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논문 기본 정보

자료유형
학술저널
저자정보
Baek, Nam-In (Department of Life Sciences and Institute of Life Science & Resources, Kyunghee University) Choi, Soo-Young (Department of Genetic Engineering, Division of Life Sciences, Hallym University) Park, Jin-Kyu (Korea Ginseng & Tobacco Research Institute) Cho, Sung-Woo (Department of Biochmeistry, College of Medicine, University of Ulsan) Ahn, Eun-Mi (Department of Life Sciences and Institute of Life Science & Resources, Kyunghee University) Jeon, Seong-Gyu (Department of Genetic Engineering, Division of Life Sciences, Hallym University) Lee, Byung-Ryong (Department of Genetic Engineering, Division of Life Sciences, Hallym University) Bahn, Jae-Hoon (Department of Genetic Engineering, Division of Life Sciences, Hallym University) Kim, Yong-Kyu (Korea Ginseng & Tobacco Research Institute) Shon, Il-Hwan (Daelim Industrial Co. Daeduk R&D Center)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제22권 제2호
발행연도
1999.1
수록면
219 - 224 (6page)

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In our search for the anticonvulsant consitutent of Gastrodia elata repeated column chromatographies guided by activity assay led to isolation of an active compound, which was identified as gastrodin on the basis of spectral data. Brain succinic semialdehyde dehydrogenase (SSADH) was inactivated by preincubation with gastrodin in a time-dependent manner and the reaction was monitored by absorption and fluorescene spectroscopic methods. The inactivation followed pseudo-first-order kinetics with the second-rate order constant of $1.2{\times}10^{3} M^{-1} min^{-1}$. The time course of the reaction was significantly affected by the coenzyme NAD^{+}$, which affected complete protection against the loss of the catalytic activity, whereas substrate succinic semialdehyde failed to prevent the inactivation of the enzyme. It is postulated that the gastrodin is able to elevate the neurotransmitter GABA levels in central nervous system by inhibitory action on one of the GABA degradative enzymes, SSADH.

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