Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum

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 phar...

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Publicado: 1997
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_07423098_v23_n1_p40_Princ
http://hdl.handle.net/20.500.12110/paper_07423098_v23_n1_p40_Princ
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spelling paper:paper_07423098_v23_n1_p40_Princ2023-06-08T15:44:42Z Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum 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 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. 1997 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_07423098_v23_n1_p40_Princ http://hdl.handle.net/20.500.12110/paper_07423098_v23_n1_p40_Princ
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic 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
spellingShingle 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
Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum
topic_facet 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
description 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.
title Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum
title_short Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum
title_full Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum
title_fullStr Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum
title_full_unstemmed Melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum
title_sort melatonin's antioxidant protection against δ-aminolevulinic acid-induced oxidative damage in rat cerebellum
publishDate 1997
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_07423098_v23_n1_p40_Princ
http://hdl.handle.net/20.500.12110/paper_07423098_v23_n1_p40_Princ
_version_ 1768541899090558976