Increase of manganese superoxide dismutase, but not of Cu/Zn-SOD, in experimental optic neuritis

Xiaoping Qi, John Guy, Harry Nick, John Valentine, Narsing Rao

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Purpose. To evaluate the role of manganese superoxide dismutase (Mn- SOD) and copper/zinc superoxide dismutase (Cu/Zn-SOD) in cellular protection of the optic nerve against the oxidative injury that contributes to demyelination in experimental allergic encephalomyelitis (EAE). Methods. Immunocytochemistry for Mn-SOD and Cu/Zn-SOD and ultracytochemical localization of hydrogen peroxide (H2O2) were performed on the optic nerves of guinea pigs with EAE and normal guinea pigs. Cell-specific enzyme expression of SOD was quantitated by computerized morphometric analysis. Results. Light microscopy showed a perivascular distribution of Mn-SOD- positive cells in the optoic nerves of animals with EAE. Electron microscopy showed that the Mn-SOD immunogold was confined exclusively to mitochondria, whereas Cu/Zn-SOD immunogold was found in the cytoplasmic matrix and nucleus of cells of the optic nerve in both animals with EAE and normal animals. Results of quantitative analysis of the optic nerves of animals with EAE showed an 8-fold increase in Mn-SOD immunogold in astroglial cells and a 13- fold increase in microglial/phagocytic cells in comparison with that of normal animals. Increases in Mn-SOD immunogold were contiguous to H2O2- derived reaction product. No increases in Cu/Zn-SOD immunogold were detected in EAE. Conclusions. Increases in Mn-SOD activity in astroglial cells and microglial/phagocytic cells may contribute to the relative sparing of these cells from injury in EAE, whereas the low level of Mn-SOD in oligodendroglial cells and axons may increase their vulnerability ot the effects of superoxide-induced injury that results in demyelination.

Original languageEnglish
Pages (from-to)1203-1212
Number of pages10
JournalInvestigative Ophthalmology and Visual Science
Volume38
Issue number6
StatePublished - Jun 11 1997
Externally publishedYes

Fingerprint

Optic Neuritis
Autoimmune Experimental Encephalomyelitis
Superoxide Dismutase
Optic Nerve
Demyelinating Diseases
Phagocytes
Wounds and Injuries
Guinea Pigs
Cell Nucleus
Superoxides
Hydrogen Peroxide
Axons
Zinc
Copper
Microscopy
Electron Microscopy
Mitochondria
Immunohistochemistry
Light
Enzymes

Keywords

  • antioxidant enzymes
  • experimental optic neuritis
  • free radicals
  • immunocytochemistry
  • superoxide dismutases

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Increase of manganese superoxide dismutase, but not of Cu/Zn-SOD, in experimental optic neuritis. / Qi, Xiaoping; Guy, John; Nick, Harry; Valentine, John; Rao, Narsing.

In: Investigative Ophthalmology and Visual Science, Vol. 38, No. 6, 11.06.1997, p. 1203-1212.

Research output: Contribution to journalArticle

Qi, Xiaoping ; Guy, John ; Nick, Harry ; Valentine, John ; Rao, Narsing. / Increase of manganese superoxide dismutase, but not of Cu/Zn-SOD, in experimental optic neuritis. In: Investigative Ophthalmology and Visual Science. 1997 ; Vol. 38, No. 6. pp. 1203-1212.
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abstract = "Purpose. To evaluate the role of manganese superoxide dismutase (Mn- SOD) and copper/zinc superoxide dismutase (Cu/Zn-SOD) in cellular protection of the optic nerve against the oxidative injury that contributes to demyelination in experimental allergic encephalomyelitis (EAE). Methods. Immunocytochemistry for Mn-SOD and Cu/Zn-SOD and ultracytochemical localization of hydrogen peroxide (H2O2) were performed on the optic nerves of guinea pigs with EAE and normal guinea pigs. Cell-specific enzyme expression of SOD was quantitated by computerized morphometric analysis. Results. Light microscopy showed a perivascular distribution of Mn-SOD- positive cells in the optoic nerves of animals with EAE. Electron microscopy showed that the Mn-SOD immunogold was confined exclusively to mitochondria, whereas Cu/Zn-SOD immunogold was found in the cytoplasmic matrix and nucleus of cells of the optic nerve in both animals with EAE and normal animals. Results of quantitative analysis of the optic nerves of animals with EAE showed an 8-fold increase in Mn-SOD immunogold in astroglial cells and a 13- fold increase in microglial/phagocytic cells in comparison with that of normal animals. Increases in Mn-SOD immunogold were contiguous to H2O2- derived reaction product. No increases in Cu/Zn-SOD immunogold were detected in EAE. Conclusions. Increases in Mn-SOD activity in astroglial cells and microglial/phagocytic cells may contribute to the relative sparing of these cells from injury in EAE, whereas the low level of Mn-SOD in oligodendroglial cells and axons may increase their vulnerability ot the effects of superoxide-induced injury that results in demyelination.",
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N2 - Purpose. To evaluate the role of manganese superoxide dismutase (Mn- SOD) and copper/zinc superoxide dismutase (Cu/Zn-SOD) in cellular protection of the optic nerve against the oxidative injury that contributes to demyelination in experimental allergic encephalomyelitis (EAE). Methods. Immunocytochemistry for Mn-SOD and Cu/Zn-SOD and ultracytochemical localization of hydrogen peroxide (H2O2) were performed on the optic nerves of guinea pigs with EAE and normal guinea pigs. Cell-specific enzyme expression of SOD was quantitated by computerized morphometric analysis. Results. Light microscopy showed a perivascular distribution of Mn-SOD- positive cells in the optoic nerves of animals with EAE. Electron microscopy showed that the Mn-SOD immunogold was confined exclusively to mitochondria, whereas Cu/Zn-SOD immunogold was found in the cytoplasmic matrix and nucleus of cells of the optic nerve in both animals with EAE and normal animals. Results of quantitative analysis of the optic nerves of animals with EAE showed an 8-fold increase in Mn-SOD immunogold in astroglial cells and a 13- fold increase in microglial/phagocytic cells in comparison with that of normal animals. Increases in Mn-SOD immunogold were contiguous to H2O2- derived reaction product. No increases in Cu/Zn-SOD immunogold were detected in EAE. Conclusions. Increases in Mn-SOD activity in astroglial cells and microglial/phagocytic cells may contribute to the relative sparing of these cells from injury in EAE, whereas the low level of Mn-SOD in oligodendroglial cells and axons may increase their vulnerability ot the effects of superoxide-induced injury that results in demyelination.

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