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Biomedical subjects

E Hayashi

Publications and source records attributed to E Hayashi.

At least 163 records · Page 9Linked to original sources
PubMed1978

Effects of purine compounds on cholinergic nerves. Specificity of adenosine and related compounds on acetylcholine release in electircally stimulated guinea pig ileum.

The action of 21 purine compounds on the twitch response of the electrically stimulated guinea pig isolated ileum has been investigated. Adenosine and related compounds produced a dose-dependent depression of the response. Adenosine was the most potent and 2'-deoxyadenosine had one hundredth the potency of adenosine. Adenine, hypoxanthine, inosine, IMP, ITP, xanthine, xanthosine, XMP, XTP, guanine, GMP and GTP were ineffective at concentrations less than 1 mM. Adenosine (30 microgram) reduced the electrically induced ACh output from the ileal strips. The dose--depression curve for adenosine (0.1--30 microgram) was shifted to the right in the presence of xanthine derivatives and of these, theophylline was the most potent inhibitor of adenosine. On the other hand, dipyridamole (0.1--1 microgram) and hexobendine (0.1--1 microgram) shifted the curve to the left. They markedly inhibited 3H-adenosine uptake into the ileum. Theophylline (0.1 mM), dipyridamole (0.3 microgram) and hexobendine (0.3 microgram) did not affect tetrodotoxin-, adrenaline-, strychnine- and morphine-induced inhibition of the twitch response. The present investigations have revealed that adenosine and related compounds reduce ACh release from the intramural cholinergic nerves in the guinea pig ileum possibly in a specific manner (or through a specific receptor site) different from that of other inhibitors such as morphine.

Acetylcholine↗
PubMed1978

The development of tachyphylaxis to electrical stimulation in guinea-pig ileal longitudinal muscles and the possible participation of adenosine and adenine nucleotides.

1 Electrically (30 Hz) induced contractions of guinea-pig isolated ileal longitudinal muscles were reduced by tetrodotoxin (1 micron), adenosine (30 micron) and morphine (10 micron). 2 When stimulated with 10 or 30 Hz for 10 s at 1 min intervals, a progressive decline of amplitude of the contraction was seen (development of tachyphylaxis). At this time, the contractile response to 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) (10 micron) was also greatly reduced. 3 The smaller responses to electrical stimulation and DMPP during tachyphylaxis were restored to their initial amplitude by the addition of theophylline (10 micron). The appearance of tachyphylaxis was prevented by pretreatment with theophylline (1 to 10 micron) and was greatly accelerated by pretreatment with dipyridamole (0.1 1 micron). 4 In [14C]-choline or [3H]-adenosine preloaded muscle strips, electrical stimulation (30 Hz) increased the 14C- or 3H-output, the effect being sensitive to tetrodotoxin blockade. The tachyphylaxis to electrical stimulation was accompanied by a considerable and sustained increase in 3H-output, an effect that was accelerated by dipyridamole (1 micron). The 14C-output initially increased but fell off gradually with the development of tachyphylaxis at which time theophylline (30 micron) reversed the fall. 5 There was a marked increase in the proportion of released [3H]-adenosine to its derivatives during the development of tachyphylaxis. Approximately 60% of the released total radioactivity after tachyphylaxis was found to be [3H]-adenosine. 6 These results suggest that the development of tachyphylaxis may be closely associated with the release of endogenous adenosine derivatives (mostly adenosine) which have presynaptic inhibitory actions on the cholinergic elements in guinea-pig ileum.

Acetylcholine↗
PubMed1978

Phthalate and 4-hydroxyphthalate metabolism in Pseudomonas testosteroni: purification and properties of 4,5-dihydroxyphthalate decarboxylase.

Phthalate is degraded through 4,5-dihydroxyphthalate and protocatechuate in Pseudomonas testosteroni NH1000. The ezyme 4,5-dihydroxyphthalate decarboxylase, catalyzing the conversion of 4,5-dihydroxyphthalate to protocatechuate and carbon dioxide, was purified approximately 130-fold from phthalate-induced cells of a protocatechuate 4,5-dioxygenase-deficient mutant of P. testosteroni. The most purified preparation showed a single protein band on sodium dodecyl sulfate-acrylamide disc gel electrophoresis with a molecular weight of 38,000. The apparent molecular weight of the native enzyme determined by Sephadex G-200 column chromatography was 150,000. Among the substrate analogs tested, only 4-hydroxyphthalate served as a substrate, which was decarboxylated to form m-hydroxybenzoate. The apparent Km values for 4,5-dihydroxyphthalate and 4-hydroxyphthalate were estimated to be 10.5 micrometer and 1.25 mM, respectively, and the Vmax for the former was 10 times larger than that for the latter. Whereas the wild-type strain could utilize 4-hydroxyphthalate as a sole source of carbon, none of the following could grow with the compound: 4,5-dihydroxyphthalate decarboxylase-deficient, m-hydroxybenzoate-nondegradable, and protocatechuate 4,5-dioxygenase-deficient mutants. Since one-step revertants of these mutants could utilize 4-hydroxyphthalate, the compound appears to be metabolized through m-hydroxybenzoate and protocatechuate in P. testosteroni NH1000.

Biodegradation, Environmental↗
PubMed1978

Isolation of TOL and RP4 recombinants by integrative suppression.

We obtained genetic and molecular evidence of non-thermosensitive recombinants of RP4 (Kmr Tcr Cbr/Apr) and the thermosensitive TOL plasmid. As first isolated in Pseudomonas aeruginosa PAO, the recombinant plasmid pTN1 specified noninducible synthesis of TOL enzymes and was transmissible to Escherichia coli on selection for the transfer of kanamycin resistance. The phenotypic expression of TOL genes of pTN1 in E. coli was low and also noninducible. A spontaneous segregant, pTN2, appearing from pTN1, conferred inducible synthesis of TOL enzymes. These plasmids carry all of the TOL determinants as evidenced by the ability of Pseudomonas putida carrying recombinant plasmids to grow on toluene, xylene, and m-toluate. In E. coli the expression of TOL genes with normal regulation (pTN2) appears to be extremely low without induction, and the induced expression is comparable to that with defective regulation (pTN1). The measurement of the molecular weight of pTN2 by electron microscopy gave a value of about 74 X 10(6).

Conjugation, Genetic↗
PubMed1978

Fundamental studies on physiological and pharmacological actions of L-ascorbate 2-sulfate. VI. Effects of L-ascorbate 2-sulfate on lipid metabolism in guinea pigs.

Effects of L-ascorbate 2-sulfate (AAS) on lipid metabolism were studied in guinea pigs maintained on diet I with sufficient L-ascorbic acid (AA) supplement or on diet II without AA supplement. AAS(300 mg/kg) inhibited an increase in serum and liver levels of lipids to a greater degree than AA (175 mg/kg), a reference compond, in hyperlipidemic guinea pigs induced by cholesterol feeding with diets I or II. AAS also induced a decrease in serum and liver levels of lipids in guinea pigs which had been previously maintained for 6 weeks on diet II containing 1.0% cholesterol. AA administration significantly increased AA level in various organs of animals maintained on both the diets containing cholesterol. It also rectified the AA level lowered by previous maintenance on diet II containing cholesterol. AAS showed a slight AA replacing effect on the AA level. Both AA and AAS exerted preventive and curative effects on several symptoms due to chronic AA deficiency.

Animals↗
PubMed1978

Fundamental studies on physiological and pharmacological actions of L-ascorbate 2-sulfate. V. On the hypolipidemic and antiatherosclerotic effects of L-ascorbate 2-sulfate in rabbits.

Effects of L-ascorbate 2-sulfate (AAS) on lipid metabolism and on pathological changes of aorta and visceral organs were investigated in cholesterol fed rabbits, with ascorbic acid (AA) and clofibrate (CPIB) as reference compounds. Administration of AAS (300 and 150 mg/kg) inhibited an increase in the levels of serum total cholesterol, free cholesterol, triglycerides and phospholipids caused by cholesterol feeding. A high dose of AAS prevented an increase of liver weight. An increase in the level of liver cholesterol was inhibited by a high dose of AAS. Both doses of AAS effectively prevented an accumulation of cholesterol in the aorta. The area rate of atheromatous plaque in aorta was less in specimens from both groups of AAS than in those from control I. Pathological changes in intima and media of aorta were milder in specimens from both groups of AAS. Developed of patholoigcal changes in arteries of various organs were prevented with both doses of AAS.

Animals↗