Search PubMed⌕ Search

Biomedical subjects

C H Kuo

Publications and source records attributed to C H Kuo.

At least 145 records · Page 8Linked to original sources
PubMed1981

Induction of drug-metabolizing enzymes and toxicity of trans-stilbene oxide in rat liver and kidney.

The effect of trans-stilbene oxide (TSO) on organ function and morphology and on drug-metabolizing enzymes was determined in male Sprague-Dawley rats. TSO (300 or 600 mg/kg) was administered i.p., once daily for 5 consecutive days. At a dose of 3400 mg/kg, TSO did no alter body weight, but increased liver weight. The higher dose (600 mg/kg) markedly decreased body weight. TSO treatment (300 mg/kg) induced several drug-metabolizing enzymes. Epoxide hydrolase activity was enhanced in the liver, kidney and lung. In contrast, arylhydrocarbon hydroxylase activity was not significantly altered. Glutathione S-transferase activity, with 1-chloro-2,4-dinitrobenzene as substrate, and uridine diphosphoglucuronyl transferase activity, with p-nitrophenol as substrate, were also increased in the liver and kidney after TSO treatment. It appears that TSO induces hepatic and renal enzyme activities in a similar manner. Treatment with the higher dose of TSO depressed accumulation of p-amino-hippurate by renal cortical slices and increased blood urea nitrogen concentration. Histological examination of kidney sections after treatment with TSO revealed no abnormality. The lower dose led to negligible alteration in liver and the higher dose resulted in mild to moderate hepatic cellular.

Animals↗
PubMed1980

Subsynaptosomal distribution of 45Ca taken up by synaptosomes in high-potassium medium.

The 45Ca uptake of synaptosomes was stimulated by high K+, and the K-stimulated uptake was temperature dependent and reached a plateau level within 20 sec at 30 degrees C. The synaptosomes which took up 45Ca in high-K+ medium for 20 sec was disrupted, and subsynaptosomal distribution of 45Ca was examined. The percentage increases of 45Ca labeling of fractions D (vesicles), C (myelin), B (synaptic plasma membrane), and A (mitochondria) induced by high potassium were 27.7 +/- 10.3%, 28.7 +/- 10.4%, 31.0 +/- 4.0%, and 48.1 +/- 5.5%, respectively. However, total counts of K-stimulated 45Ca labeling in fraction B was equal to that in fraction A, and those in fractions C and D were less. These observations indicate that Ca binding on the synaptic plasma membrane may be as important as a Ca reservoir or regular of Ca2+ in nerve terminals as the mitochondria.

Absorption↗
PubMed1980

Ascorbic acid, an endogenous factor required for acetylcholine release from the synaptic vesicles.

The ACh-releasing factor, which is required for ACh release in presence of 2 mM ATP, 2 mM Mg and 10(-5) M Ca from isolated synaptic vesicles, was purified from the synaptosomal cytoplasm of rat brain by Sephadex G-15, DEAE-Sephadex, Sephadex G-10 and AG50W-2X column chromatographies and identified as ascorbic acid. A low concentration of L-ascorbic acid (5 x 10(-6) M) produced a release of ACh from the vesicles in the presence of ATP, MgCl2 and CaCl2, as did synaptosomal cytoplasm. This release of ACh induced by L-ascorbic acid was found to be dissociable from formation of lipid peroxide. These findings are discussed in relation to the physiological role of L-ascorbic acid in the brain.

Acetylcholine↗
PubMed1980

Inhibition of N-methyl-N'-nitro-N-nitrosoguanidine-activated guanylate cyclase by anticarcinogenic agents.

Recent studies have demonstrated that nitroso chemical carcinogens markedly activate guanylate cyclase, which catalyzes the production of guanosine 3',5'-monophosphate (cyclic GMP). We therefore examined the effect of inhibitors of carcinogenic compounds on guanylate cyclase activation by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). An antioxidant group of anticarcinogenic compounds was effective. Disulfiram and phenethyl isothiocyanate exhibited the most potent inhibition. Inhibitor constants (Ki) for disulfiram and phenethyl isothiocyanate were 1.2 x 10(-5) M and 4.9 x 10(-5) M, respectively. Sodium diethyldithiocarbamate, phenyl isothiocyanate, butylated hydroxyanisole and ethoxyquin showed moderate inhibitory effects. Sodium selenide decreased the MNNG-activated guanylate cyclase activity to about 30%, and it was inhibitory at the low concentration of 10(-5) M. The present data suggest that one of the mechanisms by which anticarcinogenic compounds exert their effect may in part be related to the inhibition of guanylate cyclase.

Animals↗
PubMed1979

Effect of L-leucine on p-aminohippurate accumulation by mammalian renal cortical slices.

The effect of several amino acids (L-glutamate, L-phenylalanine, L-leucine, glycine, L-tryptophan, L-histidine, L-valine) on p-aminohippurate accumulation was evaluated in rat, mouse and rabbit kidneys. Only leucine was found to enhance p-aminohippurate accumulation in rat and mouse renal cortical slices but not in rabbit slices. Leucine had no effect on tetraethylammonium accumulation. In rat renal cortical slices, leucine increased the uptake and decreased the runout of p-aminohippurate, each effect contributing to the increase in p-aminohippurate accumulation. The apparent Km of p-aminohippurate uptake was decreased by leucine with no change in the apparent V. Aminooxyacetate (an inhibitor of transamination of leucine) partially depressed the stimulating effect of leucine on p-aminohippurate accumulation, whereas alpha-ketoisocaproic acid (a metabolite of leucine formed by transamination) enhanced p-aminohippurate accumulation, suggesting that the metabolism of leucine in kidney slices may be necessary for the stimulating effect on p-aminohippurate transport.

Amino Acids↗
PubMed1979

Subcellular ascorbic acid in scorbutic guinea pig brain.

In scorbutic guinea pigs fed an ascorbic acid-deficient diet for 18 days, the ascorbic acid contents of the liver and plasma were less than 4% those of the control animals, while the content in the brain was about one-third that of the controls. In normal animals, the concentration of ascrobic acid was highest (7.55 +/- 1.46 micrograms of ascorbic acid/mg protein) in the S3 fraction and was also fairly high (5.37 +/- 0.91) in the P2p fraction (cytoplasm of nerve terminals). During ascorbic acid deficiency, the contents in the P2p and microsome fractions decreased slightly faster than those in other fractions. Even after 18 days' deficiency, no significant change was found in the acetylcholine content of the brain.

Acetylcholine↗
PubMed1978

Effects of synaptic plasma membranes on release of acetylcholine from synaptic vesicles.

The influences of synaptic plasma membranes on release of acetylcholine (ACh) from synaptic vesicles isolated from rat brain were examined. In the presence of ATP, Mg++ and Ca++ but absence of cytoplasm from the nerve endings, the synaptic plasma membranes did not increase ACh release indicating absence of a stimulating factor which is known to be present in the cytoplasm. In presence of ATP, Mg++, Ca++ and the cytoplasm, the synaptic plasma membranes inhibited ACh release from the synaptic vesicles in high K+ medium, though not in high Na+ medium. Binding of Ca++ by the synaptic plasma membranes was dependent on ATP, inhibited by Na+ and stimulated by K+. Thus, the synaptic plasma membranes may inhibit ACh release in high K+ medium due to reduction in the concentration of free Ca++.

Acetylcholine↗