Effect of high-dose methylprednisolone on anti-oxidant enzymes after experimental SAH

Daniela Lombardi, Paolo Gaetani, Fulvio Marzatico, Carla Cafe, Riccardo Rodriguez y Baena

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Lipid peroxidation has been considered one of the most important factors involved in the pathogenesis of neuronal damage following subarachnoid hemorrhage. In the brain, the protective systems most involved against peroxidative and free radicals generated reactions are superoxide-dismutase (SOD) and glutathione-peroxidase (GSH-Px). Since these activities are subjected to a significant reduction following experimental SAH induction in rats, we investigated in the present study if the beneficial effect of high-dose methylprednisolone (MP) in inhibiting lipid peroxidative processes in SAH is possibly linked to an influence on anti-oxidant enzymatic activities. In brain cortex, after MP treatment, CuZn SOD activity in the early phase and more dramatically in the late phase after SAH was restored (4.06 ± 0.06 and 4.07 ± 0.14 enzymatic units/mg of protein, respectively) if compared to hemorrhagic non-treated controls (3.69 ± 0.16 and 2.96 ± 0.06 enzymatic U/mg of protein) while Mn-SOD and GSH-Px activities were improved in treated animals only in the early and late phases after SAH, respectively. In the hippocampus, in treated rats CuZn activity was partially restored only at 6 h, while Mn-SOD activity recovered at 48 h after SAH; no significant changes in GSH-Px activity were found in treated animals at any time. In the brain stem, in treated animals, CuZn SOD activity was restored in the early phase (3.86 ± 0.12 enzymatic U/mg of protein) up to control values of non-hemorrhagic rats (3.44 ± 0.30 enzymatic U/mg of protein), while GSH-Px activity recovered in the late phase. A possible effect of MP exerted through a reduction of lipid peroxidative processes and the consequent preservation of anti-oxidant enzymatic activities is suggested.

Original languageEnglish
Pages (from-to)13-19
Number of pages7
JournalJournal of the Neurological Sciences
Volume111
Issue number1
DOIs
Publication statusPublished - 1992

Fingerprint

Methylprednisolone
Oxidants
Superoxide Dismutase
Enzymes
Proteins
Lipids
Brain
Subarachnoid Hemorrhage
Glutathione Peroxidase
Lipid Peroxidation
Brain Stem
Free Radicals
Hippocampus

Keywords

  • Anti-oxidant systems
  • Glutathione peroxidase
  • Methylprednisolone
  • Subarachnoid hemorrhage
  • Superoxide dismutase

ASJC Scopus subject areas

  • Ageing
  • Clinical Neurology
  • Surgery
  • Neuroscience(all)
  • Developmental Neuroscience
  • Neurology

Cite this

Effect of high-dose methylprednisolone on anti-oxidant enzymes after experimental SAH. / Lombardi, Daniela; Gaetani, Paolo; Marzatico, Fulvio; Cafe, Carla; Rodriguez y Baena, Riccardo.

In: Journal of the Neurological Sciences, Vol. 111, No. 1, 1992, p. 13-19.

Research output: Contribution to journalArticle

Lombardi, Daniela ; Gaetani, Paolo ; Marzatico, Fulvio ; Cafe, Carla ; Rodriguez y Baena, Riccardo. / Effect of high-dose methylprednisolone on anti-oxidant enzymes after experimental SAH. In: Journal of the Neurological Sciences. 1992 ; Vol. 111, No. 1. pp. 13-19.
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abstract = "Lipid peroxidation has been considered one of the most important factors involved in the pathogenesis of neuronal damage following subarachnoid hemorrhage. In the brain, the protective systems most involved against peroxidative and free radicals generated reactions are superoxide-dismutase (SOD) and glutathione-peroxidase (GSH-Px). Since these activities are subjected to a significant reduction following experimental SAH induction in rats, we investigated in the present study if the beneficial effect of high-dose methylprednisolone (MP) in inhibiting lipid peroxidative processes in SAH is possibly linked to an influence on anti-oxidant enzymatic activities. In brain cortex, after MP treatment, CuZn SOD activity in the early phase and more dramatically in the late phase after SAH was restored (4.06 ± 0.06 and 4.07 ± 0.14 enzymatic units/mg of protein, respectively) if compared to hemorrhagic non-treated controls (3.69 ± 0.16 and 2.96 ± 0.06 enzymatic U/mg of protein) while Mn-SOD and GSH-Px activities were improved in treated animals only in the early and late phases after SAH, respectively. In the hippocampus, in treated rats CuZn activity was partially restored only at 6 h, while Mn-SOD activity recovered at 48 h after SAH; no significant changes in GSH-Px activity were found in treated animals at any time. In the brain stem, in treated animals, CuZn SOD activity was restored in the early phase (3.86 ± 0.12 enzymatic U/mg of protein) up to control values of non-hemorrhagic rats (3.44 ± 0.30 enzymatic U/mg of protein), while GSH-Px activity recovered in the late phase. A possible effect of MP exerted through a reduction of lipid peroxidative processes and the consequent preservation of anti-oxidant enzymatic activities is suggested.",
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