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Biomedical subjects

M Terada

Publications and source records attributed to M Terada.

At least 613 records · Page 34Linked to original sources

Fundamental studies on physiological and pharmacological actions of L-ascorbate 2-sulfate. I. On the hypolipidemic effects.

The effects of L-ascorbate 2-sulfate (AAS) on the lipid metabolism were examined in Triton-induced hyperlipemic mice, hypercholesterolemic and normal rats, the following results being obtained. 1) In Triton-induced hyperlipemic mice, AAS (300 mg/kg) significantly decreased the serum cholesterol level, while L-ascorbate (AA, 175 mg/kg) was found ineffective. 2)In hypercholesterolemic rats fed 0.5% cholesterol diet, the consecutive administration of AAS decreased the level of serum cholesterol and liver triacylglycerols. AA only slightly affected these levels. However, both AAS and AA prevented the unordinal increase in the liver weight caused by cholesterol feeding. 3)In normal rats, the administration of AAS over a 4-week period decreased the levels of serum cholesterol and liver triacylglycerols.

Animals↗

Specific receptors for glucocorticoid in the cytoplasm of the liver of AH 130 tumor-bearing rats.

Specific receptors for dexamethasone (11beta, 17alpha, 21-trihydroxy-9alpha-fluoro-16alpha-methyl-1,4-pregnadiene-3,20-dione) in the cytoplasm of the liver from AH 130 (solid type) tumor-bearing rats markedly increased in the advanced stage of tumor growth. The cytoplasmic receptors of the livers of normal and tumor-bearing rats differed in their affinities for dexamethasone, and their apparent equilibrium (dissociation) constants (K) for dexamethasone were 4.0 and 2.6 X 10(-9) M, respectively. The rates of dissociation of dexamethasone-receptor complexes and the heat denaturations of the receptors in the livers of normal and tumor-bearing rats were similar. The glucocorticoid receptors of tumor-bearing rat liver had slightly higher affinities than did those of normal liver for all the steroids tested. Only a trace amount of receptors for dexamethasone could be detected in the cytoplasm of AH 130 ascites cells.

Animals↗

[Experimental studies on anthelmintics (XXVI). Biochemical and pharmacological studies of 4-iodothymol on Ascaris lumbricoides suum].

We have shown previously that 4-iodothymol (IT) produces a contraction in Ascaris muscle, probably due to the myogenic action. In this paper, the effects of IT on the carbohydrate metabolism in Ascaris muscle have been investigated in comparison with those of hexylresorcinol (Hex), santonin (S) and piperazine (Pip). (1) Hex (200 approximately 400 mug/ml) showed a strong nonspecific inhibition on the formation of succinate from fumarate in muscle homogenate, the phosphofructokinase (PFK) activity in cytoplasm, and the electron transfer activity in mitochondria. (2) S(100 approximately 400 mug/ml) and Pip (100 approximately 400 mug/ml) were inneffective on these activities. (3) IT inhibited the formation of succinate from glucose and fumarate in muscle homogenate (100 approximately 400 mug/ml), the PFK activity in cytoplasm (400 mug/ml), and the mitochondrial succinate oxidase system (25 approximately 400 mug/ml). These results suggest that IT elicits the wormcidal action by inhibiting the energy metabolism of Ascaris muscle mitochondria.

Animals↗

Mitigation of caffeine-induced teratogenicity in mice by prior chronic caffeine ingestion.

Pregnant A/J female mice, which had drunk tap water or a 0.05% caffeine solution for 8-19 weeks after weaning, were each injected sc with 150 or 250 mg/kg caffeine once on day 13 of gestation. After 150 mg/kg caffeine the frequencies at term of fetal death, external malformation, and subcutaneous hematomas were significantly lower in the caffeine- than water-drinking group. After 250 mg/kg caffeine the frequency of fetal death but not of malformations and hematomas was lower in the group with caffeine pretreatment. These findings were explained by assuming that long-term ingestion of caffeine induced and increased rate of degradation of caffeine administered during pregnancy.

Abnormalities, Drug-Induced↗

Induction of erythroid differentiation by dimethylsulfoxide in cells infected with Friend virus: relationship to the cell cycle.

Cells infected with Friend virus can be induced to erythroid differentiation by culture with 2% dimethylsulfoxide. This study was designed to determine if dimethylsulfoxide causes the expression of erythroid differentiation by an effect on a particular phase of the cell division cycle. The infected cells were synchronized by exposure to 2 mM thymidine. It is shown that dimethylsulfoxide must be present during DNA synthesis (S-phase) and, possibly, shortly thereafter, to induce differentiation assayed by measuring hemoglobin synthesis. In order to achieve an effective intracellular incorporation of dimethylsulfoxide, cells must be exposed to the agent for at least 24-30 hr before the critical S phase. It is suggested that induction of erythroid differentiation in cells infected with Friend virus involves an effect of dimethylsulfoxide, or a metabolic product, that alters the program of transcription, during or immediately after DNA synthesis.

Cell Differentiation↗

Induction of erythroid differentiation in murine virus infected eythroleukemia cells by highly polar compounds.

Murine-virus-infected erythroleukemia cells cultured in a medium with dimethylsulfoxide or N,N-dimethylformamide are induced to differentiate to erythroid cells. A number of highly polar compounds have a similar effect in inducing erythroid differentiation of the virus-infected cells, as assayed by the appearance of hemoglobin. These compounds are 1-methyl-1-2-piperidone, N,N-dimethylacetamide, N-methylpyrrolidinone, N-methylacetamide, 2-pyrrolidinone, propionamide, pyridine-N-oxide, piperidone, N-methylformamide, acetamide, and triethylene glycol. It has been previously reported that dimethylsulfoxide must be present during DNA synthesis and, possibly, shortly therafter, to induce differentiation. These findings are consistent with the hypothesis that dimethylsulfoxide and related polar compounds act by changing the conformation of DNA or a DNA-protein complex, causing an alteration in transcription that leads to the expression of the program of erythroid differentiation.

Acetamides↗