J Korean Soc Neonatol.  2003 Nov;10(2):235-240.

The Effect of Repetitive Hypoxia on Production of Lipid Peroxidation in Newborn Rat Brain

• Kim IS
• Suk HJ
• Park JS
• Park MS
• Park MS

Abstract

PURPOSE
Among many pathophysiologic mechanisms of hypoxic-ischemic brain injury, reactive oxygen species (ROS) cause or contribute to brain damage relates to their ability to attack the fatty acid moiety of plasma and subcellular membranes. Because ROS are generated by hypoxia-ischemia especially during reperfusion period of recovery, repetitive hypoxia-reoxygenation in newborn brain may result in more severe damage than a similar single insult. It is to determine whether repetitive hypoxia-reoxygenation may produce more ROS than a similar single insult in newborn rat brain. METHODS: We compared the production of lipid peroxidation in 3 days old rat brain following normoxia, repetitive hypoxia-reoxygenation and an equal duration of sustained hypoxia-reoxygenation by measuring 8-isoprostane-F2alpha. 8-isoprostane-F2alpha is free radical catalyzed metabolites of arachidonic acid, which is produced independent of cyclooxygenase. RESULTS: Compared to a single duration hypoxia-reoxygenation, repetitive hypoxia- reoxygenation produce more ROS (8-isoprostane-F2alpha) in newborn rat brain (P < 0.005). CONCLUSION: It can be speculated that repetitive hypoxia is more detrimental than equal duration of single insult in new born rat brain. Relations between increased ROS production and brain injury following repetitive hypoxia-reoxygenation should be evaluated.

Keyword

Hypoxic-ischemic brain damage; Reactive oxygen species; 8-isoprostane-F2alpha; Hypoxia-reoxygenation; Lipid peroxidation

MeSH Terms

Animals
Anoxia*
Arachidonic Acid
Brain Injuries
Brain*
Humans
Infant, Newborn*
Lipid Peroxidation*
Membranes
Plasma
Prostaglandin-Endoperoxide Synthases
Rats*
Reactive Oxygen Species
Reperfusion
Arachidonic Acid
Prostaglandin-Endoperoxide Synthases
Reactive Oxygen Species