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Biomedical subjects

I K Ho

Publications and source records attributed to I K Ho.

At least 253 records · Page 14Linked to original sources
PubMed1980

Inhibition of mouse brain synaptosomal ATPases and ouabain binding by chlordecone.

The effect of chlordecone on the mouse brain synaptosomal Na+-K+ ATPase, Mg2+ ATPase and p-nitrophenyl phosphatase (PNPPase) activities was determined. In addition, the effect of chlordecone on [3H] ouabain binding to synaptosomes was also investigated. The in vitro data show that chlordecone inhibits PNPPase, Na+-K+ ATPase, and Mg2+ ATPase activities with ID50 values of 4, 5 and 7 micrograms respectively. Treatment of mice with symptomatogenic doses of chlordecone resulted in a decreased synaptosomal Na+-K+ and oligomycin-sensitive (mitochondrial) Mg2+ ATPases. The decrease was dose-dependent. The oligomycin-insensitive Mg2+ ATPase activity was unaffected either in vitro or in vivo. The binding of [3H] ouabain to synaptosomal membranes was inhibited by chlordecone in a dose-dependent manner in both in vitro and in vivo experiments. The binding of [14C] chlordecone to synaptosomes occurs even at nanomolar concentrations. The marked inhibition of brain synaptosomal ATPases and ouabain binding by chlordecone suggests that chlordecone may impair active transport mechanisms in synaptosomal membranes.

4-Nitrophenylphosphatase↗
PubMed1980

Assessment of photomirex toxicity in the mouse.

Toxicity in the mouse was produced after oral administration of photomirex at 10, 25 and 50 mg/kg.d in corn oil. Mortality began to occur 4, 7, and 16 d after daily administration of photomirex at 50, 25, and 20 mg/kg, respectively. In all cases, the cumulative LD50 for photomirex was estimated as 225-250 mg/kg. The effect of photomirex on food and water consumption varied depending on dose. Daily oral administration of photomirex caused a dose-dependent loss of body weight. No overt behavioral changes were observed during the experiments. Body temperature was unaffected. Biochemical studies also showed that photomirex did not affect plasma glucose and free fatty acid content and brain biogenic amine levels. It appears that photomirex is similar to mirex in terms of peripheral toxicity.

Amines↗
PubMed1980

The inhibition and potentiation of procarbazine on hepatic mixed-function oxidases in phenobarbital tolerant and nontolerant mice.

The effect of procarbazine on mixed-function oxidases was investigated in naive and pentobarbital tolerant mice. In mice receiving procarbazine, 200 mg/kg, i.p. 1 hr earlier, metabolisms of pentobarbital, aniline and ethylmorphine in vitro and cytochrome P-450 content of hepatic microsomes were significantly decreased. The drug binding of either aniline or pentobarbital to cytochrome P-450 was also decreased. However, procarbazine failed to exert this effect after the enzymes had been induced by continuous administration of pentobarbital. Interestingly, procarbazine enhanced the barbiturate induced hepatic microsomal mixed-function oxidase activities when it was administered before the implantation of pentobarbital pellet. Both cytochrome P-450 and cytochrome b5 content after pentobarbital pellet implantation were further increased by pretreatment with procarbazine. This finding was further substantiated by the increase in pentobarbital and aniline binding to cytochrome P-450. The present studies may provide another model for studying the nature of hepatic mixed-function oxidase induction process.

Animals↗
PubMed1980

Enhancement of carbon tetrachloride elevated glutamate oxalacetate transaminase and glutamate pyruvate transaminase by acute and continuous pentobarbital administration in mice.

The results demonstrated that both acute and continuous administration of pentobarbital enhanced the CCl4-induced elevation of SGOT and SGPT activities. The potentiation of pentobarbital on CCl4-elevated SGOT and SGPT activities showed both time- and dose-dependent actions. The CCl4-induced elevation of both serum enzyme activities after continuous exposure of pentobarbital was still significant 6 days after the termination of pentobarbital. The CCl4-elevated SGOT and SGPT activities were also affected by various doses of Na-pentobarbital, although the degree of potentiation was less than the results obtained by pentobarbital pellet implantation. The present results further support the contention that proliferation of hepatic cells by barbiturates enhances CCl4-induced toxicity.

Alanine Transaminase↗
PubMed1980

Effect of patulin on hepatic monooxygenase in male mice.

The in vivo effects of patulin on hepatic monooxygenase enzymes in male mice were examined after single and multiple exposures (i.p.) to the mycotoxin. The animals were exposed to a single dose of 1, 3 or 4.5 mg patulin/kg or daily doses of 1.0 mg/kg for 5 or 14 days. After single exposure no significant effect was observed on hexobarbital hydroxylation while aniline hydroxylase increased significantly at 3 mg/kg and at 48 hr. The demethylation of aminopyrine and ethylmorphine increased significantly 48 and 72 hr after 3.0 or 4.5 mg patulin/kg doses. A 12% increase was observed in cytochrome P-450 content 48 hr after exposure to 1 or 3 mg/kg. NADPH-cytochrome C reductase was enhanced significantly at all 3 dose levels at 48 hr. At 24 hr hepatic NADPH-dependent dehydrogenase activity increased 38 and 46% in animals exposed to a single dose of 3 mg patulin/kg, respectively. No effect of patulin was observed on the hepatic drug metabolizing enzymes examined except hexobarbital oxidation in mice exposed to multiple doses of patulin. Patulin at best was a weak inducer of the hepatic mixed function oxidase system.

Animals↗
PubMed1979

Effects of the aflatoxins on ATPase activities in mouse and rat liver.

The effects of the aflatoxins on ATPase activities in mouse and rat tissues were investigated in vitro. The hepatic oligomycin-sensitive (O.S.) Mg++ ATPase was inhibited significantly. The order of inhibition was G1 greater than B1 greater than G2 greater than B2. Mouse O.S. Mg++ ATPase was more sensitive than the corresponding rat enzyme. The oligomycin-insensitive (O.I.) Mg++ ATPase activities in rat and mouse liver were not altered. Although aflatoxins G1 and B1 were more potent inhibitors of hepatic O.S. Mg++ ATPase, no concentration-response was observed, whereas aflatoxins G2 and B2 inhibited enzyme activity in a concentration-dependent manner. Spectral analysis of aflatoxin G1 solutions suggested that solubility was not related to the observed effects. In addition, the effects of aflatoxin B1 and G1 on mouse brain microsomal Na+-K+ ATPase were examined. Although aflatoxin B1 was more potent that G1, both mycotoxins significantly inhibited enzyme activity in a concentration-dependent fashion.

Adenosine Triphosphatases↗
PubMed1979

Enhancement of pharmacologic responses of pentobarbital by dopram.

The effect of Dopram (doxapram hydrochloride, A. H. Robins Co.) on the pharmacologic responses to pentobarbital was evaluated. In naive and pentobarbital-tolerant mice, Dopram was shown to enhance significantly sodium pentobarbital-induced narcosis in a dose-related manner. The effect of the duration of action of Dopram on pentobarbital narcosis also was assessed. It was observed that Dopram (40 mg/kg, i.p.) significantly increased pentobarbital-induced narcosis even when administered 2 hr prior to challenge with sodium pentobarbital (60 mg/kg, i.p.) A significantly increased hypothermic response to sodium pentobarbital was seen in Dopram-treated animals. The half-life of pentobarbital in brain and serum was shown to be increased significantly in animals receiving Dopram, 40 mg/kg, i.p. The waking brain and serum pentobarbital concentrations were not significantly different in either group. These studies show that Dopram potentiates pentobarbital's effects. Further study is necessary to determine the sites of operation and mechanism of this potentiation.

Animals↗
PubMed1979

Effects of acute and continuous morphine administration on catecholamine-sensitive adenosine triphosphatase in mouse brain.

The catecholamine-stimulated adenosine triphosphatase (ATP-ase) activities in mouse brain synaptosomes were inhibited by morphine both in vitro and in vivo. Morphine up to 10(-3) M had no effect on basal ATPase activities but at 10(-4) M significantly inhibited dopamine-sensitive ATPase activities in vitro. The morphine effect was antagonized by an opiate antagonist, naloxone. The catecholamine-sensitive ATPase activities were also inhibited by acute administration of morphine. The inhibition was dose-dependent. However, naloxone partially antagonized the morphine inhibition of depamine-sensitive ATPase activity but not norepinephrine-sensitive ATPase activity. A significant decrease in the sensitivity of synaptosomal ATPase to catecholamines was observed in mice rendered tolerant by morphine pellet implantation. The Na+,K+-ATPase was more affected by morphine as compared to Mg++-ATPase activity. The dopamine-sensitive Na+,K+-ATPase activity was restored by 50% in precipitated withdrawal mouse brain synaptosomes. Norepinephrine-sensitive ATPase activity was also restored partially in precipitated withdrawal animals. These results suggest that in mouse brain synaptosomes morphine may be interacting with ATPase at or near the catecholamine-active sites.

Adenosine Triphosphatases↗
PubMed1979

Effects of acute and chronic administration of pentobarbital on catecholamine uptake in mouse brain synaptosomes.

The studies showed that pentobarbital at concentrations up to 10(-4) M failed to exhibit any effect on catecholamine uptakes in vitro. In mice treated both acutely and chronically with pentobarbital, there was a significant attenuation in both dopamine and norepinephrine uptakes into synaptosomal preparations. The decrease in both catecholamine uptakes during the course of the development of tolerance to pentobarbital was demonstrated to be time dependent. The ability of catecholamine uptake processes was restored by abrupt withdrawal of pentobarbital by the removal of pentobarbital pellet. It appears that both acute and chronic effects of pentobarbital on catecholamine uptakes may be associated with the development of tolerance to pentobarbital.

Animals↗
PubMed1978

Lipid accumulation in mouse hepatocytes after morphine exposure.

After morphine injection lipid accumulation in mouse hepatocytes begins within 2 h and continues for 24 h when most hepatocytes are filled with lipid droplets. In spite of morphine maintenance the liver recovers as the accumulated lipids are coupled with protein and subsequently transported and released into the perisinusoidal space of Disse.

Animals↗