations without ALA, melatonin markedly reduced (36-40%) the basal levels of lipid peroxidation when compared with the corresponding controls. ALA uptake and porphyrin accumulation were increased 30% in incubations with 1.0-2.0 mM ALA for 4 hr in the presence of 2.0 mM melatonin, providing evidence for the involvement of ALA-promoted ROS in the damage of enzymes related to porphyrin biosynthesis. These results are further support for the protective role of melatonin against oxidative damage induced by ALA; this protective action of melatonin is probably due to melatonin's antioxidant and free radical scavenger properties. The development of a new therapeutic approach for AIP patients employing melatonin alone or in combination with conventional treatments should be considered.

Registro:

Documento: Artículo
Título:Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum
Autor:Princ, F.G.; Juknat, A.A.; Maxit, A.G.; Cardalda, C.; Batlle, A.
Filiación:Ctro. Invest. sobre Porfirinas y P., Depto. de Quim. Biológica, Universidad de Buenos Aires, 1428 Buenos Aires, Argentina
Viamonte 1881-10o A, 1056 Buenos Aires, Argentina
Palabras clave:Melatonin; Porphyrinogenesis; Rat cerebellum; Reactive oxygen species; δ-aminolevulinic acid; aminolevulinic acid; antioxidant; malonaldehyde; melatonin; porphyrin; reactive oxygen metabolite; animal; article; cerebellum; drug effect; lipid peroxidation; male; metabolism; rat; Aminolevulinic Acid; Animals; Antioxidants; Cerebellum; Lipid Peroxidation; Male; Malondialdehyde; Melatonin; Porphyrins; Rats; Reactive Oxygen Species
Año:1997
Volumen:23
Número:1
Página de inicio:40
Página de fin:46
DOI: http://dx.doi.org/10.1111/j.1600-079X.1997.tb00333.x
Título revista:Journal of Pineal Research
Título revista abreviado:J. Pineal Res.
ISSN:07423098
CODEN:JPRSE
CAS:Aminolevulinic Acid, 106-60-5; Antioxidants; Malondialdehyde, 542-78-9; Melatonin, 73-31-4; Porphyrins; Reactive Oxygen Species
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_07423098_v23_n1_p40_Princ

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Citas:

---------- APA ----------
Princ, F.G., Juknat, A.A., Maxit, A.G., Cardalda, C. & Batlle, A. (1997) . Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum. Journal of Pineal Research, 23(1), 40-46.
http://dx.doi.org/10.1111/j.1600-079X.1997.tb00333.x
---------- CHICAGO ----------
Princ, F.G., Juknat, A.A., Maxit, A.G., Cardalda, C., Batlle, A. "Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum" . Journal of Pineal Research 23, no. 1 (1997) : 40-46.
http://dx.doi.org/10.1111/j.1600-079X.1997.tb00333.x
---------- MLA ----------
Princ, F.G., Juknat, A.A., Maxit, A.G., Cardalda, C., Batlle, A. "Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum" . Journal of Pineal Research, vol. 23, no. 1, 1997, pp. 40-46.
http://dx.doi.org/10.1111/j.1600-079X.1997.tb00333.x
---------- VANCOUVER ----------
Princ, F.G., Juknat, A.A., Maxit, A.G., Cardalda, C., Batlle, A. Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum. J. Pineal Res. 1997;23(1):40-46.
http://dx.doi.org/10.1111/j.1600-079X.1997.tb00333.x