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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2017.7
- 수록면
- 503 - 514 (12page)
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초록· 키워드
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Nicotinamide (NAM) plays essential roles in physiology through facilitating NAD+ redox homeostasis. Importantly, at high doses, it protects cells under oxidative stresses, and has shown therapeutic effectiveness in a variety of disease conditions. In our previous studies, NAM lowered reactive oxygen species (ROS) levels and extended cellular life span in primary human cells. In the treated cells, levels of NAD+/NADH and SIRT1 activity increased, while mitochondrial content decreased through autophagy activation. The remaining mitochondria were marked with low superoxide levels and high membrane potentials (Δψm); we posited that the treatment of NAM induced an activation of mitophagy that is selective for depolarized mitochondria, which produce high levels of ROS. However, evidence for the selective mitophagy that is mediated by SIRT1 has never been provided. This study sought to explain the mechanisms by which NAM lowers ROS levels and increases Δψm. Our results showed that NAM and SIRT1 activation exert quite different effects on mitochondrial physiology. Furthermore, the changes in ROS and Δψm were not found to be mediated through autophagy or SIRT activation. Rather, NAM suppressed superoxide generation via a direct reduction of electron transport, and increased Δψm via suppression of mitochondrial permeability transition pore formation. Our results dissected the effects of cellular NAD+ redox modulation, and emphasized the importance of the NAD+/NADH ratio in the mitochondria as well as the cytosol in maintaining mitochondrial quality.
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참고문헌 (63)
참고문헌 신청
Ayoub, I. A. / 2002 / Therapeutic window for nicotinamide following transient focal cerebral ischemia / Neuroreport 13:213~216
Bayrakdar, E. T. / 2014 / Ex vivo protective effects of nicotinamide and 3-aminobenzamide on rat synaptosomes treated with Abeta(1-42) / Cell Biochem. Funct 32:557~564
Bernardi, P. / 1992 / Modulation of the mitochondrial permeability transition pore. Effect of protons and divalent cations / J. Biol. Chem 267:2934~2939
Cheng, Y. / 2011 / Activation of the permeability transition pore by Bax via inhibition of the mitochondrial BK channel / Cell Physiol. Biochem 27:191~200
최호진 / 2015 / High-Dose Nicotinamide Suppresses ROS Generation and Augments Population Expansion during CD8+ T Cell Activation / Molecules and Cells 38(10):918~924
Bayrakdar, E. T. / 2014 / Ex vivo protective effects of nicotinamide and 3-aminobenzamide on rat synaptosomes treated with Abeta(1-42) / Cell Biochem. Funct 32:557~564
Bernardi, P. / 1992 / Modulation of the mitochondrial permeability transition pore. Effect of protons and divalent cations / J. Biol. Chem 267:2934~2939
Cheng, Y. / 2011 / Activation of the permeability transition pore by Bax via inhibition of the mitochondrial BK channel / Cell Physiol. Biochem 27:191~200
최호진 / 2015 / High-Dose Nicotinamide Suppresses ROS Generation and Augments Population Expansion during CD8+ T Cell Activation / Molecules and Cells 38(10):918~924
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