Distinct roles of oxidative stress and antioxidants in the nucleus dorsalis and red nucleus following spinal cord hemisection.
Oxidative stress plays an important role in the pathogenesis of neurodegeneration after the acute central nervous system injury. We reported previously that increased nitric oxide (NO) production following spinal cord hemisection tends to lead to neurodegeneration in neurons of the nucleus dorsalis (ND) that normally lacks expression of neuronal NO synthase (nNOS) in opposition to those in the red nucleus (RN) that constitutively expresses nNOS. We wondered whether oxidative stress could be a mechanism underlying this NO involved neurodegeneration. In the present study, we examined oxidative damage evaluated by the presence of 4-hydroxynonenal (HNE) and iron accumulation and expression of putative antioxidant enzymes heme oxygenase-1 (HO-1) and superoxide dismutase (SOD) in neurons of the ND and RN after spinal cord hemisection. We found that HNE expression was induced in neurons of the ipsilateral ND from 1 to 14 days following spinal cord hemisection. Concomitantly, iron staining was seen from 7 to 14 days after lesion. HO-1, however, was only transiently induced in ipsilateral ND neurons between 3 and 7 days after lesion. In contrast to the ND neurons, HNE was undetectable and iron level was unaltered in the RN neurons after spinal cord hemisection. HO-1, SOD-Cu/Zn and SOD-Mn were constitutively expressed in RN neurons, and lesion to the spinal cord did not change their expression. These results suggest that oxidative stress is involved in the degeneration of the lesioned ND neurons; whereas constitutive antioxidant enzymes may protect the RN neurons from oxidative damage.
Xu
Mei
M
Department of Biology, Georgia State University, Atlanta, GA 30303, USA.
Yip
George Wai-Cheong
GW
Gan
Le-Ting
LT
Ng
Yee-Kong
YK
D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002452:Cell Count / Q000379:methods; D007839:Functional Laterality; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D006651:Histocytochemistry / Q000379:methods; D007150:Immunohistochemistry / Q000379:methods; D007501:Iron / Q000378:metabolism; D008297:Male; D020645:Mediodorsal Thalamic Nucleus / Q000473:pathology*; D009474:Neurons / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012012:Red Nucleus / Q000473:pathology*; D013119:Spinal Cord Injuries / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D013194:Staining and Labeling / Q000379:methods; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors
D000447:Aldehydes; D000975:Antioxidants; D007501:Iron; D013482:Superoxide Dismutase; C027576:4-hydroxy-2-nonenal