• Microbiology and Biotechnology Letters
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• v.24 no.4
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• pp.485-492
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• 1996

myo-Inositol, a growth factor for Saccharomyces cerevisiae (S. cerevisiae), has been known to be incorporated into phosphatidylinositol (PI), which is a kind of phospholipid in the cell membrane, by a membrane-associated PI-synthesizing enzyme. The deficiency of myo-inositol in S. cerevisiae adversely affected the membrane structure and function. On the basis of biochemical functions of myo-inositol, the effect of deficiency of myo-inositol on the aerobic glucose metabolism was investigated by measuring specific oxygen uptake rate (Q$_{O2}$) used as an indicator representing the respiratory capacity of S. cerevisiae in batch and continuous cultures. The respiratory capacity of aerobic glucose metabolism in S. cerevisiae was also monitored after glucose pulse-addition in a continuous culture (D=0.2, 1/hr), in which glucose was utilized through respiratory metabolism. The deficiency of myo-inositol was found to lead to both the decrease of the maximum specific oxygen uptake rate (Q$_{O2max}$) observed from the batch as well as in the continuous culture experiment and the decrease of the respiratory capacity of aerobic glucose metabolism of S. cerevisiae determined from the glucose pulse-addition experiment, in which the glucose flux into respiratory and fermen- tative metabolism was quantitatively analyzed.

• Environmental Analysis Health and Toxicology
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• v.9 no.1_2
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• pp.1-8
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• 1994

Nerve conduction impairment in lead neuropathy has been empirically linked to altered nerve myo-inositol metabolism. In most cases of neuropathy, abnormal myo-inositol metabolism is associated with abnormal $Na^+/K^+$ATPase provides a potential mechanism to relate defects of the myo-inositol metabolism in the peripheral nerve treated with lead. Therefore, the effect of lead on the rat sciatic nerve $Na^+/K^+$ATPase and other ATPase of sciatic nerve was studied. ATPase activity was measured enzymatically in sciatic nerve homogenates from 2-wk lead treated neuropathy rats and age-mached controls administered myo-inositol. $Na^+/K^+$ATPase components were assessed by ouabain inhibition or the omission of sodium and potassium ions. Lead reduced 50% reduction in the $Na^+/K^+$ATPase activity in homogenates of sciatic nerve. The 50% reduction in the $Na^+/K^+$ ATPase activity was selectively prevented by myo-inositol treatment. This study suggests that the toxic mechanism of the lead on peripheral nerve may be through reduction in $Na^+/K^+$ATPase activity which has been linked to axonal transport slowing in the rat model of lead neuropathy, via direct changes by the perturbation of the intracelluar sodium or potasium level.

• Bulletin of the Korean Chemical Society
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• v.23 no.3
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• pp.515-517
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• 2002

• Microbiology and Biotechnology Letters
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• v.46 no.2
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• pp.102-110
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• 2018

A bacterial strain capable of metabolizing myo-inositol (MI) and converting to other substances was isolated from soil of orchard. The isolate, named YB-46, was grown on minimal medium supplemented with MI as the sole carbon source and was presumed to belonging to genus Enterobacter according to the 16S rDNA sequence. Escherichia coli transformant converting MI into unknown metabolites was selected from a metagenomic library prepared with fosmid pCC1FOS vector. Plasmid was isolated from the transformant, and the inserted gene was partially sequenced. From the nucleotide sequence, an iolG gene was identified to encode myo-inositol dehydrogenase (IolG) consisting of 336 amino residues. The IolG showed amino acid sequence similarity of about 50% with IolG of Enterobacter aerogenes and Bacillus subtilis. The His-tagged IolG (HtIolG) fused with hexahistidine at C-terminus was produced and purified from cell extract of recombinant E. coli. The purified HtIolG showed maximal activity at $45^{\circ}C$ and pH 10.5 with the highest activity for MI and D-glucose, and more than 90% of maximal activity for D-chiro-inositol, D-mannitol and D-xylose. $K_m$ and $V_{max}$ values of the HtIolG for MI were 1.83 mM and $0.724{\mu}mol/min/mg$ under the optimal reaction condition, respectively. The activity of HtIolG was increased 1.7 folds by $Zn^{2+}$, but was significantly inhibited by $Co^{2+}$ and SDS.

• Journal of environmental and Sanitary engineering
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• v.14 no.1
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• pp.88-96
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• 1999

The effect of acute cadmium-neuropathy on phospholipid metabolism in rat sciatic nerve was investigated. An animal model of cadmium neuropathy was induced by feeding diet containing cadmium to Sprague-Dawley rat for two weeks. Four weeks aged Sprague-Dawley rats were divided into four groups : normal control group, 10ppm-cadmium treated group, 100ppm-cadmium treated group, 1000ppm-cadmium treated group, reference drug, myo-inositol-treated group. All rats were sacrificed at the end of two weeks. The rate of incorporation of 2-[3H]myo-inositol into polyphosphinositide was significantly decreased while the rates of incorporation into phospholipid of titratedserine, ethanolamine and choline were unchanged in sciatic nerve obtained from cadmium-treated rat. Continuously the activities of three enzymes concerned with inositol phospholiped metabolism were measured in homogenates of rat sciatic nerves. Cystidine diglyceride transferase and phophatidylinositol kinase showed significantly decreased activities while phosphatidylinositol-4-phosphate kinase did not show any significant change in activity by cadmium treatment. However these deficits of inositol phospholipid metabolism were ameliorated by myo-inositol administration and these effectiveness were more potent in lower dose cadmiumtreated rats than higher dose cadmium-treated rats. These results suggest that cadmium intoxicated peripheral nerve with perturbation of the ployphosphoinositide metabolism and alteration of the enzyme activity which concerned with myo-inositol metabolism.

• Journal of environmental and Sanitary engineering
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• v.10 no.3
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• pp.45-55
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• 1995

This study was carried out to elucidate the toxic mechanism of cadmium in peripheral nerve. An animal model of cadmium neuropathy was induced by feeding diet containing cadmium to Sprague- Dawley rat (or two weeks. Four weeks aged Sprague- Dawley rats were divided into four groups : normal control group, 10ppm- cadmium treated group, 100ppm- cadmium treated group, 1000ppm- cadmium treated group, reference drug- treated group. All rats were sacrificed at the end of two weeks for assessing the development of cadmium neuropathy, These results obtained were summarized as follows : 1. Cadmium reduced peripheral flow of both acetylcholinesterase and cholinesterase in rat sciatic nerve. 2. The toxic mechanism of cadmium might be the result of an reduction of myo-inositol concentration in peripheral nervous system 3. Reduction in myo-inositol content of peripheral nerve resulted from the inhibition of sodium- Potassium ATPase activity, which is responsible for myo-inositol transport, by cadmium 4. Oral administration of myo-inositol improved the flow of both acetylcholinesterase and cholinesterasenerve in cadmium intoxicated rat. These results suggest that mild cadmium neuropathy might be diagnosed by checking nervous myo-inositol content and oral administraion of myo-inositol might prevent the development of severe cadmium neuropathy with special reference to detective axonal transport.

• Journal of Life Science
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• v.7 no.2
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• pp.119-126
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• 1997

Phytase(myo-inositol hexkisphosphate phosphohydrolase ; EC 3.1.3.8) was purified from the mucoas of rat intestinal. The molecular weight of enzyme was determined to be 160kDa by sephacryl S-200 gel filtration. Analysis of the purified enzyme o SDS-polyacrylamide gel electrophoresis(SDS-PAGE) showen that it was composed of two different subunits and the molecular weight of its subunit was found to be 70kDa and 90kDa respectively, indicating that this enzyme is hetrodimer. The enzyme activities were activated in the presence of $ MgCl_{2}$, but inhibited by $ZnCl_{2}$, $MnCl_{2}$, and EDTA. The substrates tested, phytase showed the highest affinity for the enzyme at the physiological ph. The Km value for phytic acid(inositol-hexakisphosphate)was 0.31 mM at pH 7.4. rat intestinal mucosa phytase seems to play an important in the metabolism of inositol.

• Korean Journal of Food Science and Technology
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• v.5 no.4
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• pp.240-248
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• 1973

Reduction of penta-O-acetyl-myo-inosose-2 by catalytic hydrogenation and with sodium-amalgam was carried out in alcohol solution of pH $3{\sim}4$. The former reduction product was axial-alcohol, and the latter equatorial-alcohol. On reduction of penta-O-acetyl-DL-epi-inosose-2 with sodium borohydride and sodium-amalgam in the previous condition, ax.-alcohol and eq.-alcrhol have been obtained. The synthesis of various inositol-p-hydroxybezoate are described. The esters have been characterized by paper chromatography and saponification, and their antimicrobial activities on some microbes were tested for the application of food industry. As the result, it was found that the antimicrobiol activity of epi-inositol ester was superior to its analogues.

• Journal of Life Science
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• v.19 no.1
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• pp.147-151
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• 2009

D-pinitol, another chemical structure of 3-O-methyl-D-chiro-inositol, is an important insulin-sensitizer. The purpose of this review is to examine the characteristics of pinitol and other analogs as functional food biomaterials which were well known to reduce blood glucose levels. Pinitol can be converted to chiro-inositol in normal humans, while diabetic patients can not use the molecule, resulting in exhibiting low level of chiro-inositol in their urine. Recently, it is reported that pinitol can trigger phospholipase C/D, thus the rate of glucose metabolism accelerates to use as fuel for human body. To not only reduce insulin resistance of diabetic patients, but also alleviate the symptoms of diabetes, obesity, and muscle contraction, pinitol and its dietary supplementation is needed.

• Natural Product Sciences
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• v.4 no.3
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• pp.170-173
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• 1998

A new derivative of allo-inositol has been isolated from the aerial parts of Stocksia brahuica and named as brahol (1). The structure of 1 was elucidated with the help of extensive 2D-NMR spectroscopic techniques and identified as 5-O-methyl-allo-inositol. The structure was reconfirmed by acetate derivative (2).