Superoxide dismutase functional regulation in neonatal hypoxia: effect of glucose, oxygen and epinephrine.

Hypoxia is one of the major causes of damage to the fetal and neonatal brain and cardiac functions. In earlier studies, we have reported the brain damage caused by hypoxia and resuscitation with oxygen and epinephrine and have found that glucose treatment to hypoxic rats and hypoxic rats treated with oxygen shows a reversal of brain damage. The neonatal rats are shown to be deficient in free radical scavenging system, which offers a high risk of oxidative stress. In the present study, we induced hypoxia in neonatal Wistar rats and resuscitated with glucose, oxygen and epinephrine. Heart tissue and cerebral cortex were used to study the kinetics of superoxide dismutase activity in experimental groups of rats to assess the free radical status. Results showed that glucose supplementation in hypoxia (Hx + G) and hypoxic + oxygen (Hx + O) had an efficient free radical scavenging capability, compared to all other experimental groups. The observation was ascertained by studying the activity of catalase, another antioxidant enzyme in the body. Our results suggested that in neonatal rats during hypoxic condition, damage to heart and brain was more prominent in all groups, except when supplemented with glucose. These findings may have clinical significance in the proper management of heart and brain function.