Protective effect of 1-methylated beta-carbolines against 3-morpholinosydnonimine-induced mitochondrial damage and cell viability loss in PC12 cells
- Authors
- Choi, WT; Youn, YC; Han, ES; Lee, CS
- Issue Date
- Oct-2004
- Publisher
- KLUWER ACADEMIC/PLENUM PUBL
- Keywords
- cell death; differentiated PC12 cells; 1-methylated beta-carbolines; mitochondrial membrane permeability; reactive nitrogen species
- Citation
- NEUROCHEMICAL RESEARCH, v.29, no.10, pp 1807 - 1816
- Pages
- 10
- Journal Title
- NEUROCHEMICAL RESEARCH
- Volume
- 29
- Number
- 10
- Start Page
- 1807
- End Page
- 1816
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/24753
- DOI
- 10.1023/B:NERE.0000042206.46554.e4
- ISSN
- 0364-3190
1573-6903
- Abstract
- The present study investigated the effect of 1-methylated beta-carbolines ( harmaline, harmalol and harmine) on change in the mitochondrial membrane permeability and cell death due to reactive nitrogen species in differentiated PC12 cells. beta-Carbolines, caspase inhibitors (z-LEHD. fmk and z-DQMD. fmk) and antioxidants (N-acetylcysteine, dithiothreitol, melatonin, carboxy-PTIO and uric acid) depressed cell viability loss due to 3-morpholinosydnonimine (SIN-1) in PC12 cells. beta-Carbolines inhibited the nuclear damage, the decrease in mitochondrial transmembrane potential, the cytochrome c release, the formation of reactive oxygen species and the depletion of GSH caused by SIN-1 in PC12 cells. beta-Carbolines decreased the SIN-1-induced formations of 3-nitrotyrosine, malondialdehyde and carbonyls in PC12 cells. The results show that 1-methylated beta-carbolines attenuate SIN-1-induced mitochondrial damage. This results in the inhibition of caspase-9 and -3 and apoptotic cell death in PC12 cells by suppressing the toxic actions of reactive oxygen and nitrogen species, including the GSH depletion.
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