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7810860 
Journal Article 
Retinoic acid reduces apoptosis and oxidative stress by preservation of SOD protein level 
Ahlemeyer, B; Bauerbach, E; Plath, M; Steuber, M; Heers, C; Tegtmeier, F; Krieglstein, J 
2001 
Yes 
Free Radical Biology and Medicine
ISSN: 0891-5849
EISSN: 1873-4596 
PERGAMON-ELSEVIER SCIENCE LTD 
OXFORD 
30 
10 
1067-1077 
11369496 
WOS:000168654700002 
Retinoic acid (RA) has already been shown to exert antiapoptotic and antioxidative activity in various cells. In this study, we determined the effect of RA on the mRNA and protein levels of the Cu-,Zn-superoxide dismutase (SOD-1) and Mn-superoxide dismutase (SOD-2) during staurosporine-induced apoptosis in primary cultures from neonatal rat hippocampus. Exposure to staurosporine (300 nM, 24 h) increased the percentage of apoptotic neurons to 62% compared with 18% in controls. We determined an increase in the reactive oxygen species (ROS) content from 4 up to 48 h after the induction of the injury. Treatment with staurosporine did not significantly change the mRNA levels of SOD-1 and SOD-2. However, the SOD-1 and SOD-2 protein levels markedly decreased 24 and 48 h after the addition of staurosporine. Compared with staurosporine-exposed controls. RA (10 nM)-treated cultures showed a significant increase in neuronal survival, a reduced neuronal ROS content, and enhanced protein levels of SOD-l and SOD-2 24 and 48 h after the start of the exposure to staurosporine. The results suggest that RA reduced staurosporine-induced oxidative stress and apoptosis by preventing the decrease in the protein levels of SOD-1 and SOD-2, and thus supported the antioxidant defense system. (C) 2001 Elsevier Science Inc. 
apoptosis; neurons; staurosporine; retinoic acid; reactive oxygen species; superoxide dismutase; antioxidant defense system; free radicals