• BMB Reports
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• v.29 no.1
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• pp.81-87
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• 1996

The relationship of S-thiolation and oxidation of glycogen phosphorylase b and peroxidation of phosphatidyl choline liposome by xanthine oxidase (XOD), 2,2'-azobis(2-amidinopropane) hydrochloride (AAPH), and 2,2'-azobis(dimethylvaleronitrile) (AMVN)-generated free radicals was investigated, Glycogen phosphorylase b was S-thiolated in the presence of glutathione and oxidized in the absence of it by XOD, AAPH and AMVN. In XOD-initiated reaction, the rates of S-thiolation and oxidation of phosphorylase were very similar and addition of liposome to the reaction mixture showed little inhibition of the modifications. In AAPH-initiated reaction, the rate of oxidation was higher than that of S-thiolation and addition of liposome increased oxidation of the protein but had no effect on S-thiolation. In AMVN-initiated reaction, S-thiolation was higher than oxidation and addition of liposome increased S-thiolation remarkably but showed no effect on oxidation. The effect of liposome on modifications of protein in AAPH and AMVN reaction seemed to be caused by certain reactive degradation products or intermediates of liposome by free radical attack. Peroxidation of liposome was not observed in XOD-initiated reaction. Liposome was gradually peroxidized by AAPH reaction. The peroxidation was inhibited by addition of GSH and phosphorylase. Peroxidation of liposome by AMVN was extreamly fast, and was not affected by GSH and phosphorylase.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.18 no.2
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• pp.138-143
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• 2015

Glycogen storage disease type IX (GSD IX) is caused by a defect in phosphorylase b kinase (PhK) that results from mutations in the PHKA2, PHKB, and PHKG2 genes. Patients usually manifest recurrent ketotic hypoglycemia with growth delay, but some may present simple hepatomegaly. Although GSD IX is one of the most common causes of GSDs, its biochemical and genetic diagnosis has been problematic due to its rarity, phenotypic overlap with other types of GSDs, and genetic heterogeneities. In our report, a 22-month-old boy with GSD IX is described. No other manifestations were evident except for hepatomegaly. His growth and development also have been proceeding normally. Diagnosed was made by histologic examination, an enzyme assay, and genetic testing with known c.3210_3212del (p.Arg1070del) mutation in PHKA2 gene.

• Journal of Nutrition and Health
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• v.28 no.5
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• pp.426-434
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• 1995

The purpose of this study were to investigate the effect of fasting and vitamin B6 repletion on tissue concentration of pyridoxal 5-phosphate and urinary excreteion of 4-pyridoxic acid in vitamin B6 deficient rats. Sixty six rats(6 per group) were fed either a vitamin B6 deficient diet (-B6) or a control diet (+B6) for 6 weeks and then rats were repleted with +B6 diet for 2 weeks. Rats were fasted for 1 and 3 days and for 3 days after repletion. Pyridoxal 5-phosphate (PLP) concentration in plasma, liver, skeletal muscle, and heart muscle and urinary 4-pyridoxic acid (4-PA) excretion were compared. Fasting resulted in a significant increase in PLP concentration in the plasma, liver and heart muscle of rats fed the -B6 diet. Skeletal muscle PLP concentration was significantly decreased in +B6 rats but not in -B6 rats. Following vitamin B6 repletion, PLP concentration in the plasma, liver and heart muscle in previously -B6 rats was similar to the respective concentration in +B6 rats while PLP concentration in the skeletal muscle of previously -B6 rats increased, but it was not reached to that of +B6 rats. At day 1 and 2 of the fast, urinary 4-PT excretion increased in both +B6 and -B6 rats although there was no supply of vitamin B6 due to fasting. These results suggest that vitami B6 is redistributed as PLP when there is a caloric deficit and PLP is supplied by an endogenous source, possibly PLP bound to skeletal muscle glycogen phosphorylase.

• Journal of Microbiology
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• v.45 no.3
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• pp.268-271
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• 2007

In Korea, the Mycobacterium tuberculosis K-strain is the most prevalent clinical isolates and belongs to the Beijing family. In this study, we conducted comparative porteomics of expressed proteins of clinical isolates of the K-strain with H37Rv, H37Ra as well as the vaccine strain of Mycobacterium bovis BCG following phagocytosis by the human monocytic cell line U-937. Proteins were analyzed by 2-D PAGE and MALDI-TOF-MS. Two proteins, Mb1363 (probable glycogen phosphorylase GlgP) and MT2656 (Haloalkane dehalogenase LinB) were most abundant after phagocytosis of M. tuberculosis K-strain. This approach provides a method to determine specific proteins that may have critical roles in tuberculosis pathogenesis.

• Journal of Ginseng Research
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• v.47 no.6
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• pp.784-794
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• 2023

Background: ginsenoside Rg5 is a rare ginsenoside with known hypoglycemic effects in diabetic mice. This study aimed to explore the effects of ginsenoside Rg5 on skin wound-healing in the Lepr^db/db mutant (db/db) mice (C57BL/KsJ background) model and the underlying mechanisms. Methods: Seven-week-old male C57BL/6J, SLC7A11-knockout (KO), the littermate wild-type (WT), and db/db mice were used for in vivo and ex vivo studies. Results: Ginsenoside Rg5 provided through oral gavage in db/db mice significantly alleviated the abundance of apoptotic cells in the wound areas and facilitated skin wound healing. 50 μM ginsenoside Rg5 treatment nearly doubled the efferocytotic capability of bone marrow-derived dendritic cells (BMDCs) from db/db mice. It also reduced NF-κB p65 and SLC7A11 expression in the wounded areas of db/db mice dose-dependently. Ginsenoside Rg5 physically interacted with SLC7A11 and suppressed the cystine uptake and glutamate secretion of BMDCs from db/db and SLC7A11-WT mice but not in BMDCs from SLC7A11-KO mice. In BMDCs and conventional type 1 dendritic cells (cDC1s), ginsenoside Rg5 reduced their glycose storage and enhanced anaerobic glycolysis. Glycogen phosphorylase inhibitor CP-91149 almost abolished the effect of ginsenoside Rg5 on promoting efferocytosis. Conclusion: ginsenoside Rg5 can suppress the expression of SLC7A11 and inhibit its activity via physical binding. These effects collectively alleviate the negative regulations of SLC7A11 on anaerobic glycolysis, which fuels the efferocytosis of dendritic cells. Therefore, ginsenoside Rg5 has a potential adjuvant therapeutic reagent to support patients with wound-healing problems, such as diabetic foot ulcers.