Biomedical subjects
Publications and source records attributed to R Sato.
Hypolipidemic effects of S-methylmethionine (MMSC) were compared with clofibrate in 3 experimental procedures. In results, the characteristic effect of MMSC is discussed from therapeutic viewpoint.
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The intact, amphipatic form of cytochrome b5 could bind to unsealed ghosts, but not to resealed ghosts, suggesting that the cytochrome could bind only to the inner (cytoplasmic) surface of the ghost membrane. This was further confirmed by the finding that the cytochrome could bind to closed, inside-out vesicles prepared from the ghosts. This asymmetric binding was not due to the exclusive localization of sialic acid and sugar chains on the outer surface of the ghosts membrane, because the cytochrome could not bind to ghosts even after enzymatic removal of these components. Although liposomes consisting of phosphatidylcholine or both phosphatidylcholine and sphingomyelin could effectively bind the cytochrome, this binding capacity was progressively decreased as increasing amount of cholesterol was included in the composition of phosphatidylcholine liposomes. Removal of cholesterol from resealed ghosts by incubation with egg phosphatidylcholine liposomes resulted in the binding of cytochrome b5 to the outer surface of the treated ghosts. The possibility is discussed that the asymmetric binding is due to preferential localization of cholesterol in the outer leaflet of the lipid bilayer that constitutes the ghost membrane.
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A series of 7-nitro- and amino-N,'-bis(4-quinaldinyl)-alpha, omega-diaminoalkanes related to the 6-amino derivative 1 was synthesized and tested in the mouse P-388 lymphocytic leukemia screen. There of the 7-nitro derivatives (12, 14, and 15) were found to have moderate activity (T/C 140-150%), while other nitro derivatives (11 and 13) were devoid of any antitumor properties. All five 7-amino compounds (2-6) were moderately to strongly active (T/C 134-196%). In addition, binding of amino derivatives 2-6 to DNA was examined by their ability to (1) stabilize DNA to thermal denaturation and (2) inhibit the DNA-dependent RNA polymerase reaction in vitro. Tm data suggest that these compounds bind to DNA and are strong inhibitors of the polymerase reaction (I50 = 6-9 X 10(-6) M).
A CO-binding heme protein was solubilized and partially purified from the inner membrane fraction of rat liver mitochondria by a modification of a method [Imai, Y. & Sato, R. (1974) Biochem. Biophys. Res. Commun. 60, 8-14] developed to purify cytochrome P-450 from liver microsomes. The partially purified preparation contained protoheme and its spectral properties are characteristic of the heme proteins of the cytochrome P-450 family. The isolated cytochrome P-450 preparation could reconstitute a CO-sensitive, NADPH-dependent 26-hydroxylation activity for 5beta-cholestane-3alpha,7alpha,-12alpha-triol when supplemented with NADPH-adrenodoxin reductase and adrenodoxin, both purified from bovine adrenocortical mitochondria. Unlike a cytochrome P-450 purified from liver microsomes of drug-untreated rats, however, the liver mitochondrial cytochrome P-450 could not catalyze NADPH-dependent benzphetamine N-demethylation in the presence of adrenodoxin reductase and adrenodoxin or function with the purified microsomal NADPH-cytochrome c reductase plus Emulgen 913 as an electron-donating system. It is concluded that the rat liver inner mitochondrial membrane houses a species of cytochrome P-450 functional in 5beta-cholestane-3alpha,7alpha,12alpha-triol 26-hydroxylation.
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The 2nd c-wave is a new wave of corneoretinal potential which is an on-response with a long latency (65-98 sec), and appears following the end of the c-wave of ERG. It suggested that the 2nd c-wave is based on the tail of the late receptor potential of the retina.
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A mouse strain, ICR/SLC, was involved in spontaneous amyloidosis with high incidence. The amyloid deposition in this strain was seen mainly in the mucosal propria of duodenum and terminal ileum, liver, spleen, adrenal cortices, and renal glomeruli. The mice, orally administered more than 300 mg/kg of organic germanium for 22 months since 5 weeks old, did not develop amyloidosis. Half of the mice, given 30 mg/kg of organic germanium for 22 months developed amyloidosis. The mice given 5% carboxymethylcellulose, the solvent of organic germanium, were affected with systemic amyloidosis with high frequency. The results showed that the organic germanium successfully inhibited the occurrence of senile amyloidosis with dose response. The agent did not have any apparent relation to the incidence of hepatic cell carcinoma or pulmonary adenoma which is frequently combined with aged mice. Although the actual mechanism involved is not clear, the evidence of the inhibition of senile amyloidosis by organic germanium may give a light to elucidate the pathogenesis of amyloidosis.
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