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Biomedical subjects

S W Cho

Publications and source records attributed to S W Cho.

100 records · Page 6Linked to original sources
PubMed1989

Inactivation of bakers' yeast glucose-6-phosphate dehydrogenase by aluminum.

Preincubation of yeast glucose-6-phosphate dehydrogenase (G6PD) with Al(III) produced an inactive enzyme containing 1 mol of Al(III)/mol of enzyme subunit. None of the enzyme-bound Al(III) was dissociated by dialysis against 10 mM Tris-HCl, pH 7.0, containing 0.2 mM EDTA at 4 degrees C for 24 h. Citrate, NADP+, EDTA, or NaF protected the enzyme against the Al(III) inactivation. The Al-(III)-inactivated enzyme, however, was completely reactivated only by citrate and NaF. The dissociation constant for the enzyme-aluminum complex was calculated to be 4 x 10(-6)M with NaF, a known reversible chelator for aluminum. Modification of histidine and lysine residues of the enzyme with diethyl pyrocarbonate and acetylsalicylic acid, respectively, inactivated the enzyme. However, the modified enzyme still bound 1 mol of Al(III)/mol of enzyme subunit. Circular dichroism studies showed that the binding of Al(III) to the enzyme induced a decrease in alpha-helix and beta-sheet and an increase in random coil. Therefore, it is suggested that inactivation of G6PD by Al(III) is due to the conformational change induced by Al(III) binding.

Aluminum↗
PubMed1989

Ribonuclease inhibitor from pig brain: purification, characterization, and direct spectrophotometric assay.

The ribonuclease inhibitor from pig brain has been purified 1,500-fold by a combination of ammonium sulfate fractionation, ion-exchange chromatography, hydroxylapatite chromatography, and gel filtration. The inhibitor has a Mr 50,000. It is a noncompetitive inhibitor for pancreatic ribonuclease A with a Ki of 1 nM, forming a 1:1 complex. Both ribonuclease A and B, but not ribonuclease U1 and T1, are inactivated by the inhibitor. The inhibition capacity was abolished by sulfhydryl reagents such as p-chloromercuribenzoate. Incubation of the enzyme-inhibitor complex with the sulfhydryl reagent caused dissociation into active ribonuclease and inactive inhibitor. Dithiothreitol was required during purification to retain the activity of the inhibitor.

Amino Acids↗
PubMed1989

Time-dependent inactivation of glucose-6-phosphate dehydrogenase from yeast by aluminum.

Aluminum inhibited yeast glucose-6-phosphate dehydrogenase (EC 1.1.1.49) by a pseudo-first-order reaction. The inhibition was proportional to the incubation time and the concentration of aluminum. Double reciprocal plots gave a straight line with a kinact of 8.3 min-1 and indicated the presence of a binding step prior to inhibition. The kinetic study showed that 1 mol of aluminum was bound per mol of enzyme subunit.

Aluminum↗
PubMed1989

Inactivation of glucose-6-phosphate dehydrogenase isozymes from human and pig brain by aluminum.

Prolonged intake of low levels of aluminum from the drinking water has been found to increase the aluminum content in rat brain homogenates and to reduce the activity of hexokinase and glucose-6-phosphate dehydrogenase (G6PD). To determine the interaction of G6PD with aluminum in the brain, we have recently purified two isozymes of G6PD (isozymes I and II) from human and pig brain. Unlike isozyme I, isozyme II also had 6-phosphogluconate dehydrogenase (6-PGD) activity. We report here that G6PD isozymes I and II from human and pig brain purified to apparent homogeneity are inactivated by aluminum. Aluminum did not affect the 6-PGD activity of isozyme II. The aluminum-inactivated enzyme contained 1 mol of aluminum/mol of enzyme subunit. The protein-bound metal ion was not dissociated by exhaustive dialysis at 4 degrees C against 10 mM Tris-HCl (pH 7.0) containing 0.2 mM EDTA. Preincubation of aluminum with citrate, NADP+, EDTA, NaF, ATP, and apotransferrin protected the G6PD isozymes against aluminum inactivation. However, when the G6PD isozymes were completely inactivated by aluminum, only citrate, NaF, and apotransferrin restored the enzyme activity. The dissociation constants for the enzyme-aluminum complex of the isozymes varied from 2 to 4 microM, as measured by using NaF, a known chelator for aluminum. Inhibition of G6PD by low levels of aluminum further strengthens the suggested role of aluminum toxicity in the energy metabolism of the brain.

Aluminum↗
PubMedDate not supplied

Portal vein aneurysm of the umbilical portion: imaging features and the relationship with portal vein anomalies.

BACKGROUND: We evaluated the imaging features of portal vein aneurysm occurring at the umbilical portion and the relation between portal vein aneurysm of the umbilical portion and portal vein anomaly. METHODS: Retrograde analysis was performed in 18 patients with portal vein aneurysm of the umbilical portion of the portal vein. We analyzed the size, shape, and imaging findings of portal vein aneurysm. In addition, we evaluated associated portal vein anomalies, specifically, the branching pattern of the intrahepatic portal vein and the position of the umbilical portion of the left portal vein. RESULTS: The diameter of the portal vein aneurysm ranged from 1.5 to 2.2 cm and the shape of the portal vein aneurysm was saccular (n = 14) or fusiform (n = 4). Imaging findings of the portal vein aneurysm of the umbilical portion were typical for its vascular nature. Portal vein anomalies were seen in eight of 18 patients (44%): the right anterior segmental portal vein (n = 7) or the right anterior and posterior segmental portal veins (n = 1) originating from the umbilical portion of the left portal vein and a rightward deviation of the umbilical portion of the left portal vein (n = 4). CONCLUSION: Due to its vascular nature, noninvasive diagnostic modalities can enable the detection of portal vein aneurysm of the umbilical portion, and there is a close relation between portal vein aneurysm of the umbilical portion and portal vein anomaly.

Adult↗
PubMedDate not supplied

Comparison of antiproliferative effects of 1-histamine-2 receptor antagonists, cimetidine, ranitidine, and famotidine, in gastric cancer cells.

In the immune system, histamine is known to suppress cytotoxic T-lymphocytes and nitrogen induced lymphocyte thymidine uptake, down-regulate some cytokines, and activate suppressor T-lymphocytes, and in the gastrointestinal system, histamine was reported to have trophic effects on gastrointestinal epithelial cells. Enhanced rates of cell proliferation by histamine are implicated in the pathogenesis. This study was designed since there is a lack of comparative data about the cell proliferations of histamine-2 receptor antagonist (H2-RA), cimetidine, ranitidine, and famotidine, in gastric cancer. KATO-III and AGS cell lines were used in this experiment. The concentrations of the histamine and cimetidine were 10(-5)-10(-8) M, respectively and those of ranitidine and famotidine were 10(-6)-10(-9)M, respectively. Cell proliferation after drug treatment was evaluated by direct cell counting, [3H]thymidine incorporation, and MTT assay. Activities of ornithine decarboxylase (ODC), a rate limiting enzyme in polyamine synthesis, were measured after each drug treatment. Protein kinase A, a cAMP-dependent protein kinase system, was assayed using [alpha-32P]ATP. Histamine showed statistically significant cell proliferating effects in a dose-dependent manner (P < 0.001), the maximal effect in 10(-5) M concentration. ODC activities were increased in accordance with the increment of cell numbers after histamine treatment. Cimetidine reversed the histamine-stimulated cell proliferation significantly, the maximal effect in 10(-5) M concentration (P < 0.01). Although ranitidine showed the tendency to attenuate the cell proliferation dose-dependently, but without statistical significance, famotidine did not show such an effect at all. cAMP-dependent protein kinase activities were significantly increased following 10(-5) M histamine treatment, also reversed significantly by cimetidine co-administration (P < 0.01). Beneficial clinical outcomes could be anticipated from cimetidine treatment in patients with gastric cancer by anti-proliferating effects against gastric cancer cells. These effects of H2-RA are likely to be mediated by specific interactions at the H2-receptor.

Adenocarcinoma↗
PubMedDate not supplied

Effects of 2-bromopropane on spermatogenesis in the Sprague-Dawley rat.

In 1995, 2-bromopropane (2-BP) was associated with occupational reproductive and hematopoietic toxicity in Korea. The effect of 2-BP on spermatogenesis, or Leydig cells, has not been determined in adult rats. In the present study, 40 ten-week-old Sprague-Dawley (SD) rats were treated orally with 3.5 g/kg/d of 2-BP for 3 consecutive days. At 1, 3, 5, 7, 14, 28, 42, and 70 d after treatment, testes were perfused with Karnovsky's solution or immersed in Bouin's solution, embedded in plastic or Epon and evaluated with light and electron microscopy. DNA ploidy distributions of testicular suspensions were determined by flow cytometry, which allowed comparison of quantitative spermatogenesis with histopathologic observations. Degeneration of spermatogonia was observed during Stages I-IV in seminiferous tubules on Day 1 after treatment. Spermatocytes, spermatids, Sertoli cells, and Leydig cells appeared normal in the early stage of the study. Whereas spermatid retention in Stages IX-XI was observed on Day 7 after treatment, depletion of spermatocytes and spermatids continued over time, followed by a marked increase of germ cells on Day 42 after treatment. However, the seminiferous tubules did not completely recover by study termination. Leydig cell cellularity increased mildly without any significant morphologic modification at the end of the study. Immunohistochemistry using an antibody against proliferating cell nuclear antigen (PCNA), showed an increased number of immunoreactive Leydig cells in the interstitium. In the flow cytometry analysis, proportions of diploid and tetraploid cells gradually decreased time-dependently until Day 28 after treatment, but showed an increase on Day 42, followed by a decrease on Day 70 after treatment. These data are strengthened by qualitative descriptions of lesions observed by histopathology. These results suggest that a high dose of 2-BP can decrease spermatogenesis by adversely affecting spermatogonia followed by depletion of spermatocytes, spermatids, and spermatozoa, with subsequent testicular atrophy. The atrophied testes may not regenerate completely. The number of Leydig cells may increase mildly with 10 weeks of recovery.

Animals↗
PubMedDate not supplied

Effects of transferrin on the modulation of cytokine production on mouse spleen cells.

In order to investigate the the effects of transferrin(Tf) on the production of cytokines, mouse spleen cells were treated with various concentrations of apo- and holo-Tf, and then the production of IL-6, IFN gamma and the expression of mRNA for TNF alpha was determined. The distribution of Tf, macrophages and T cells in the mouse mammary glands was also examined. IL-6 and IFN gamma producing capabilities of the unstimulated spleen cells in the presence of apo and holo-Tf were increased in a dose dependent manner, while the cells stimulated with anti-CD3 had no significant effects on production in thd presence of graded concentrations of Tf. The relative abundance of TNF alpha mRNA was significantly affected by the concentration of TF. During early involution almost all of the secretory epithelial cells and the secretion in the alveoli showed a very strong positive reaction to transferrin antibody, and macrophages and T cells were distributed in the lumen, alveolar epithelial layer and connective tissue area. These findings suggest that the upregulated patterns of these cytokines and distribution of immune cells may play a beneficial role in the augmentation of host's defense mechanisms during involution.

Animals↗