Increases of antioxidants are related to more delayed neuronal death in the hippocampal CA1 region of the young gerbil induced by transient cerebral ischemia.

In age-related studies, young animals are resistant to ischemic damage. In present study, we investigated the neuronal death of pyramidal neurons and compared changes in the immunoreactivities and levels of antioxidants, Cu/Zn-SOD (SOD1), Mn-SOD (SOD2), catalase (CAT) and glutathione peroxidase (Gpx), in the hippocampal CA1 region between adult and young gerbils after 5 min of transient cerebral ischemia. In the adult ischemia-group, only a few (12%) of CA1 pyramidal neurons survived 4 days after ischemia-reperfusion (I-R); however, in the 4 days after I-R the young group, most of CA1 pyramidal neurons survived. Seven days after I-R, many (about 39%) of CA1 pyramidal neurons survived, thereafter, the neuronal death in the CA1 pyramidal neurons was not significantly changed. The immunoreactivities of all the antioxidants were well detected in CA1 pyramidal neurons in the adult sham-groups; in the young sham-groups, they were distinctively low compared to those in the adult sham-group. Four days after I-R in the adult group, all the immunoreactivities in the pyramidal neurons were dramatically deceased. However, at this time after I-R in the young groups, they were dramatically increased in the pyramidal neurons. From 7 days after I-R, all the immunoreactivities in the pyramidal neurons in the young ischemia-groups were distinctively decreased. In addition, the levels of all the antioxidants in the CA1 region of the young sham-groups were lower than those in the adult sham-group. Four days after I-R in the adult groups, the levels of all the antioxidants were dramatically deceased; however, at this time in the young ischemia-groups, they were distinctively increased in the CA1 region. Seven days after I-R, all the antioxidants levels in the CA1 region were distinctively decreased. In brief, we conclude that the increased antioxidants levels were related to a less and much delayed neuronal death in the CA1 pyramidal neurons in the young group following I-R injury.