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Biomedical subjects

M Arai

Publications and source records attributed to M Arai.

At least 649 records · Page 36Linked to original sources
PubMed1983

Effect of ethanol administration on the metabolism of ethanol in baboons.

To determine the mechanism whereby alcohol consumption accelerates ethanol metabolism, baboons were fed a diet containing ethanol (50% of calories) or an isocaloric control diet for 2 to 7 years. In alcohol-fed animals, the rate of ethanol metabolism per kilogram of body weight was accelerated by 34% at 50 mM concentrations of blood ethanol and liver size (estimated radiologically) increased by 23%. However, the rate of ethanol metabolism per gram of liver was not significantly increased. There was a 35% decrease in alcohol dehydrogenase (ADH) activity expressed per gram of liver and a 19% decrease per kilogram of body weight. Furthermore, the mitochondrial capacity to handle reducing equivalents was strikingly decreased as assessed by the rate of oxygen consumption at state 3 with glutamate and by the decrease in the activities of NADH and glutamate dehydrogenases. Thus, both factors presumed to be rate limiting for the ADH pathway (ADH activity and NADH reoxidation) were found to be decreased after chronic alcohol feeding. Therefore, even taking the increased liver size into consideration, the ADH pathway could not account for the rate of ethanol metabolism. By contrast, it was found that the activity of the microsomal ethanol-oxidizing system increased significantly after chronic alcohol consumption (by 22% expressed per gram of liver and by 54% expressed per kilogram of body weight). There were no significant changes in the content of cytochrome P-450.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Oxidoreductases↗
PubMed1983

[A study of temperature sensitivity of choriocarcinoma cells in vitro--their cell proliferation and morphology in hyperthermic environment].

The possibility of hyperthermic therapy for choriocarcinoma was fundamentally analyzed in an in vitro study. The temperature sensitivity of choriocarcinoma cells designated GCH-nu-YS clone was examined using a severely controlled temperature gradient incubator (T.G.I.). The cells were placed into an atmosphere at various temperatures (37.0-41.2 degrees C) for about 2 weeks and the inhibitory effect on cell proliferation was chronologically investigated in addition to degenerative changes in cellular morphology. When the temperature was not higher than 39.2 degrees C the proliferation of YS clone was nearly the same as that of the cells cultured at 37.0 degrees C. Proliferation at 39.5-39.6 degrees C, however, was slightly inhibited. And when cultured at over 39.9 degrees C, it was markedly inhibited. Above 40.4 degrees C, cell proliferation was impossible, thus resulting in destruction of the cells. These data suggest that the temperature upper limit for viability (TLV) is approximately 40.4-40.6 degrees C and the temperature upper limit for proliferation (TLP) is approximately 40.1-40.2 degrees C. When Okumura's method of classification according to temperature sensitivity is applied, the choriocarcinoma cells may be regarded as having the characteristics of adenocarcinoma. Morphological findings for cells treated at TLV revealed enlargement of the cytoplasm, an increase in the number of perinuclear granules and the appearance of deformed cells such as bizarre cells.

Cell Survival↗
PubMed1983

Differences in susceptibility to sodium saccharin among various strains of rats and other animal species.

Differences in the susceptibilities to sodium saccharin of the urinary bladder epithelium in various strains of rats and other animal species were examined. In Experiment 1, male ACI, Wistar, F344 and Sprague-Dawley rats were administered 5.0% sodium saccharin in the diet for 52 weeks. Rats were killed after weeks 12, 24, 36 and 52. In ACI rats, sodium saccharin induced not only preneoplastic lesions of the urinary bladder, but also tumors. However, in other strains it did not. The urinary bladder of ACI rats given sodium saccharin had the most marked lesions under scanning electron microscopy, with less marked changes in Wistar and F344 rats. Sprague-Dawley rats were resistant to sodium saccharin. In Experiment 2, male F344 rats, B6C3F1 mice, Syrian golden hamsters, and Hartley guinea pigs were given 5.0% sodium saccharin in the diet for 20 weeks. The animals were sacrificed sequentially. Rats developed urinary bladder lesions during the experiment, as detected by light microscopy and scanning electron microscopy. Increased DNA synthesis of the urinary bladder epithelium was detected in rats by autoradiography. However, mice, hamsters and guinea pigs were resistant to sodium saccharin. These results indicate that there are strain and species differences in the urinary bladder response to sodium saccharin.

Animals↗
PubMed1982

Lack of correlation between hepatic mitochondrial membrane structure and functions in ethanol-fed rats.

A current hypothesis suggests that alterations in the chemical composition and the subsequent changes in the structure of the membrane could account for the functional derangements observed in the hepatic mitochondria of animals fed ethanol for extended periods. An examination of this hypothesis reveals that the liver mitochondria of ethanol-fed rats show a dissociation between the respiratory functions and the lipid composition and microviscosity of the membranes.

Animals↗
PubMed1982

Pachymeningitis cervicalis hypertrophica.

Presented here is an autopsy case of pachymeningitis cervicalis hypertrophica. A 77-year-old female had the initial symptoms of cervical radiculopathy which terminated in the syndrome of spinal cord transection. Prior to the onset of radiculopathy, the patient had been admitted to the hospital because of a fever and had been shown to have granulomatous sinusitis. Autopsy revealed chronic granulomatous pachymeningitis of the cervical spinal cord, the lesion being mostly restricted to this region. From histopathologic similarities, the extension of sinusitis to cervical pachymeningitis was assumed, but this was not confirmed. An attempt to discover the causative micro-organisms was unsuccessful. The possibility of a limited form of Wegener's granulomatosis could be excluded in view of the absence of true angiitis. Corresponding to the levels of pachymeningitis, the spinal cord was also severely damaged, which was principally due to circulatory disturbance as a result of pachymeningitis.

Aged↗
PubMed1982

Hepatotoxicity of vitamin A and ethanol in the rat.

To study the possible hepatotoxicity of vitamin A supplementation and its potentiation by ethanol, rats were fed diets with either normal or fivefold increased vitamin A content, both with or without ethanol. Ethanol with a normal vitamin A diet produced the expected proliferation of the smooth endoplasmic reticulum and moderate mitochondrial lesions. Vitamin A supplementation by itself produced endoplasmic reticulum proliferation, slight enlargement of mitochondria, and moderate decrease in cytochrome oxidase activity and cytochrome aa3 content. The combination of high vitamin A and ethanol resulted in much more striking lesions, with giant mitochondria containing paracrystalline inclusions and depression of oxygen consumption in state-3 respiration with five different substrates, including palmitate and palmitoyl coA. The depression of fatty acid oxidation may have contributed to the lipid accumulation. The blood levels of vitamin A were unaffected whereas liver levels of vitamin A were increased by vitamin A supplementation and decreased by ethanol. As a net result the liver vitamin A content of the high-A-ethanol groups was not greater than that of the normal-A-control group, suggesting that a metabolite of vitamin A rather than vitamin A itself may have been responsible for the potentiation of vitamin A toxicity by ethanol. Mitochondrial toxicity reflected itself also in decreased content of various cytochromes and reduced activity of enzymes, including glutamate dehydrogenase. The activity of the latter was increased in the serum. Implications of these findings for the routine treatment of alcoholics with vitamin A and the monitoring for possible signs of toxicity are discussed.

Animals↗