The Anti-apoptotic Action of 5-Hydroxyindole: Protection of Mitochondrial Integrity

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  • Bae Sung Jin
    Department of Pharmacy, Pusan National University Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University
  • Lee Jun Sik
    Department of Microbiology and Immunology, College of Medicine, BK21 Medical Science Education Center, Pusan National University
  • Lee Eun Kyeong
    Department of Pharmacy, Pusan National University Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University
  • Kim Ji Min
    Department of Pharmacy, Pusan National University Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University
  • Choi Jehun
    Department of Pharmacy, Pusan National University Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University
  • Heo Hyoung-Sam
    Department of Pharmacy, Pusan National University Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University
  • Yu Byung Pal
    Department of Physiology, The University of Texas Health Science Center at San Antonio
  • Chung Hae Young
    Department of Pharmacy, Pusan National University Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University

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5-Hydroxyindole (5HI), 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 (Δψm), 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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