Expression of DNA Repairing Enzymes in the Cerebral Tissue of the Rat Fetus After Hypoxic Injury.
10.11637/kjpa.2012.25.2.67
- Author:
Kyung Jin LEE
1
;
Jung Woo KIM
;
Byung Woon MIN
;
Nan Young BAE
;
Ki Young KANG
Author Information
1. Department of Anatomy, College of Medicine, Seonam University, Korea. anatomy@medigate.net
- Publication Type:Original Article
- Keywords:
Hypoxia;
Apoptosis;
OGG1;
APE1;
BDNF
- MeSH:
Animals;
Anoxia;
Apoptosis;
Blotting, Western;
Brain-Derived Neurotrophic Factor;
Caspase 3;
Cerebral Cortex;
DNA;
DNA Damage;
DNA Repair;
Ether, Ethyl;
Fetal Development;
Fetus;
Guanine;
Humans;
Infant;
Infant Mortality;
Nerve Growth Factors;
Neurons;
Rats;
Rats, Sprague-Dawley
- From:Korean Journal of Physical Anthropology
2012;25(2):67-76
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Hypoxia is one of the major causes of neonatal mortality. Hypoxia-induced tissue injuries are resulted from complex mechanisms such as DNA damage and apoptosis. In this study, we aimed to elucidate the changes in the expression of DNA repairing enzymes such as 8-hydroxyguanine glycosylase 1 (OGG1) and apurinic/apyrimidinic endonuclease 1 (APE1) and brain derived neurotrophic factor (BDNF) in the fetal cerebral tissue after intrauterine hypoxic injury. For this study, pregnant Sprague-Dawley rats were exposed to hypoxic gas (10% O2, 5% CO2, 85% N2) for 2 or 4 hours at postconception day 14.5 and 15.5. After 24 hours, the animals were anesthetized with ethyl ether and fetuses were obtained by laparatomy. Hematoxylin-eosin stain, immunohistochemical stain, and western blot were employed for analysis. The caspase-3 immunolabeled cells were significantly increased within the cerebral cortex after hypoxic injury. The expressions of OGG1, APE1, and BDNF were also increased in the cerebral tissue after hypoxic injury at post-conception day 14.5, in a dose-dependent manner. However, the expression of BDNF was significantly decreased in the cortical tissue exposed to hypoxic injury at postconception day 15.5. These results demonstrate that fetal hypoxic injury induces apoptosis of the nerve cells and promotes the expressions of the DNA repairing enzymes and neurotrophic factors. In addition, these results suggest that protection mechanisms against hypoxic injury alter along the progression of the fetal development.
