Search PubMed⌕ Search

Biomedical subjects

I K Ho

Publications and source records attributed to I K Ho.

At least 271 records · Page 15Linked to original sources
PubMed1978

Effects of rubratoxin B on the kinetics of cationic and substrate activation of (Na+-K+)-ATPase and p-nitrophenyl phosphatase.

Rubratoxin B, a lactone-containing bisanhydride metabolite of certain toxigenic molds, inhibited (Na+-K+)-stimulated ATPase activity of mouse brain microsomes in a dose-dependent manner with an estimated IC50 of 6 x 10(-6) M. Hydrolysis of ATP was linear with time and enzyme concentration, with or without rubratoxin in reaction mixtures. Altered pH and activity curves for (Na+-K+)-ATPase demonstrated comparable inhibition by rubratoxin in buffered acidic, neutral, and alkaline pH ranges. Kinetic studies of cationic-substrate activation of (Na+-K+)-ATPase indicated classical competitive inhibition for Na+ and K+. Results also showed competitive inhibition for K+ activated p-nitrophenyl phosphatase as demonstrated by altered binding site parameters without change in the catalytic velocity of dephosphorylation of the enzyme . phosphoryl complex. Noncompetitive inhibition with regards to activation by ATP and p-nitrophenyl phosphate was indicated by altered Vmax values with no change in Km values. Inhibition was partially restored by repeated washings. Preincubation with sulfhydryl agents protected the enzyme from inhibition. Cumulative inhibition studies with rubratoxin and ouabain indicated possible interaction between the two inhibitors of (Na+-K+)-ATPase. Rubratoxin appeared to exert its effects on (Na+-K+)-ATPase by interacting at Na+ and K+ sites.

4-Nitrophenylphosphatase↗
PubMed1978

Sensitivity to continuous administration of pentobarbital in different strains of mice.

The comparisons of responses to pentobarbital by pellet implantation method with respect to cumulative mortality, narcosis and tolerance development on five strains (ICR, ddY, ddN, C57BL, and C3H) of mice were studied. C3H mice showed most susceptible and sensitive to pentobarbital among the five strains of mice tested. ICR mice were most resistant to the treatment. It appears that the effects of genetic variation could be of importance for future studies in gaining insight of the mechanism of barbiturate tolerance.

Animals↗
PubMed1978

Evaluation of Dopram(R) and its effects on hexobarbital narcosis.

The effect of Dopram(R) on hexobarbital induced narcosis and hypothermia was determined. Sodium hexobarbital (70mg/kg, i.p.) sleeping times were assessed in saline, Dopram(R), 20 and 40 mg/kg, i.p., administered mice. A dose-response increase in sodium hexobarbital induced narcosis was produced by Dopram(R). The duration of Dopram(R) effect on hexobarbital narcosis was also assessed. Dopram(R) potentiated significantly hexobarbital sleeping times when administered two hours prior to sodium hexobarbital challenge. Dopram(R) also was observed to significantly increase the hypothermic response to hexobarbital. The effect of the individual components of Dopram(R) (doxapram hydrochloride and chlorobutanol) on hexobarbital narcosis and hypothermia was evaluated. It was found that doxapram hydrochloride (20 and 40 mg/kg, i.p.) and chlorobutanol (5 and 10 mg/kg, i.p.) potentiated sodium hexobarbital narcosis and hypothermia. It seems that doxapram hydrochloride and chlorobutanol are both responsible for the potentiation of hexobarbital narcosis and hypothermia by Dopram(R).

Animals↗
PubMed1977

Pentobarbital distribution in discrete brain areas of tolerant and nontolerant mice.

Uptake and distribution of pentobarbital in tolerant and nontolerant mice were studied. Mice were implanted with pentobarbital or placebo pellets s.c. 3 days prior to the injection of 60 mg/kg sodium pentobarbital i.p. One group of animals was sacrificed when they first awakened. Whole brain, five discrete brain areas, and plasma were assayed for pentobarbital by gas chromatography. In a second group, time studies were performed on brain sections and plasma. In tolerant vs nontolerant animals, sleeping time was markedly decreased (10-20 vs 50-70 min); whole brain, brain sections, and plasma levels on awakening were not significantly different; linear and exponential curves of pentobarbital levels vs time showed an increase in slope (-1.05 vs-0.40) and a decrease in T 1/2 (10.2 VS 35.7 min). These findings suggest that the tolerance development to pentobarbital in the central nervous system is due to functional mechanism rather than brain dispositional mechanism.

Animals↗