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Biomedical subjects

T Meguro

Publications and source records attributed to T Meguro.

At least 109 records · Page 6Linked to original sources

Classification of maximal expiratory flow-volume types observed in non-smoking healthy young subjects.

Pulmonary function tests were performed on 234 healthy non-smoking young subjects (189 males and 45 females free from respiratory and allergic symptoms). Maximal expiratory flow-volume (MEFV) curves were visually classified into five MEFV types: Type A, convex or straight flow changes; types B, C, and D, concave-convex-concave flow changes; and type E, sudden flow-fall and accompanying decreased flow rates at lower lung volumes. The reproducibility of MEFV patterns were shown by one way analysis of variance (ANOVA) of MEFV data obtained from 4 groups each consisting of 3-4 males and representing different MEFV types. Distribution of MEFV types was different between males and females; the rate of type A was higher in females than in males and those of types B and E were higher in males than in females. When analyzed in terms of three fractional flow rates, Fr-75, Fr-50, and Fr-25, these values could also be classified into 5 types similarly to the visual MEFV type analysis. It is concluded that MEFV type analysis is useful in assessing health conditions.

Adult↗

Exhaled metallic mercury in acatalasemic, hypocatalasemic and normal mice injected with mercury (II) chloride.

To clarify the relationship between the catalase activity in mouse organs and the amounts of metallic mercury exhaled, normal, homozygous hypocatalasemic and acatalasemic mice were injected with mercuric chloride. The cumulative amount of metallic mercury exhaled by mice was evidently expressed in the descending order of acatalasemic, hypocatalasemic, and normal mice. Statistically significant differences in the cumulative exhaled metallic mercury levels were observed between acatalasemic and hypocatalasemic mice, between normal and hypocatalasemic mice, and between acatalasemic and normal mice using the method of one way analysis of variance (ANOVA). A linear relationship was obtained through logarithm of catalase activity in the lungs or the blood, and logarithm of the cumulative amount of the exhaled mercury.

Animals↗

Effect of heptachlor on hepatic mitochondrial oxidative phosphorylation in rat.

In a study of the hepatotoxicity of heptachlor (1,4,5,6,7,8,8-heptachlor 3a, 4,7,7 a-tetrahydro-4,7-methanoindene), a major compound of chlordane, the effect of heptachlor on the respiratory activity (oxidative phosphorylation and electron transport) of rat liver mitochondria was investigated. Heptachlor at a final concentration of 50 microM with succinate as substrate decreased the respiratory control index (RCI) due to a marked inhibition of state 3 respiration and a slight inhibition of state 4 respiration. One hundred microM heptachlor with succinate as substrate suppressed the states 3 and 4 respiration almost completely. On the other hand, heptachlor at a final concentration ranging from 50 to 100 microM with beta-hydroxybutylate (beta-HB) slightly decreased the RCI and decreased the RCI hardly at all with ascorbate plus N,N,N',N', -tetramethylphenylene diamine (TMPD) as substrate. Heptachlor at a concentration of 50 microM in the presence of succinate also decreased the ADP/O ratio of mitochondria. The mode of inhibition of succinate oxidation by heptachlor apparently is a noncompetitive inhibition, as shown by Lineweaver-Burk plot.

Animals↗

Methemoglobin formation in the blood of Japanese subjects and mice suffering from acatalasemia in response to methemoglobin inducers.

Hemolysates or erythrocytes prepared from Japanese normal and acatalasemic subjects were exposed to nitrogen monoxide or nitrogen dioxide, and methemoglobin formation was determined. Concentrations of methemoglobin in human and mouse acatalasemic hemolysates exposed to nitrogen monoxide or nitrogen dioxide were higher than those in the normal hemolysates. Results similar to Japanese acatalasemic hemolysates or erythrocytes were obtained with mouse hemolysates or erythrocytes. When acatalasemic mice were exposed to nitrogen monoxide, the methemoglobin concentration in the blood was higher than that in the normal mice. Similar results on methemoglobin formation were obtained after exposing mice to nitrogen dioxide, although the rate of methemoglobin formation was lower in the blood of nitrogen dioxide-exposed mice. The methemoglobin concentration in erythrocytes of acatalasemic mice after the addition of sodium nitrite was higher than that in red cells of normal ones. Methemoglobin concentration in the blood of mice receiving sodium nitrites in vivo was determined, and found that the methemoglobin concentration in the blood of acatalasemic mice was higher than that in the blood of normal ones. These results indicated that the formation of methemoglobin from hemoglobin with nitrogen monoxide, nitrogen dioxide and nitrite ion appears to be controlled by the blood catalase.

Animals↗

Uptake of metallic mercury and mercuric ion by human erythrocytes.

Uptake of metallic mercury (Hg degrees) and mercuric ion (Hg2+) by erythrocytes was studied by incubating erythrocytes with various concentrations of radioactive metallic mercury and mercuric ion in phosphate-buffered saline (pH 6.8) or plasma at 25 degrees C for 30 min. Radioactivity taken up in the cytosol (endsome) and stroma were determined with a gamma scintillation counter. The radioactivity ratio of the mercury recovered in the cytosol fraction to metallic mercury incubated in the saline was significantly higher than the ratio of that to mercuric ion. Similar findings were observed in erythrocytes incubated with metallic mercury and mercuric ion in plasma, although the recovered radioactivity of mercury in the cytosol of erythrocytes incubated with metallic mercury or mercuric ion in plasma was less than that incubated in phosphate-buffered saline. Thus, erythrocytes incubated with metallic mercury took up a larger amount of mercury than those incubated with mercuric ion. Discussion is made on these findings.

Catalase↗

[Stimulative effect of chlordanes on guinea pig polymorphonuclear leukocytes].

To investigate the toxicity of chlordane, an organochlorine insecticide, effects of cis-Chlordane, trans-Chlordane, Heptachlor and Heptachlor epoxide were examined on stimulus responses of guinea pig polymorphonuclear leukocytes (PMNs). Results obtained were as follows. These chlordane-related compounds stimulated superoxide (O2-) generation, altered membrane potential and increased intracellular Ca2+ concentration ((Ca2+]i). As a significant tendency was not found in the stimulating effects of these compounds, the relationship between the effect and molecular structure of these substances remains unknown. Of these response reactions of PMN stimulated by chlordanes, stimulation of O2- generation lagged behind the others. Increase in [Ca2+]i was due to both acceleration of extracellular Ca2+ influx and Ca2+ release from intracellular pool. These results indicate that these chlordane-related compounds stimulate PMN and suggest a causal relationship between the stimulation of O2- generation by these substances and their toxicity.

Animals↗

Effect of aminotriazole on mercury uptake by the fetus of normal and acatalasemic mice exposed to metallic mercury.

Pregnant normal (N) and acatalasemic (A) mice treated with aminotriazole (AT) were exposed to metallic mercury. The mercury contents of the fetus and maternal organs were subsequently determined. The fetal and placental mercury contents were the highest in the AT-treated A mice (A-AT), and the contents decreased in the order of AT-treated N mice (N-AT), non-treated N mice (N-C) and non-treated A mice (A-C). Statistically significant differences in the fetal mercury levels were observed between N-C and A-C, A-C and N-AT, and N-AT and A-AT. The ratios of the mercury concentration in the fetus to that in the maternal blood decreased in the order of A-AT, N-AT, A-C and N-C. The differences in the ratio were significant between these groups. Similar results were obtained when the ratios of the maternal liver level to the maternal blood level or the ratios of the placental level to the maternal blood level were compared. The effect of AT on mercury uptake is remarkable in the fetus of both normal and acatalasemic mice exposed to metallic mercury.

Acatalasia↗

The level and stability of residual catalase in cultured acatalasemic skin fibroblasts.

In an attempt to determine the level and heat stability of residual catalase in somatic cells of acatalasemic Japanese, skin fibroblasts from an acatalasemic subject were cultured, and the catalase activity of the cultured fibroblasts was compared with that of cultured normal fibroblasts. Catalase activity was determined using an oxygen electrode. The residual catalase activity in cultured acatalasemic fibroblasts was 10% of the normal. The heat stability at 55 degrees C of residual catalase in the acatalasemic fibroblasts was similar to that of normal fibroblasts.

Acatalasia↗

Metallic mercury in the arterial blood of normal and acatalasemic mice exposed to metallic mercury vapor.

Concentration of metallic mercury in the arterial blood was higher in acatalasemic mice after exposure to 3.45 mg/m3 for 10 minutes in comparison with normal mice, whereas concentration of mercuric ion was lower in acatalasemic mice than in normal mice. Thus, the ratio of metallic mercury to total mercury in the arterial blood of acatalasemic mice was 5.86 +/- 3.61%, which was statistically significantly higher than the value (1.36 +/- 0.65%) of corresponding normal mice. The mercury concentration and distribution in the brain and liver of acatalasemic mice were higher than those in normal mice. Data indicate that the concentration of metallic mercury in the arterial blood of acatalasemic mice was higher than that of normal mice and that metallic mercury soluble in lipids is likely transferred to the brain and liver from the blood. Conclusively, metallic mercury in the arterial blood is the biologically active form for transferring mercury from blood to organs.

Acatalasia↗