21 research outputs found
Studies on hepatotoxicity induced by chlorinated hydrocarbons. II. Lipid metabolism and absorption spectrum of microsomal lipid in the mice exposed to 1, 1, 2, 2-tetrachloroethane
Female Cb mice weighing 20-23 g were exposed to 800 ppm (in average) of 1, I, 2, 2.tetrachloroethane for 3 hours. Both triglyceride and phospholipid in the liver and plasma were determined at varying times after the exposure. On the other hand, there were observed the ultraviolet
absorption spectra of microwmallipids in the liver at 90 minutes after the 1, 1,2, 2-tetrachloroethane or the carbon tetrachloride exposure. The results thus obtained are summarized as follows: 1. The increase of hepatic triglyceride contents attained the maximum level in the period between 20 and 25 hours after the exposure and declined to the initial levels at 90 hours later. 2. The plasma triglyceride levels decreased until 25 hours after the exposure, then tended to increase significantly and were much higher than the control levels in the period between 70 and 90 hours later. 3. Both liver and plasma phospholipid levels decreased gradually up to 25 hours after the exposure, then slowly recovered with almost the same rate of increase. 4. It was suggested that the inhalation of the above vapors induced a little change in microsomal lipids in the liver.</p
Studies on hepatotoxicity induced by chlorinated hydrocarbons. Lipid and ATP metabolisms in the liver of mice exposed to 1,1,2,2-tetrachloroethane
With a constant gas-exposure chamber newly devised, the author had Cb mice (females weighing 16.0 ± 1.5 g) inhale 600 ppm (in average) of 1, 1, 2, 2-tetrachloroethane for 3 hours. Then, the total Iipid, triglyceride and ATP levels in the liver were estimated before, immediately after, 4
hours and 8 hours after the exposure. The results of the observations are briefly summarized as follows:
1. It has been demonstrated by the chemical quantitative analyses of total lipid and others that the exposure to 1, 1,2, 2-tetrachloroethane induces fatty liver in mice.
2. Both total lipid and triglyceride levels increased almost linearly from the time of exposure up to 8 hours later. The ratio, triglyceride: total lipid, increased with lapse of time after the exposure, and of the lipid
components, the increase of triglyceride was marked.
3. The hepatic ATP level decreased almost linearly from the time of exposure to 8 hours later. The value, total lipid × ATP, hardly differed from that of the control even after the exposure, and there was observed a parallel relationship between the rate of increase in total lipid level and the rate of decrease in the hepatic ATP level. 4. The intensity of hepatotoxicity of 1, 1, 2, 2-tetrachloroethane proved to be practically the same at that of carbon tetrachloride.</p
Catalatic activity of immature and mature red blood cells in Japanese acatalasemia (difference between Japanese and Swiss acatalasemia)
We fractionated the red cells of Japanese acatalasemic individuals (four individuals in two families) by SAss's method and counted the number of reticulocytes and determined the catalatic activity by manometric and perborate methods on each fraction containing reticulocytes in the descending order from the upper to the lower layers. We also incubated
each of these fractions at 37°C for 4, 10,24 and 48 hours, to see the catalatic activity along with the maturation of reticulocytes. Heat stability of
catalatic fraction separated by DEAE column was also examined. The results of the study may briefly be summarized as follows. 1. a. There was no parallel relationship between the number of reticulocytes and the catalatic activity in Japanese acatalasemic red cells.
b. There could be seen no decrease in catalatic activity while the number of reticulocytes did decrease by the incubation. 2. Heat stability of crude catalatic fraction from acatalasemic blood is approximately the same as that of crude catalase fraction from normal blood.</p
Metabolism of 14 C-iodochlorohydroxyquinoline (chinoform) in mice
In order to know the organ distribution of Chinoform, I4C.Chinoform was injected into the tail vein of the mice, and radioactivity was measured in the chloroform soluble fractions in some organs and tissues containing non.conjugated Chinoform. The results obtained are as follows. 1. Uptake of Chinoform by the visceral organs was found to be in the following ascending order: fat tissue, kidney, spleen, liver, small intestine, (blood), muscle and eye, and marked uptake by the fat tissue and kidney was observed. 2. The presence of radioactive Chinoform in the chloroform soluble fraction of the central nervous system was recognized and it was almost in the same degree of specific radioactivity as that of blood. 3. A higher uptake in the chloroform soluble fraction of the sciatic nerve than that of central nervous system was recognized, and the value of the former was about 3 to 8 times as high as that of the latter. 4. The presence of Chinoform in the chroloform soluble fraction of the bile, although it increased after incu bation of the bile with j9-glucuro.
nidase was observed. High radiogctivity of chinoform in the total fraction of the bile suggests a possible presence of "liver-intestine-circulation" of
the drug.</p
Studies on hepatotoxicity induced by chlorinated hydrocarbons. Lipid and ATP metabolisms in the liver of mice exposed to 1,1,2,2-tetrachloroethane
With a constant gas-exposure chamber newly devised, the author had Cb mice (females weighing 16.0 ± 1.5 g) inhale 600 ppm (in average) of 1, 1, 2, 2-tetrachloroethane for 3 hours. Then, the total Iipid, triglyceride and ATP levels in the liver were estimated before, immediately after, 4
hours and 8 hours after the exposure. The results of the observations are briefly summarized as follows:
1. It has been demonstrated by the chemical quantitative analyses of total lipid and others that the exposure to 1, 1,2, 2-tetrachloroethane induces fatty liver in mice.
2. Both total lipid and triglyceride levels increased almost linearly from the time of exposure up to 8 hours later. The ratio, triglyceride: total lipid, increased with lapse of time after the exposure, and of the lipid
components, the increase of triglyceride was marked.
3. The hepatic ATP level decreased almost linearly from the time of exposure to 8 hours later. The value, total lipid × ATP, hardly differed from that of the control even after the exposure, and there was observed a parallel relationship between the rate of increase in total lipid level and the rate of decrease in the hepatic ATP level. 4. The intensity of hepatotoxicity of 1, 1, 2, 2-tetrachloroethane proved to be practically the same at that of carbon tetrachloride.</p