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NAD+ treatment can block rotenone‐induced nuclear apoptotic changes of PC12 cells
Author(s) -
Hong Yunyi,
Shao Jiaxiang,
Xia Weiliang,
Ying Weihai
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.965.6
Subject(s) - nad+ kinase , rotenone , apoptosis , mitochondrion , pharmacology , dna laddering , oxidative stress , nuclear dna , chemistry , biology , microbiology and biotechnology , biochemistry , mitochondrial dna , programmed cell death , dna fragmentation , enzyme , gene
Our previous study has shown that NAD+ can prevent astrocyte necrosis induced by oxidative stress and DNA alkylating agents. We have further found that intranasal administration of NAD+ can profoundly reduce ischemic brain damage. The goal of this current study is to determine the effects of NAD+ on the apoptotic changes of cells. We found that the mitochondrial Complex I inhibitor rotenone at 0.1 to 1 micromolar dose‐dependently induced nuclear condensation of PC12 cells: 0.75 micromolar rotenone induced an approximately 50% decrease in the nuclear size of the cells. Treatment of the cells with 0.25 to 1 mM NAD+ dose‐dependently attenuate rotenone‐induced nuclear condensation ‐‐‐ a hallmark of apoptosis: the rotenone‐induced nuclear condensation was nearly completely prevented by 1 mM NAD+. Our preliminary results have also shown that NAD+ treatment can prevent alkylating agent‐induced DNA laddering of astrocytes. Collectively, our results suggest that NAD+ treatment can significantly decrease toxic agent‐induced necrosis as well as apoptotic changes, thus providing information for understanding the mechanisms underlying the NAD+‐produced reductions of ischemic brain injury (Supported by a Key Research Grant of Shanghai Municipal Scientific Committee 08JC1415400 (WY), Pujiang Scholar Program Grant (WY)).