Abstract:
:The neonatal brain appears to be selectively vulnerable to oxidative stress. Several potential mechanisms associated with altered reactive oxygen species metabolism would explain the increased susceptibility. They include increased accumulation of hydrogen peroxide with subsequent neurotoxicity. This enhanced neurotoxicity from H2O2 accumulation may be related to inadequate scavenging abilities of the immature nervous system, such as lower glutathione peroxidase activity. Contributing to the immaturity of the scavenging enzymes is the inability of the developing nervous system to maintain glutathione stores. The immature nervous system is rich in iron, and has more free iron than the mature nervous system. As H2O2 accumulates because of these improper defense mechanisms, it is exposed to this free iron. This exposure results in the generation of OH radical (Fenton reaction), a more potent free radical that can cause severe damage. The rapid conversion of H2O2 to OH in the setting of free iron sets up the immature nervous system for increased cytotoxicity. Understanding the molecular mechanisms of oxidative stress will lead to better therapies for neonatal hypoxia-ischemia.
journal_name
Dev Neuroscijournal_title
Developmental neuroscienceauthors
Ferriero DMdoi
10.1159/000046143keywords:
subject
Has Abstractpub_date
2001-01-01 00:00:00pages
198-202issue
3eissn
0378-5866issn
1421-9859pii
46143journal_volume
23pub_type
杂志文章,评审abstract::The distribution of the noradrenergic system within the rat cerebellar cortex following low-level X-irradiation was studied using tyrosine hydroxylase immunocytochemistry. X-Irradiation treatments consisted of 1, 3, or 5 successive daily dose beginning on postnatal day 1. When studied 24 h after the last exposure, a d...
journal_title:Developmental neuroscience
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journal_title:Developmental neuroscience
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更新日期:2007-01-01 00:00:00
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journal_title:Developmental neuroscience
pub_type: 杂志文章
doi:10.1159/000112695
更新日期:1982-01-01 00:00:00
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pub_type: 杂志文章
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更新日期:1981-01-01 00:00:00
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更新日期:2000-09-01 00:00:00
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更新日期:2004-03-01 00:00:00
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更新日期:1994-01-01 00:00:00
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