Toshio Obata1, Michiko Nakashima2. 1. School of Nursing, Faculty of Health Sciences, Osaka Aoyama University, 2-11-1 Niina, Mino City, Japan. Electronic address: t-obata@osaka-aoyama.ac.jp. 2. Department of Nursing, School of Health Sciences, Asahi University, 1851 Hozumi, Mizuho City, Gifu, Japan.
Abstract
BACKGROUND: Semicarbazide-sensitive amine oxidase (SSAO; EC; 1.4.3.6.) has widespread tissue distribution, and the physiological role of SSAO is quite well known through its involvement in several pathological states. AIMS: The present study examined modulators of SSAO which might be present in the rat heart cytosol and looked for changes in SSAO modulatory activity. METHODS: An endogenous inhibitor of SSAO was separated by gel filtration from 105,000g supernate of T4-treated rat heart cytosol. SSAO inhibition fraction was referred to as "endogenous SSAO inhibitor". RESULTS: The inhibition by this inhibitor was concentration-dependent. Inhibition of SSAO was not enhanced by varying the time of preincubation of the enzyme, indicating reversible inhibition of SSAO. The molecular weight of this inhibitor was estimated to be 1000-1100 by gel filtration. The isoelectric point (pI) value was determined to be 4.8 isoelectric focusing. This inhibitor was found to be heat-stable and resistant to protease treatment. SSAO inhibition activity was much lower in the cytosol of thyroidectomized, non-T4-treated rats than T4-treated rats, suggesting that this inhibitor was induced by thyroid hormone T4. SSAO activity in rat heart might be regulated by the level of this inhibitor. CONCLUSION: These results suggest the presence of SSAO inhibitor in T4-treated rat cytosol and that the level of this inhibitor is regulated by thyroid hormone.
BACKGROUND:Semicarbazide-sensitive amine oxidase (SSAO; EC; 1.4.3.6.) has widespread tissue distribution, and the physiological role of SSAO is quite well known through its involvement in several pathological states. AIMS: The present study examined modulators of SSAO which might be present in the rat heart cytosol and looked for changes in SSAO modulatory activity. METHODS: An endogenous inhibitor of SSAO was separated by gel filtration from 105,000g supernate of T4-treated rat heart cytosol. SSAO inhibition fraction was referred to as "endogenous SSAO inhibitor". RESULTS: The inhibition by this inhibitor was concentration-dependent. Inhibition of SSAO was not enhanced by varying the time of preincubation of the enzyme, indicating reversible inhibition of SSAO. The molecular weight of this inhibitor was estimated to be 1000-1100 by gel filtration. The isoelectric point (pI) value was determined to be 4.8 isoelectric focusing. This inhibitor was found to be heat-stable and resistant to protease treatment. SSAO inhibition activity was much lower in the cytosol of thyroidectomized, non-T4-treated rats than T4-treated rats, suggesting that this inhibitor was induced by thyroid hormone T4. SSAO activity in rat heart might be regulated by the level of this inhibitor. CONCLUSION: These results suggest the presence of SSAO inhibitor in T4-treated rat cytosol and that the level of this inhibitor is regulated by thyroid hormone.
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