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Biomedical subjects

C H Kuo

Publications and source records attributed to C H Kuo.

At least 127 records · Page 7Linked to original sources
PubMed1983

Effects of age and sex on hexachloro-1,3-butadiene toxicity in the Fischer 344 rat.

Effects of age and sex on hexachloro-1,3-butadiene (HCBD) nephrotoxicity were determined 24 hours after a single dose (0, 25, 50, 100 or 200 mg/kg) in 28- and 63-day-old Fischer 344 rats. HCBD treatment significantly increased the kidney to body weight ratio but had little effect on the liver to body weight ratio. The 28-day-old rats were more susceptible to HCBD nephrotoxicity judged by elevated blood urea nitrogen, decreased renal cortical accumulation of p-aminohippurate and tetraethylammonium. Adult female rats (63-day-old) appeared to be more susceptible to HCBD nephrotoxicity than males at the low dose (50 mg/kg).

Aging↗
PubMed1983

Influence of tooth-to-denture-base discrepancy on space closure following premature loss of deciduous teeth.

Influence of tooth-to-denture-base discrepancy on so-called physiologic migration of the first molar was studied on serial dental casts of 116 boys and girls, obtained through a dental health program for school children in an area in which there was no dentist. The alteration of spaces following premature loss of deciduous molars was examined comparing the anterior to posterior discrepancies between tooth and denture base. Modes of space alteration showed positive correlation with the size of the discrepancy, especially in the mandibular dental arches. The space deficiency in the posterior region seemed to have a positive effect on the mesial migration of the first molar. Mesial migration of the first molar seems to be pathologic rather than physiologic and is strongly affected by tooth-to-denture-base discrepancies. Space maintenance does not seem to be useful, because it is not necessary in minimum discrepancy cases and is not effective in severe discrepancy cases.

Adolescent↗
PubMed1983

Lipid peroxidation: a possible mechanism of cephaloridine-induced nephrotoxicity.

Cephaloridine produces renal cortical injury, but the precise mechanism responsible for this nephrotoxicity remains unclear. Recently cephaloridine has been shown to deplete reduced glutathione (GSH) concentration selectively in renal cortex. Cephaloridine nephrotoxicity can be potentiated by diethyl maleate (a GSH depletor), but no glutathione conjugate can be detected. Thus, it was of interest to investigate further the mechanism of depletion of renal cortical GSH by cephaloridine. In the present study, cephaloridine markedly decreased GSH in rat and rabbit renal cortex while concomitantly increasing oxidized glutathione (GSSG). Furthermore, cephaloridine increased lipid peroxidation specifically in renal cortical cells. Conjugated diene formation (an index of lipid peroxidation) was increased in renal cortex but not in the liver shortly following administration of cephaloridine. Removal of selenium and/or vitamin E from the diet, which should enhance lipid peroxidation, potentiated cephaloridine nephrotoxicity and enhanced cephaloridine-induced morphological damage in the kidney. These findings are consistent with a major role of lipid peroxidation in the etiology of cephaloridine nephrotoxicity.

Animals↗
PubMed1983

Analysis of a distinctive protein in chick retina during development.

Soluble proteins from the chick retina were analyzed at various developmental stages by SDS-polyacrylamide gel electrophoresis. A peptide of about 24,000 daltons (24 Kd protein) appeared in the 14-day embryo and gradually increased with embryonic age, maintaining a fairly steady level after hatching. Polypeptides which correspond to actin and tubulin, however, remained almost unchanged during development. The 24 Kd protein was not detected in the cerebrum, tectum, pigment epithelium or vitreous body at any age. To characterize this protein, it was partially purified by gel filtration and ion exchange column chromatography, and its isoelectric point was measured. It was focused in a diffuse spot at about pH 5.5. In the bovine retina, a protein was observed at 24,000 daltons on SDS-polyacrylamide gel, but its isoelectric point was more basic than that of chick retina. It is suggested that the 24 Kd protein is one of the distinctive proteins that increase in concentration during the chick retinal development, and would be closely associated with retinal functions.

Animals↗
PubMed1983

Nuclear structure: determination of the fate of the nuclear envelope in Drosophila during mitosis using monoclonal antibodies.

Libraries of monoclonal antibody against nuclear proteins of Drosophila melanogaster have been established recently to investigate nuclear structure and function. Some of the antibodies have been characterized as being directed against the nuclear envelope. Further studies detailed in this paper describe the fate of the nuclear envelope during mitosis. Indirect immunofluorescence staining of whole developing Drosophila embryos has been used as a system in which nuclear events can be studied both synchronously and in a longitudinal gradient of mitotic structures. The results show a pattern of breakdown and reconstruction of the nuclear envelope in which the antigen is always present in particulate structures. In addition, the processes of antigen rearrangement are shown to be spatially determined throughout mitosis.

Animals↗
PubMed1983

Effect of piperonyl butoxide on organic anion and cation transport in rabbit kidneys.

Piperonyl butoxide has been shown to reduce accumulation of cephaloridine in rabbit renal cortex; however, the mechanism responsible for this effect remains unclear. Cephaloridine is a zwitterion and its accumulation in renal cortex has been suggested to be regulated by both organic anion and cation transport systems. Thus, it was of interest to determine the effect of piperonyl butoxide on renal transport of p-aminohippurate (PAH, an organic anion) and tetraethylammonium (TEA, an organic cation). Although pretreatment with piperonyl butoxide markedly inhibited renal cortical uptake of cephaloridine, the same treatment had less inhibitory effect on either PAH or TEA uptake. Efflux of PAH from preloaded renal cortical slices was enhanced by pretreatment with piperonyl butoxide; however, TEA efflux was unaffected. Thus, piperonyl butoxide appears to have effects on renal membrane functions which result in differential effects on PAH, TEA, and cephaloridine transport.

Aminohippuric Acids↗
PubMed1983

Effects of piperonyl butoxide on cephalosporin nephrotoxicity in the rabbit. An effect on cephaloridine transport.

To evaluate the hypothesis that cytochrome P-450 mixed-function oxidase (MFO) activity may have a causal role in the production of cephalosporin nephrotoxicity, the effects of the MFO inhibitors cobaltous chloride and piperonyl butoxide on the nephrotoxicity of cephaloridine in the rabbit were examined. Although cobaltous chloride had no effect on cephaloridine nephrotoxicity, piperonyl butoxide had a significant protective effect. However, in correlated studies of the effects on the renal cortical uptake and disappearance of cephaloridine, it was found that piperonyl butoxide significantly reduces (by 50%) the cortical concentrations of the cephalosporin, both decreasing its uptake by and increasing its disappearance from tubular cells. Finally, we evaluated the effect of piperonyl butoxide on the nephrotoxicity of cephaloglycin, a more toxic cephalosporin that lacks the thiophene side-ring proposed as the target of MFO activation in earlier studies with cephaloridine. No protection against cephaloglycin was found. It is concluded that these inhibitors of MFO activity do not reduce cephalosporin nephrotoxicity in general, and that the reduction of cephaloridine toxicity by piperonyl butoxide can be explained by an effect on the intracellular concentrations of that particular cephalosporin.

Acute Kidney Injury↗
PubMed1982

Depletion of renal cortical glutathione and nephrotoxicity by cephaloridine, cephalothin and gentamicin in male Sprague-Dawley rats.

Cephaloridine and gentamicin are selectively accumulated in renal cortex and produce necrosis or proximal tubular cells. However, the mechanisms responsible for renal cortical accumulation of these two antibiotics are quite different; therefore the early pathogenetic processes may not be the same. In the present study, effects of two cephalosporins (cephaloridine and cephalothin) and an aminoglycoside (gentamicin) on rat renal cortical glutathione were determined. Cephaloridine produced a dose-related depletion of renal cortical glutathione one hour following a single administration of the drug. In contrast, cephalothin in equivalent doses did not reduce renal cortical glutathione. Gentamicin had no effect on renal cortical glutathione, even when an acutely lethal dose (1000 mg/kg) was used. Pretreatment of rats with diethyl maleate (0.4 ml/kg) markedly depleted renal cortical glutathione and this pretreatment also potentiated cephaloridine nephrotoxicity. These results suggest that glutathione may play a protective role against cephaloridine but not gentamicin nephrotoxicity.

Animals↗
PubMed1982

A library of monoclonal antibodies to nuclear proteins from Drosophila melanogaster embryos. Characterization by a cultured cell assay.

To study the structure and function of the cell nucleus, a library of 170 monoclonal antibodies was produced to nuclear antigens from 3-6 h old Drosophila embryos. In preparation for immunization, nuclei were separated, at neutral pH and in the presence of polyamines, into two fractions containing either urea-soluble non-histone nuclear proteins or histones plus small quantities of non-histone proteins complexed to DNA. The antibodies were characterized in a rapid, indirect immunofluorescent assay employing cultured Drosophila cells (Schneider's line 2). Low backgrounds and high specific fluorescence were achieved in this assay by purifying the rhodamine-labelled second antibody on a polystyrene resin and washing the cells with optimal concentrations of detergents. The assay categorized antigens according to their cellular locations: in nuclei, in nuclei plus cytoplasm, or primarily in cytoplasm. A subset of nuclear antigens reacted specifically with the nuclear envelope. In addition, some antibodies were characterized by their reactions with polytene chromosomes. The cultured cell assay provides a new, efficient method for expanding this antibody library. The monoclonal antibodies in the library now provide highly specific tools for investigating structural nuclear proteins and proteins that may be regulatory during embryonic development.

Animals↗
PubMed1982

Effects of drug-metabolizing enzyme inducers on cephaloridine toxicity in Fischer 344 rats.

High doses of cephaloridine produce necrosis of renal proximal tubular cells and this nephrotoxicity has been shown to be reduced by piperonyl butoxide (a mixed-function oxidase inhibitor) in rats and rabbits, and potentiated by phenobarbital (a mixed-function oxidase inducer) in rabbits but not rats. Phenobarbital is known to increase rabbit but not rat renal mixed-function oxidase activities; however, several other compounds such as polybrominated biphenyls (PBB), trans-stilbene oxide (TSO) and beta-naphthoflavone (BNF) have been shown to induce renal enzyme activities in rats. Thus, it was of interest to determine the effects of PBB, TSO and BNF on cephaloridine toxicity in Fischer 344 rats. Nephrotoxicity was estimated by measuring alterations in the kidney-to-body weight ratio, blood urea nitrogen and accumulation of p-aminohippurate (PAH) and tetraethylammonium by renal cortical slices. Hepatotoxicity was quantified as changes in serum glutamic pyruvic transaminase (SGPT) activity. Cephaloridine produced only minor changes in SGPT activity. Animals fed diet supplemented with 100 ppm of PBB for 10 days became less susceptible to cephaloridine nephrotoxicity. Similarly, pretreatment of animals with TSO (300 mg/kg) or BNF (100 mg/kg) for 4 days decreased cephaloridine toxicity. Thus, these results suggest that induction of renal drug-metabolizing enzyme activities by these 3 inducers may enhance some detoxification pathway(s) which convert cephaloridine to a non-toxic metabolite(s). Alternatively, treatments with these inducers may alter cephaloridine pharmacokinetics and decrease renal cortical accumulation of cephaloridine.

Animals↗
PubMed1982

5-hydroxytryptamine stimulates [3H]dopamine release from the fish retina.

Serotonin (5-hydroxytryptamine, 5-HT; 0.5 micro M and above) stimulated the release of [3H]dopamine ([3H]DA) from particulate fractions of the carp (Cyprinus carpio) retina. The 5-HT effect was dose- and Ca2+-dependent, and was structurally specific. A similar response was not elicited by the other indoles (5,6-dihydroxytryptamine, 5,7-dihydroxytryptamine, 5-hydroxytryptophan, or 5-hydroxyindoleacetic acid) examined. An increase in [3H]DA release was elicited by addition of 5-HT agonists (5-methoxytryptamine, 5-methoxy-N,N-dimethyltryptamine, and tryptamine), but not antagonized by three 5-HT antagonists (metergolin, methysergide, and spiperone). Either DA alone or noradrenaline (0.5 mM) produced a large increase in [3H]DA release from the particulate fractions, but this action was Ca2+-independent. Further, no significant release of [3H] gamma-aminobutyric acid could be evoked by 5-HT (0.5 mM) under similar experimental conditions. Taken together, the present data suggest that 5-HT stimulates [3H]DA release from the fish retina through a specific receptor-mediated mechanism on dopaminergic terminals, but not through an exchange or nonspecific phenomenon.

5-Methoxytryptamine↗
PubMed1982

Metabolism of acetaminophen by the isolated perfused kidney.

Acetaminophen (APAP) produces proximal tubular necrosis in the Fisher 344 rat. This lesion may result from the covalent binding of reactive intermediates of APAP to cellular macromolecules when glutathione (GSH) is sufficiently depleted. Experiments were designed to evaluate the ability of the kidney to convert APAP to reactive electrophilic metabolites capable of depleting renal GSH by quantifying GSH concentrations in isolated perfused kidneys perfused with APAP. Perfusion without APAP reduced (3 X 10(-5) -3 X 10(-5) M) to the perfusion medium further reduced renal GSH content. Treatment of rats with polybrominated biphenyls enhanced the ability of 3 X 10(-8) M APAP to deplete GSH. In contrast, treatment with piperonyl butoxide reduced the depletion of GSH produced by 3 X 10(-5) M APAP. At 3 X 10(-5) M APAP, the glucuronic acid, sulfate and the mercapturic acid conjugates were excreted by the isolate perfused kidneys. After treatment with polybrominated biphenyls, mercapturic acid excretion increased 4-fold, whereas the glucuronic acid and sulfate conjugate excretions were unaffected. These data suggest that the kidney can produce an electrophilic metabolite of APAP which can combine with and deplete renal GSH. An electrophilic metabolite of APAP produced by the kidney may initiate APAP induced renal necrosis.

Acetaminophen↗
PubMed1982

Renal cortical accumulation of phenobarbital in rats and rabbits: lack of correlation with induction of renal microsomal monooxygenases.

Subchronic treatment with phenobarbital induces renal cortical microsomal monooxygenase activities (e.g., ethoxycoumarin O-deethylase, benzphetamine N-demethylase and arylhydrocarbon hydroxylase) and cytochrome P-450 content in rabbits but not in rats. The mechanism responsible for this species-specific difference in renal cortical enzyme induction remains unknown, but may be the result of differences in the renal cortical accumulation of phenobarbital by these two species. Rabbit kidneys may be capable of accumulating more phenobarbital than rat kidneys. In the present study, accumulation of phenobarbital by renal cortical slices and the disposition of phenobarbital in vivo were determined. Both rat and rabbit renal cortical accumulation of phenobarbital was partially energy-dependent and inhibited by SKF-525A. Renal cortical accumulation of phenobarbital in rats was also inhibited by piperonyl butoxide. Accumulation of phenobarbital in rabbit renal cortical slices was not greater than that in rat renal cortical slices. Furthermore, rabbit renal cortex did not accumulate more phenobarbital in vivo than rat renal cortex. These results suggest that the different enzyme inducing effects of phenobarbital in rat and rabbit kidneys is not due to quantitative differences in accumulation of phenobarbital in renal cortex.

Animals↗
PubMed1981

Ouabain binding to chick embryo neuroretina during development in ovo and in monolayer cultures.

Eight-day-old embryo neuroretinas (NR) were dissociated and cultured as monolayer. [3H]Ouabain binding was investigated during the culture period. [3H]Ouabain binding to NR increases continuously until around the tenth day of culture, but after that it gradually decreased. On the other hand, [3H]ouabain binding to NR during in ovo development continued to increase until the embryo was 20 days old. Na-K-ATPase activity was also compared with [3H]ouabain binding during development in ovo and in monolayer culture. It was found that changes in Na-K-ATPase activity of NR in vitro and in ovo were different from those of [3H]ouabain binding activity. Exposure of NR at the second day of culture to 0.1 mM ouabain for 8 h resulted in the degeneration of some differentiated neurons (rosette-formed cells), but new rosettes were soon re-formed after the withdrawal of ouabain, and [3H]ouabain binding to the ouabain-treated NR was decreased by 30%. Ouabain-treatment of NR in 10-day-old cultures completely destroyed the aggregated neurons, but did not apparently injure the glial cell layer. [3H]Ouabain binding decreased more than 90% in the ouabain-treated NR. These results suggest that [3H]ouabain binding activity of NR and the sensitivity to ouabain toxicity are useful indicators for differentiation and development of neurons in the cultured retinal cells.

Animals↗