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Biomedical subjects

T Kanazawa

Publications and source records attributed to T Kanazawa.

At least 91 records · Page 5Linked to original sources

[Continuous infusion high-dose leucovorin with cisplatin and 5-fluorouracil for a recurrent oropharynx carcinoma].

Cisplatin and leucovorin heighten the activity of 5-fluorouracil by increasing the intracellular concentration of reduced folates. Therefore, we treated the recurrent oropharynx carcinoma case, who had received concurrent chemotherapy with low-dose cisplatin and radiotherapy, with continuous infusion high-dose leucovorin with cisplatin and 5-fluorouracil. Chemotherapy included continuous intravenous infusion of cisplatin (25 mg/m2, days 1 through 5); 5-fluorouracil (600 mg/m2, days 2 through 6); and leucovorin (200 mg/m2, days 1 through 6) administered once about every 4 weeks. Three cycles were performed, and a complete response was achieved. Grade 3 to 4 mucositis, nausea-vomiting, anemia, neutropenia, and thrombocytopenia occurred. Continuous infusion high-dose leucovorin with cisplatin and 5-fluorouracil was effective for this recurrent head and neck carcinoma. However, one must be cautious when comparing this chemotherapy in terms of toxicity.

Antineoplastic Combined Chemotherapy Protocols↗

[Successful aortic root replacement with pulmonary autograft (Ross) in two cases of congenital aortic stenosis].

Two cases of 7 and 23 year of age with congenital aortic stenosis associated with the small valve annulus underwent successful aortic root replacement with pulmonary autograft (Ross procedure). Preoperative pressure gradient and the valve size were 120 and 80 mmHg, and 16 and 18 mm, respectively. Even with the small native aortic annulus, pulmonary autografts could be implanted to aortic annulus without autograft distortion by the method of total aortic replacement. The right ventricular outflow reconstruction was performed with PTFE-valved bovine pericardial conduit with securing the posterior muscular edge by a strip of autologous aortic wall. Postoperative course in both patients was uneventful without any rhythm disturbances. During the 12 and 14 months of follow-up, both patients were in excellent clinical condition with no evidence of autograft valve regurgitation and functional deterioration of valved conduit. This procedure was thought to be a preferable method of young cases with congenital aortic stenosis.

Adult↗

[Appropriate early open heart palliation of univentricular atrioventricular connection with subaortic stenosis].

Long-term conventional pulmonary artery banding deteriorates ventricular function in patients who have univentricular atrioventricular connection with subaortic obstruction. Protection of the pulmonary vascular bed and early relief of subaortic stenosis is essential to improve the outcome after Fontan operation. From January 1995 through January 1996, three infants underwent open heart palliation because of univentricular atrioventricular connection with subaortic stenosis. All infants had discordant ventriculoarterial connection. One infant underwent the Norwood procedure (patient 1). Two infants underwent palliative arterial switch operation, one with repair of aortic arch and a Blalock-Taussig shunt (patient 2) and the other with endoluminal pulmonary artery banding (patient 3). Patient 3 required a subsequent conventional pulmonary arterial banding. The postoperative recovery period were smooth in the all infants. All infants kept sufficient PO2 ranging from 34 to 37 mmHg postoperatively. On follow-up after 16 months pulmonary artery index decreased in patient 1. On the other hand, angiogram demonstrated satisfactory pulmonary arterial growth in patient 2. There were two late death, occurring in patient 1 (sudden death) and patient 3 (pneumonia). Patient 2 awaits a Fontan type procedure. It is difficult to adjust appropriate blood flow through a Blalock-Taussing shunt and a surgically isolated pulmonary artery is capable of inducing pulmonary distortion after Damus-Norwoood type operation. Whereas natural regulation of the pulmonary arterial blood flow by a restrictive ventricular outflow tract is come up after a palliative arterial switch operation. Palliative arterial switch operation is an useful alternative open heart palliation for neonates and early infants who had univentricular atrioventricular connection with subaortic stenosis.

Aortic Valve Stenosis↗

Identification of arginyl residues located at the ATP binding site of sarcoplasmic reticulum Ca2+-ATPase. Modification with 1,2-cyclohexanedione.

Sarcoplasmic reticulum vesicles were treated with 1, 2-cyclohexanedione (CHD) in sodium borate (pH 8.0). The Ca2+-ATPase activity was completely inhibited. Inhibition of Mg.ATP and Mg.ADP binding to the high affinity ATP binding site as well as inhibition of phosphorylation with ATP occurred simultaneously with the inhibition of the Ca2+-ATPase activity. Phosphorylation with acetyl phosphate was not inhibited. The Ca2+-ATPase was strongly protected by Mg.ATP, Mg.ADP, and Mg.AMP against this inhibition. Binding of acetyl phosphate or Pi to the enzyme gave no protection. Phosphorylation with acetyl phosphate also had no protective effect. Peptide mapping of the tryptic digests, detection of peptides containing CHD-modified arginyl residues with Girard's reagent T, and sequencing revealed that Arg-489, Arg-505, and Arg-678 were modified with CHD. Arg-489 and Arg-678 were almost completely protected by Mg.ATP against this modification, but partially protected by prelabeling with fluorescein 5-isothiocyanate, which occupies the adenosine binding region in the ATP binding site. In contrast, Arg-505 was slightly protected by Mg.ATP and almost completely protected by prelabeling with fluorescein 5-isothiocyanate. Taken together, these findings suggest that Arg-489 and Arg-678 are located in or near the region occupied by the triphosphate moiety of ATP, either or both of these residues being in or close to the region occupied by the alpha-phosphoryl group in the high affinity ATP binding site and involved in the CHD-induced inhibition of this enzyme and that Arg-505 is very close to (but slightly out of) the adenosine binding region in the ATP binding site. The acetyl phosphatase activity and phosphorylation with Pi were also inhibited by the CHD treatment, but the inhibitions were considerably slower than those described above. This suggests that the arginyl residues involved in these inhibitions are distinct from that involved in the inhibition of the Ca2+-ATPase activity.

Adenosine Triphosphate↗

Reduction in water activity greatly retards the phosphoryl transfer from ATP to enzyme protein in the catalytic cycle of sarcoplasmic reticulum Ca2+-ATPase.

Cys-674 of the sarcoplasmic reticulum Ca2+-ATPase was labeled with N-acetyl-N'-(5-sulfo-1-naphthyl)ethylenediamine without a loss of the catalytic activity. The ATP-induced drop in the fluorescence of the label, which was shown in our previous studies to reflect the conformational change upon formation of the calcium.enzyme.ATP complex, was followed by the stopped-flow method. The subsequent phosphoenzyme formation was followed by the rapid quenching method. Effects of a partial substitution of organic solvents for water in the medium on the conformational change and phosphoenzyme formation were investigated in the presence of 100 microM CaCl2 at pH 7.5, 0 degrees C. The rate of the conformational change increased with increasing ATP concentration (0.1 100 microM) and was unaffected by 30% (v/v) dimethyl sulfoxide. In contrast, the rate of phosphoenzyme formation decreased sharply with increasing concentration of dimethyl sulfoxide (20-40% (v/v)), even when phosphoenzyme formation was saturated with ATP. N,N-Dimethylformamide and glycerol had essentially the same effects as dimethyl sulfoxide. These results show that the reduction in water activity does not affect the rate of the conformational change upon formation of the calcium.enzyme.ATP complex, but greatly retards the subsequent phosphoryl transfer from ATP to the enzyme protein. This strongly suggests that in this early stage of the catalytic cycle water plays a critical role in ensuring the rapid turnover of the enzyme.

Adenosine Triphosphate↗

Hypoxanthine: a low molecular weight factor essential for growth of erythrocytic Plasmodium falciparum in a serum-free medium.

A low molecular weight factor in a basal medium essential for erythrocytic Plasmodium falciparum development in a serum-free medium using a cell growth-promoting factor derived from adult bovine serum was detected. The factor was hypoxanthine. The optimal hypoxanthine concentration for parasite growth was between 15 and 120 microM. The contribution of hypoxanthine to increased parasite growth was clearly evident in cultures on day 4. Among various low molecular weight supplements tested, adenine, adenosine, AMP, ATP, cyclic AMP, guanine, guanosine, inosine, inosine monophosphate, xanthine, NAD, NADH, NADP, NADPH and deoxyguanosine triphosphate showed a similar effect to that of hypoxanthine in the serum-free culture system. On the other hand, the addition of uric acid, FAD, thymidine, uridine, orotic acid, deoxythymidine triphosphate, deoxycytidine triphosphate, deoxyadenosine triphosphate, ribose-1-phosphate, or ethanolamine was not beneficial to the parasite growth. The results presented here will not only be of practical value, but will provide important information about the developmental requirements of the parasite.

Animals↗

Chemical characterization of peroxidized low-density lipoprotein in plasma and aortic atheroma.

Hydroperoxidized cholesteryl linoleate (HPO-CL, spot X1) was produced by peroxidation of normal LDL isolated from plasma of healthy persons. Spot X stained on thin-layer chromatography plate (silica 60) between triglycerides and free fatty acids. The solvent mixture used consisted of petroleum ether 75, ethyl ether 25, and acetic acid 1. Spot X1 of plasma from healthy subjects stained slightly. It was also identified in plasma LDL of patients with atherosclerotic diseases, and in total lipids extracted from aortic atheroma obtained at autopsy. Whereas spot X1 obtained from plasma LDL of patients with atherosclerotic diseases consisted of HPO-CL, spot X1 obtained from aortic atheroma was reduced HPO-CL (hydroxide CL). Spot X1 of obtained from aortic atheroma was reduced HPO-CL (hydroxide CL). Spot X1 of aortic atheroma did not react to p-methoxydiphenylpyrenylphosphine (MP3)-an agent which shows only positive reaction to hydroperoxide chemical structures-although spot X1 of plasma LDL from atherosclerotic diseases reacted positively to MP3. Moreover, spot X1 obtained from aortic atheroma showed the same Rf value as that of the reduced HPO-CL. The IR profile of spot X1 obtained from aortic atheroma was similar to that of hydroxide CL, although the IR profiled HPO-CL was similar to that obtained from plasma LDL of atherosclerotic patients. In addition, HPO-CL was not recognized in the LDL fraction with clathrin-coated pits from aortic atheroma.

Adult↗

Peroxidized low-density lipoprotein with four kinds of hydroperoxidized cholesteryl linoleate estimated in plasma of young heavy smokers.

AIM: To clarify the mechanisms of vascular complications due to heavy smoking, it was studied whether hydroperoxidized low-density lipoprotein (HPO-LDL) was estimated in plasma of young heavy smokers. METHOD: Plasmas were separated from 15 young male students (HS-M) who smoked more than 30 cigarettes/day over 5 years, and from 10 nonsmoker students (NS-M) too. LDL was isolated by ultracentrifugation. HPO-cholesteryl linoleate (HPO-CL) was identified by thin-layer chromatography (TLC), and lipid peroxide was measured by Determiner LPO (Kyowa Medics Co., Ltd, Tokyo, Japan). The molecular structure of lipid peroxide in LDL was identified using GMS analysis, HPLC chromatography and 1H-NMR analysis. RESULTS: (1) HPO-CL was clearly observed on the TLC in LDL lipids of HS-M but from NS-M it was barely found. (2) Lipid peroxide in LDL separated from HS-M consisted of HPO-CL and reduced HPO-CL. CONCLUSION: Peroxidized LDL was estimated in plasma with young heavy smokers. Because of injurious reactions in vessels of peroxidized LDL, it is considered that heavy smoking is one of the risk factors for vascular complications in heavy smokers.

Adult↗

Batroxobin accelerates lipid accumulation of peroxidized low density lipoprotein in mouse peritoneal macrophages.

Mouse peritoneal macrophages were incubated in DMEM medium with batroxobin (DF-521) to determine the effect of batroxobin on the internalization of peroxidized low-density lipoprotein (pox-LDL) by transmission electron microscopy. Although the morphology of the mouse peritoneal macrophages after incubation with DMEM, normal LDL (n-LDL) and n-LDL plus batroxobin was similar to that of the cells before incubation, they exhibited numerous cytoplasmic lipid droplets after incubation with pox-LDL for 4 h. After addition of batroxobin to the medium containing pox-LDL, the production of lipid droplets in the mouse peritoneal macrophages was tremendously accelerated. Batroxobin accelerates the phagocytosis and degradation of pox-LDL by macrophages.

Animals↗

Effect of inferior vena cava occlusion on left ventricular end-systolic pressure-volume relations in intact canine hearts--modulation by the autonomic nervous system.

The effect of inferior vena cava occlusion (IVCO) on end-systolic pressure-volume relations (ESPVR) of the left ventricle was studied in intact canine hearts. In 12 anesthetized open-chest dogs, left ventricular (LV) pressure and volume were measured simultaneously using a microtip catheter and a conductance catheter, respectively. ESPVR was constructed from LV pressure-volume loops during IVCO (10 sec) and subsequent IVCO release under 5 conditions: control, after righ or left cardiac sympathetic nerve (CSN) stimulation, bilateral vagotomy (VAT), and both VAT and bilateral CSN resection. Emax in IVCO release was significantly greater than that in IVCO in the control state. Following right or left CSN stimulation, Emax was increased increased in both IVCO and IVCO release, with the same hysteretic change in Emax. With VAT, however, no hysteretic change was observed because Emax was the same in IVCO and IVCO release. After VAT and CSN resection, Emax was decreased in both IVCO and IVCO release, and again no hysteretic change was observed. These data imply that a sudden decrease in venous return into the heart induces a decrease in afferent vagal nerve activity, and thus increases efferent CSN activity, resulting in enhanced myocardial contractility.

Animals↗

[Autoradiographic studies of oxalate distribution in rat kidney].

BACKGROUND: We performed macro and micro-autoradiographic studies using 14C-oxalate in normal and hyperoxaluric rats in order to elucidate intrarenal distribution of oxalate and to determine where calcium oxalate crystal can be adhere in the kidney. METHODS: Macro and micro-autoradiographic studies of the kidney in normal rats were carried out at intervals of 15, 30 and 90 min after intravenous administration of 14C-oxalate (37 MBq/kg BW). Hyperoxaluria was induced by vitamin B6 deficient diet. The procedure of macro and micro autoradiography is the same as that in normal rat. RESULTS: In normal rats, macroautoradiogram showed that the radioactivity of 14C-oxalate exists in the whole kidney, and microautoradiogram identified this radioactivity mainly in the extraluminal space of renal tubules at 15 min. Macro and micro-autoradiograms taken 90 min after the injection showed practically no radioactivity of 14C-oxalate in the cortex or the medulla, but it was located in the extraluminal space of the papilla. In hyperoxaluric rats, macroautoradiogram showed some spotty accumulations of 14C-oxalate in the inner medulla and papilla. Microautoradiogram revealed that these accumulations are mainly seen in the extraluminal space. CONCLUSION: These results indicate that in normal rats the injected 14C-oxalate remains in the renal papilla, especially in the extraluminal space, when nearly all oxalate was excreted by urine, and in hyperoxaluric rats 14C-oxalate exists there as calcium oxalate crystal or microlith.

Animals↗

[The changes of blood gas analysis values and platelet aggregability on acute phase in the experimental model of pulmonary embolism prepared by sephadex G-75 (SG-75) injection].

To study pathophysiologic phenomena in acute pulmonary embolism, we injected sephadex G-75 (SG-75) into rabbit auricular veins and measured the changes in blood gases and in platelet aggregability. Severe hypoxemia developed within 10 minutes of SG-75 injection. Microscopic examination of samples taken 120 minutes after SG-75 injection pulmonary artery had been embolized by the SG-75 particles, and that thrombin had formed around the particles. The lowest platelet counts were measured 10 minutes after SG-75 injection. The rates of platelet aggregation induced by adenosine diphosphate and by platelet-activating factor were abnormally low until 40 minutes after SG-75 injection. These results suggest that platelets were activated by anoxia and that the activated platelets moved around the emboli after obstruction of the pulmonary artery. We conclude that decreases in PaO2 and changes in platelet aggregability exacerbate the pathophysiologic processes in acute pulmonary embolism.

Acute-Phase Reaction↗

Sodium ionophore converts growth manner of vascular smooth muscle cells from spontaneously hypertensive rats.

OBJECTIVES: Vasoconstrictor peptides such as endothelin (ET) cause hypertrophy of vascular smooth muscle cells (VSMC) in Wistar Kyoto rats (WKY) and hyperplasia in spontaneously hypertensive rats (SHR). They also induce an increase in Na+ concentration ([Na+]i) and activate protein kinase C (PKC) independently. Therefore, we tested the hypothesis that the increase in [Na+]i may be involved in the conversion of growth manner under activated PKC in SHR VSMC. METHODS AND RESULTS: 10(-7) M phorbol ester (TPA) increased the diameter and protein content of VSMC from both strains under 18% serum conditions. Further addition of 10(-6) M gramicidin (Na+ ionophore) converted TPA-induced hypertrophy to hyperplasia, which was due to the quick transition from S to G2/M phase, only in SHR VSMC. Western blot analysis showed that serum- and TPA-induced tyrosine phosphorylation of mitogen-activated protein (MAP) kinase was potentiated by 10(-6) M gramicidin in SHR. [Na+]i, which was measured by sodium-binding benzofuran isophthalate (SBFI), was increased about 35 mM by 10(-6) M gramicidin in both strains, but TPA did not affect basal [Na+]i and the gramicidin-induced increase in [Na+]i. CONCLUSIONS: We conclude that sodium ionophore may convert hypertrophy to hyperplasia synergistically with activated PKC in SHR VSMC, possibly by MAP kinase phosphorylation.

Animals↗

Effects of the new class I antiarrhythmic agent Ro 22-9194, (2R)-2-amino-N-(2,6-dimethylphenyl)-N-[3-(3-pyridyl)propyl]propionamide D-tartrate, on ischemia- and reperfusion-induced arrhythmias in dogs: involvement of thromboxane A2 synthase inhibitory activity.

We investigated the effects of (2R)-2-amino-N-(2,6-dimethylphenyl)-N-[3-(3-pyridyl)propyl]propionamide D-tartrate (Ro 22-9194), a novel class I antiarrhythmic agent, on myocardial ischemia- and reperfusion-induced arrhythmias in dogs. The incidence of ventricular fibrillation induced by reperfusion after a 30-min coronary ligation was significantly reduced by an i.v. infusion of Ro 22-9194 (10 mg/kg for 5 min before and an additional 20 mg/kg for 30 min during coronary ligation: total, 30 mg/kg) from 73% in the vehicle-treated group to 13%. Ro 22-9194 (20 and 30 mg/kg) also dose-dependently reduced the incidence of ventricular arrhythmias, including ventricular tachycardia and ventricular fibrillation, after coronary reperfusion. Other class I antiarrhythmic agents, mexiletine (15 mg/kg) and disopyramide (7.5 mg/kg), did not inhibit the development of ventricular fibrillation. In in vitro studies, Ro 22-9194, but neither mexiletine nor disopyramide (approximately 10(-3) M), inhibited thromboxane A2 synthase and arachidonic acid-induced aggregation of human platelets (IC50: 1.2 x 10(-5) M and 3.4 x 10(-5) M, respectively). Furthermore, Ro 22-9194 (30 mg/kg) attenuated the increase in venous thromboxane B2 concentrations in the local coronary vein during coronary ligation in dogs. A thromboxane A2 synthase inhibitor, OKY-046 (2.5 mg/kg administered for 5 min before coronary ligation) also showed no evident increases in thromboxane B2 concentrations as well as an antifibrillatory effect. Venous 6-keto-prostaglandin F1 alpha concentrations were not affected by either Ro 22-9194 or OKY-046. These results demonstrate that, unlike mexiletine and disopyramide, Ro 22-9194 protects against reperfusion-induced fatal ventricular arrhythmias in dogs. They also suggest that, in addition to the class I antiarrhythmic effect, the thromboxane A2 synthase inhibitory activity may contribute to the antiarrhythmic properties of Ro 22-9194.

6-Ketoprostaglandin F1 alpha↗

The tryptophan fluorescence change upon conformational transition of the phosphoenzyme intermediate in sarcoplasmic reticulum Ca(2+)-ATPase is revealed in the absence of K+ and the presence of lasalocid.

ATP-induced changes in the tryptophan fluorescence of the Ca(2+)-ATPase were determined with sarcoplasmic reticulum vesicles at pH 7.0 and 0 degrees C by steady-state measurements in the presence of Ca2+ and the absence of K+ with and without added lasalocid (a carboxylic ionophore, 50 microM), which was previously shown to cause a predominant accumulation of the ADP-insensitive form of the phosphoenzyme intermediate (EP) (Kawashima, T., Hara, H., and Kanazawa, T. (1990) J. Biol. Chem. 265, 10993-10999). When ATP was added in the absence of lasalocid, the fluorescence decreased by 1.7%. The addition of lasalocid quenched 71% of the fluorescence but did not reduce the ATP-induced fluorescence drop. The fluorescence drop and the EP formation were also determined in the presence of lasalocid by stopped-flow spectrometry and continuous-flow rapid quenching. The observed fluorescence drop was biphasic. The first phase coincided with the formation of EP, which was largely ADP-sensitive in this early stage of the reaction. The second phase was much slower than the first phase and coincided with the accumulation of ADP-insensitive EP. When the transition of EP from the ADP-sensitive form to the ADP-insensitive form was blocked by N-ethylmaleimide treatment, the second phase disappeared, and the fluorescence drop entirely coincided with the formation of ADP-sensitive EP. These findings demonstrate that the first phase of the fluorescence drop is attributed to the formation of ADP-sensitive EP, the second phase being attributed to the transition of EP from the ADP-sensitive form to the ADP-insensitive form. The present results reveal the conditions that definitely discriminate these two phases.

Adenosine Triphosphate↗

Malignant insulinoma causing liver metastasis 8 years after the initial surgery: report of a case.

We report herein a rare case of malignant insulinoma which recurred as multiple liver metastasis 8 years after the initial resection. The patient was a 51-year-old Japanese man who originally presented in 1985 at the age of 43 years suffering from general malaise and syncope. The initial surgery in 1985 involved complete enucleation of a 15 x 13 mm insulinoma located in the uncus of the pancreas. Histopathologically, the tumor was diagnosed as a benign adenoma (insulinoma) which was immunohistochemically stained with only the anti-insulin monoclonal antibody. Macroscopically, there were no signs of either invasion or metastasis. During the subsequent 7 years, he did not show any symptoms or significant abnormality in laboratory data. However, in 1993, the patient again experienced syncope with hypoglycemia and hyperinsulinemia. Ultrasonography revealed multiple echogenic lesions in the liver and a second laparotomy confirmed multiple hepatic metastases from insulinoma, the histopathological findings of which were similar to those of the primary tumor from 8 years before. The patient is currently being treated with streptozotocin and 5-fluorouracil via a catheter in the hepatic artery.

Humans↗

Fluorometric study on conformational changes in the catalytic cycle of sarcoplasmic reticulum Ca(2+)-ATPase.

Changes in the fluorescence of N-acetyl-N'-(5-sulfo-1-naphthyl)ethylenediamine (EDANS), being attached to Cys-674 of sarcoplasmic reticulum Ca(2+)-ATPase without affecting the catalytic activity, as well as changes in the intrinsic tryptophan fluorescence were followed throughout the catalytic cycle by the steady-state measurements and the stopped-flow spectrofluorometry. EDANS-fluorescence changes reflect conformational changes near the ATP binding site in the cytoplasmic domain, while tryptophan-fluorescence changes most probably reflect conformational changes in or near the transmembrane domain in which the Ca2+ binding sites are located. Formation of the phosphoenzyme intermediates (EP) was also followed by the continuous flow-rapid quenching method. The kinetic analysis of EDANS-fluorescence changes and EP formation revealed that, when ATP is added to the calcium-activated enzyme, conformational changes in the ATP binding site occur in three successive reaction steps; conformational change in the calcium.enzyme.substrate complex, formation of ADP-sensitive EP, and transition of ADP-sensitive EP to ADP-insensitive EP. In contrast, the ATP-induced tryptophan-fluorescence changes occur only in the latter two steps. Thus, we conclude that conformational changes in the ATP binding site in the cytoplasmic domain are transmitted to the Ca(2+)-binding sites in the transmembrane domain in these latter two steps.

Animals↗

Protective effects of soy protein on the peroxidizability of lipoproteins in cerebrovascular diseases.

To study the mechanism of dyslipoproteinemia, lipoproteins [very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL)] were isolated from stroke patients and healthy persons by ultracentrifugation. Lipoproteins were dialyzed into copper dichloride solution to study the effects of soycreme administration on lipoprotein peroxidation. Blood was drawn from 15 patients with cerebral thrombosis who were not administered soycreme, 10 patients with cerebral thrombosis who were administered soycreme and 11 healthy persons. The lipoproteins were dialyzed into 5 mol/l copper dichloride solution for various lengths of time, and then lipid constituents in the lipoproteins were measured by thin-layer chromatography. After the dialysis, percentages of cholesteryl ester and triglyceride in various lipoproteins decreased significantly (P < 0.05 or 0.01) in both patient groups and in healthy persons. Spot X1 was found between triglyceride and free fatty acid on the thin-layer chromatography, and spot X2 was located between free fatty acid and free cholesterol after dialysis. Spots X1 and X2 reflect lipoprotein peroxidation. Percentages of these spots were higher in VLDL, LDL and HDL in the patient groups than in the healthy subjects. Soycreme administration suppressed the appearance of spots X1 and X2. Furthermore, blood cholesterol concentrations were reduced by the administration of soy protein. Thus, soy may be useful in the prevention and/or treatment of atherosclerosis.

Adult↗