Literature DB >> 9120219

Oxidative stress in sudden infant death syndrome.

S Huggle1, J C Hunsaker, C M Coyne, D L Sparks.   

Abstract

We investigated the hippocampus and parahippocampal cortex of victims of sudden infant death syndrome and of age-matched infants dying acutely of known causes (non-sudden infant death syndrome controls). Tissue sections were investigated for the presence of neurons expressing signs of elevated levels of free radical using immunohistochemical markers for superoxide dismutase and glutathione peroxidase. Brain tissues displayed immunopositive neurons in every infant. In control infants, an age-related decline in the number of superoxide dismutase- and glutathione peroxidase-immunoreactive neurons was apparent in the hippocampus and parahippocampal cortex. Significantly increased numbers of immunoreactive neurons were found in victims of sudden infant death syndrome under 6 months of age compared to age-matched controls. This suggests that infants who later become victims of sudden infant death syndrome may experience antemortem periods of oxidative stress, elevated levels of free radicals, and compensatory up-regulation of the free radical scavenger enzymes superoxide dismutase and glutathione peroxidase.

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Year:  1996        PMID: 9120219     DOI: 10.1177/088307389601100603

Source DB:  PubMed          Journal:  J Child Neurol        ISSN: 0883-0738            Impact factor:   1.987


  5 in total

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4.  Dentate gyrus abnormalities in sudden unexplained death in infants: morphological marker of underlying brain vulnerability.

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5.  Decreased argyrophilic nucleolar organiser region (AgNOR) expression in Purkinje cells: first signal of neuronal damage in sudden fetal and infant death.

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  5 in total

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