NITRIC-OXIDE AND ANTIOXIDANT STATUS IN GLUCOSE AND OXYGEN DEPRIVED NEONATAL AND ADULT-RAT BRAIN SYNAPTOSOMES

Nitric oxide (NO.) has been implicated in the process of cerebral isch emia/reperfusion injury. We have examined the production of NO. as ref lected by nitrite (NO2-) + nitrate (NO3-) accumulation, from synaptoso mes isolated from neonatal or adult rat brain and subjected to a perio d of glucose and oxygen deprivation. There was a significant increase in the amount of NO2- + NO3- production from adult synaptosomes under these conditions, whereas there was no difference compared to control in the production of NO2- + NO3- from the neonatal synaptosomes. The t otal antioxidant status of the synaptosomes at these different stages of brain development was found to be the same. These data suggest that the vulnerability of the adult brain to ischemia/reperfusion injury m ay be associated with the production of NO. from nerve terminals. The ratios of antioxidant capacity to NO. production under such conditions have been shown here to be different between the neonatal and adult n erve terminals. Thus the well documented resistance of neonatal brain to ischemia/reperfusion injury may involve the neonatal nerve terminal being under less oxidative stress than the adult.