Journal
BIOLOGICAL & PHARMACEUTICAL BULLETIN
Volume 33, Issue 4, Pages 550-555Publisher
PHARMACEUTICAL SOC JAPAN
DOI: 10.1248/bpb.33.550
Keywords
5-hydroxyindole; oxidative stress; mitochondrial dysfunction; apoptosis
Categories
Funding
- Medical Research Center program of the National Research Foundation of Korea [2009-0083538]
- [R01-2007-000-20852-0]
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5-Hydroxyindole (5H1), a metabolite of tryptophan, is involved in learning and memory, central neuron system regulation, and anti-oxidant activity. However, its protective action in mitochondrial function is not clear. Here, we tested whether 5HI protects against tert-butylhydroperoxide (t-BHP)-induced oxidative damage and mitochondrial dysfunction in human fibroblast cells. 5HI significantly suppressed t-BHP-induced cytotoxicity as determined by intracellular reactive species generation, lipid peroxidation, glutathione depletion, and peroxynitrite (ONOO-) generation. In addition, 5HI reduced t-BHP-induced DNA condensation. Pretreatment with 5HI significantly restored mitochondrial membrane potential (Delta psi m), suggesting that it protected cells against t-BHP-induced apoptosis. Western blot analysis also revealed that 5HI markedly inhibited cytochrome c release and caspase-3 activation, but not caspase-9 activation. Our data suggest that 5HI protects cells by attenuating oxidative stress and consequently protects against mitochondrial dysfunction.
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