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Biomedical subjects

M Sagai

Publications and source records attributed to M Sagai.

At least 91 records · Page 5Linked to original sources
PubMed1984

Studies on the biochemical effects of nitrogen dioxide. IV. Relation between the change of lipid peroxidation and the antioxidative protective system in rat lungs upon life span exposure to low levels of NO2.

This study examined the relation between lipid peroxidation and the antioxidative protective system in lungs of rats exposed to low levels of nitrogen dioxide (NO2). JCL:male Wistar rats were exposed to 0, 0.04, 0.4, and 4 ppm NO2 for 9, 18, and 27 months. Lipid peroxidation measured by TBA method, increased significantly in the 4 ppm NO2 group of the 9-month exposure and in the 0.4 and 4 ppm NO2 groups of the 18-month exposure. The activity of glutathione peroxidase measured with hydrogen peroxide as substrate decreased significantly in the 4 ppm NO2 group of the 9-month exposure and in the 0.4 and 4 ppm NO2 groups of the 18-month exposure. Furthermore, the activities of two glutathione S-transferases, aryl and aralkyl S-transferase, also decreased in the 0.4 and 4 ppm NO2 groups of the 18-month exposure, but not in any groups of the 9-month exposure. The activity of glutathione peroxidase measured with cumene hydroperoxide as substrate did not show any significant changes in any NO2 group. The activities of glucose-6-phosphate dehydrogenase and glutathione reductase were significantly higher than those in the control group for the 9-month exposure. In the 18-month exposure, however, they showed a tendency to return to control level. The activities of superoxide dismutase and disulfide reductase upon NO2 exposure for 9 and 18 months were not different from control values. To confirm that lipid peroxidation was increased with greater NO2 concentrations and exposure times, ethane and pentane exhalation in breath as an index of lipid peroxidation was examined. Ethane exhalation increased significantly following 0.04, 0.4, and 4 ppm NO2 exposure for 9 and 18 months. Furthermore, ethane formation of rats exposed to 0.04 and 0.4 ppm NO2 for 27 months also increased to twice the control level. On the other hand, after exposure to 4 ppm NO2 for 27 months, ethane levels returned to control level. Pentane formation increased significantly only in the 0.04 and 0.4 ppm groups in the 18-month exposure. Ethane exhalation in rats exposed to 0.04, 0.12, and 0.4 ppm NO2 for 9 and 18 months was similar. These results suggested that the antioxidative protective ability was decreased with prolonged exposure, while formation of cytotoxic lipid peroxides was increased.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

Relationship between survival times of rats exposed to lethal level of nitrogen dioxide and arylhydrocarbon hydroxylase activity in lungs.

A previous paper has shown that survival times of rats exposed to lethal levels of NO2 were prolonged by administration of enzyme-inducing agents prior to NO2 exposure, and that the survival time of female rats was longer than that of male rats. In order to investigate a mechanism on prolongation of survival times by administration of enzyme-inducing agents and on sex-difference, a relationship between survival times and microsomal enzyme activity in lungs of rats administered enzyme-inducing agents was examined. The survival times of rats exposed to 65 ppm NO2 were prolonged with increase of 3MC doses, and AHH activity in lungs of rats rose with increase of 3MC doses. A significant correlation between the survival time and AHH activity was observed. Induction of AHH activity of female rats administered 3MC was higher than that of male rats. NADPH-dependent cytochrome c reductase activity in lungs of male and female rats did not change with 3MC administration, and a significant relationship between the survival time and NADPH-dependent cytochrome c reductase activity was not observed. These results suggest that cytochrome P1-450 system in lung microsomes may have protective action against the toxicity of NO2.

Animals↗
PubMed1982

Biochemical studies on strain differences of mice in the susceptibility to nitrogen dioxide.

Strain differences of mice in their susceptibility to nitrogen dioxide (NO2) were examined by measuring the activities of antioxidative protective enzymes, and the amounts of antioxidants and lipid peroxides in lungs. Four strains of mice: ICR, BALB/c, ddy and C57BL/6 were used in this study and their LC50 values after exposure to NO2 for 16 hr were: 38, 49, 51 and 64 ppm, respectively (1). Genetic strain differences were observed in the enzyme activities, the antioxidant contents and lipid peroxide contents among these four different strains. The activities of glutathione peroxidase (GPX), glutathione S-transferase, and superoxide dismutase (SOD), and the contents of non-protein sulfhydryls (NPSH), alpha-tocopherol (alpha-Toc) and total lipids in lungs of the four strains were related to their LC50, while TBA reactants in lungs of the four strains were inversely related to their LC50. After exposure to 20 ppm NO2 for 16 hr, the activities of the protective enzymes and the contents of NPSH decreased, while the level of alpha-Toc increased markedly. The activities of GPX, 6-phosphogluconate dehydrogenase, SOD and disulfide reductase, and the contents of NPSH, alpha-Toc and total lipids were also related to their LC50. On the other hand, TBA reactants increased higher than those of the control groups and were inversely related to their LC50. These results suggest that the protective enzymes and the antioxidants are important factors at defence mechanism in lungs to NO2 and that the intensity of the protective systems in pigmented strains is generally greater than that in albino strains.

Animals↗
PubMed1982

Changes of gaseous exchange in the lungs of mice exposed to nitrogen dioxide and their recovery process.

To elucidate the accurate effects of NO2 on gaseous exchange in the lungs of mice during and after NO2 exposure, O2 and CO2 concentrations in the respiratory gas and respiratory rate (RR) were measured using the head-enclosed method, and arterial blood pHa, Paco2 and Pao2, lung wet weight, and lung water content were also examined. The results of the present study indicate that the gaseous exchange in the lungs of mice exposed to 20 ppm NO2 was acutely inhibited during NO2 exposure from the 3rd to 24th h, but it recovered functionally to the control level on the 3rd day after NO2 exposure.

Animals↗
PubMed1982

Studies on biochemical effects of nitrogen dioxide. II. Changes of the protective systems in rat lungs and of lipid peroxidation by acute exposure.

This work was done to clarify the relation between the change of lipid peroxidation and the protective systems in lungs after NO2 exposures. JCL:Wistar 8-wk-old male rats were exposed continuously to 10 ppm NO2 for 2 wk. Lipid peroxidation, measured by ethane exhalation in the breath of the rats and by the reaction of thiobarbituric acid with lung homogenates, increased to a maximum at 3 d after a decline at 1 d, and then returned to the initial level (of d 0). Activities of glutathione peroxidase (GPx), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), disulfide reductase (DSR), and superoxide dismutase (SOD) in the 105,000 X g supernatant of lung homogenates were depressed slightly at 1 d. Thereafter, they increased significantly to their maximum levels from 5 to 10 d, and these maximum levels were maintained until d 14. The pattern of change of these protective enzymes was symmetric to that of lipid peroxidation after 3 d. The order of the ratio of the increased value to the initial value was G6PD greater than DSR greater than 6PGD greater than GR greater than GPx greater than SOD. The time course of nonprotein sulfhydryls was similar to that of the protective enzymes. In contrast, the amounts of vitamin E increased to a maximum at 2 d and then returned to the initial level. The periodic change of vitamin E was similar to that of lipid peroxidation rather than that of the protective enzymes. These results suggest that the ability of the enzyme systems in lungs to protect against NO2 fluctuated in a complex manner and the activities of the protective enzymes varied inversely with lipid peroxidation.

Animals↗
PubMed1981

Studies on biochemical effects of nitrogen dioxide: I. Lipid peroxidation as measured by ethane exhalation of rats exposed to nitrogen dioxide.

This research was in order to follow the periodic fluctuation of lipid peroxidation by a new method in rats exposed to nitrogen dioxide. Wistar male rats were examined for lipid peroxidation as demonstrated by ethane exhalation. In rats continuously exposed to 10 ppm nitrogen dioxide for 2 weeks, the amount of ethane exhaled fluctuated in a complex manner during the exposure. Ethane exhalation decreased slightly after the first day of exposure and then increased rapidly. The maximal values were observed after the fourth day of exposure and then decreased gradually to the initial level. Furthermore, the activity of glutathione peroxidase in lungs of rats exposed to 10 ppm nitrogen dioxide varied symmetrically against the change of ethane formation. Similar changes in ethane exhalation were observed in rats exposed to the lowest levels of nitrogen dioxide (0.4, 1.2 and 4.0 ppm) for 4 months. Compared to 10 ppm nitrogen dioxide exposure for 14 days, the characteristics in rats exposed to the low levels (0.4-4.0 ppm) of nitrogen dioxide were: the decline of ethane formation, the delay in alterations, and the tendency toward gradual increase during the longer period exposure.

Animals↗
PubMed1980

Respiratory pentane: a measure of in vivo lipid peroxidation applied to rats fed diets varying in polyunsaturated fats, vitamin E, and selenium and exposed to nitrogen dioxide.

Pentane is one decomposition product of omega 6-unsaturated lipid hydroperoxides. The measurement of respiratory pentane is one of the most sensitive in vivo tests of lipid peroxidation. This measurement was applied to test the ability of a low level, short-term exposure of rats of nitrogen dioxide to induce lipid peroxidation. When exposed to 4.48 ppm nitrogen dioxide for 60 min, no increase in pentane production was detected. For 10 weeks prior to exposure, the rats were fed Torula yeast-based diets with 10% stripped lard or 10% stripped corn oil. The ratios of basal pentane production by rats fed the following antioxidants were for corn oil- and lard-fed rats, respectively: 40 I.U. vitamin E/kg and 0 selenium: 0 vitamin E and 0.1 ppm selenium: 0 vitamin E and 0 selenium, 1:2.2:5.8 and 1:1.9:3.5. Pentane production was significantly (P<0.05) greater by corn oil-fed rats than by lard-fed rats only when both vitamin E and selenium were absent from the diet.

Animals↗