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K T Chung

Publications and source records attributed to K T Chung.

At least 19 recordsLinked to original sources
PubMed1996

Effects of the nitro-group on the mutagenicity and toxicity of some benzamines.

The Ames Salmonella/microsomal assay was employed to test the mutagenicity of some benzamines (aniline, and o- and p-phenylenediamine) and their nitro-derivatives (p-nitroaniline, 2-nitro-p-phenylenediamine, 3- and 4-nitro-o-phenylenediamine), using strains TA98 and TA100 and their nitroreductase-deficient mutants, TA98NR and TA100NR, in the presence and absence of rat S9 mix. The addition of the nitro-group to benzamine molecules converted them into direct mutagens. Furthermore, the position of the nitro-group affected their mutagenic activities. Cytotoxicity testing with Chinese hamster ovary cells (CHO-K1) showed that the presence of the nitro-group in these compounds had no specific effect on toxicity. The test compounds all showed a dose-related increase in inducing chromosomal aberrations in CHO cells. However, the presence of the nitro-group did not affect potency in inducing chromosomal aberrations. Compounds containing the nitro-group had higher initial oxidation potentials and dipole moments (mu) than their nonnitro-containing counterparts. The mutagenicity and toxicity of these compounds were not related to physico-chemical properties, including oxidation potential, energy difference (deltaE) between the lowest unoccupied molecular orbital (LUMO) and the highest occupied molecular orbital (HOMO), ionization potential (I.P.), and mu.

Aniline Compounds↗
PubMed1996

Simultaneous effects of carbachol on intracellular Na+ activity, action potential, and twitch tension in guinea-pig cardiac ventricular papillary muscles.

Effects of carbachol (CCh) on the twitch tension, intracellular Na+ activity (aNai), and action potential were simultaneously measured in guinea-pig cardiac ventricular papillary muscles. In fibers driven at 60 beats/min, 100 microM CCh significantly increased the twitch tension and aNai, and decreased the action potential duration at 30 and 90% repolarization (APD30 and APD90) without changing the maximum rate of the rise of the upstroke (Vmax). Staurosporine (1 microM) alone gradually decreased the twitch tension and aNai without changing the action potential. In the presence of staurosporine, the administration of CCh restored aNai and caused the same changes in twitch tension and APD shortening with no effect on Vmax. Pretreatment with 1 microM atropine completely eliminated the effects of 100 microM CCh. Cesium (20 mM) depolarized the cell membrane and significantly increased the twitch tension and APD90 with decreases in the Vmax and aNai. CCh (100 microM) in the presence of 20 mM Cs+ biphasically decreased and increased the twitch tension and significantly decreased the Vmax and aNai with an increase in the APD90. The results suggest that the muscarinic receptor-mediated increase of aNai is protein kinase C-independent. The aNai increase is associated with the positive inotropic effect and the abbreviation of the action potential duration. In addition to the increase in aNai, the increase of the myofibrillar calcium sensitivity involved is responsible for the positive inotropic effect which is still evident after the sodium influx is inhibited by Cs+.

Action Potentials↗
PubMed1996

Effect of dietary restriction on benzo[a]pyrene (BaP) metabolic activation and pulmonary BaP-DNA adduct formation in mouse.

Hepatic microsomal xenobiotic metabolizing enzyme activities of laboratory animals can be modulated by Dietary restriction (DR). The modulation of xenobiotic metabolizing enzyme activities can affect the metabolic activation of chemical carcinogens. Acute DR (60% of the food consumption of ad libitum (AL)-fed mice for 7 weeks) reduced the body weights of the male B6C3F1 mice, and increased mouse pulmonary cytochrome P4501A1-dependent BaP metabolizing enzyme activity. The effects of DR on the formation of the specific BaP-DNA adduct, 10-(N2-deoxyguanosinyl)-7,8,9-trihydroxy-7,8,9,10-tetrahydro-BaP (BaP-N2-dG) in mouse lung can be detected by using 32P-postlabeling technique. In both AL- and DR-mice total BaP-DNA adduct formation in lung reached a peak at 48 hours after treatment with [3H]BaP and the in vivo formation of BaP-N2-dG was greater in DR mouse lung than in that of AL-animals by 22%. DR increased in vitro BaP-N2-dG formation by 39% when calf-thymus DNA was incubated with BaP using liver microsomes obtained from DR- or AL-mice as the enzyme source. The formation of the specific BaP-N2-dG adducts, measured by 32P-postlabeling, was only 20% of the total [3H]BaP-DNA adducts as determined by liquid scintillation counting. The increase of BaP-DNA adduct formation in mouse lung was correlated to the enhancement of the mouse pulmonary BaP metabolizing enzyme activity. Our results indicated that the effect of DR on the metabolic activation of BaP in mouse lung was dependent upon the mouse lung cytochrome P4501A1-dependent BaP metabolizing enzymes activities which was significantly increased by DR.

Animals↗
PubMed1995

Effect of dietary restriction on glutathione S-transferase activity specific toward aflatoxin B1-8,9-epoxide.

Dietary restriction (DR) reduced the metabolic activation of aflatoxin B1 (AFB1) in rats. This reduction may be attributed to the decrease of cytochrome P-450-mediated AFB1 epoxidation and/or increase in the detoxification of AFB1 catalyzed by hepatic glutathione S-transferase (GST) and other phase II detoxification enzymes. In this study the effect of DR on male rat liver cytosolic GST activity toward AFB1-8,9-epoxide was studied. The chemically-synthesized AFB1-8,9-epoxide was used as the substrate in this assay, and the formation of AFB1-GSH conjugate was analyzed by HPLC. Male Fischer 344 rats fed DR diets (60% of the food consumption of ad libitum (AL)-fed rats) showed a 2.4-fold increase in GST activity when AFB1-epoxide was used as the substrate. The results from the enzyme kinetic study showed that DR increased Vmax of the liver cytosolic GST but not the Km. Acute DR has little or no impact on GST activity when 1-chloro-2,4-dinitrobenzene and 2,4-dichloronitrobenzene were used as substrates. The mouse liver GST activity toward AFB1-epoxide was 3-fold greater than that of phenobarbital-induced rats, 4.5-fold greater than DR rats, and 14.7-fold greater than the GST activity of AL rats. This direct assay of liver GST activity using AFB1-epoxide as the substrate is useful for studying AFB1-induced biomarkers, such as AFB1-GSH conjugation and AFB1-DNA adducts.

Aflatoxin B1↗
PubMed1995

Mutagenicity and toxicity studies of p-phenylenediamine and its derivatives.

The mutagenicity of p-phenylenediamine and its derivatives was tested using Ames Salmonella strains TA98 and TA100. p-Phenylenediamine was weakly mutagenic to TA98 with metabolic activation. 2-Nitro-p-phenylenediamine was directly mutagenic to both strains, while 2-methyl-p-phenylenediamine required S9 mix. All the test compounds induced a dose-related increase in chromosomal aberrations in Chinese hamster ovary (CHO) cells in the absence of the S9 mix. The mutagenicity and toxicity of these compounds did not correlate with their oxidation potentials, or any other tested physicochemical properties including the energy difference between the lowest unoccupied and the highest occupied molecular orbital, ionization potential, and dipole moment.

Animals↗
PubMed1993

Effect of caloric restriction on the metabolic activation of xenobiotics.

The effect of caloric restriction (CR) on xenobiotic metabolizing enzyme activities results in alterations in the metabolic activation of chemical carcinogens, with a resultant impact on DNA-carcinogen adduct formation and DNA repair. Using aflatoxin B1 (AFB1) and benzo[a]pyrene (BP) as model carcinogens, we studied the effect of CR on the metabolic activation of these carcinogens and carcinogen-induced DNA damage and repair in terms of AFB1-DNA and BP-DNA adduct formation and removal. Male Fischer 344 rats fed calorie restricted diets (60% of the food consumption for ad libitum-fed rats) showed a reduction in the metabolic activation of AFB1 and decrease in both the in vitro and in vivo AFB1-DNA adduct formation. However, CR increased the activity of BP metabolizing enzymes resulting in an enhancement of BP-DNA adduct formation. Our results indicate that the effect of CR on metabolic activation of xenobiotics is dependent upon the selected xenobiotic metabolizing enzymes whose activities may be significantly altered by CR, and upon the nature of the chemical carcinogens which exert different structure-activity relationships during the process of chemically induced carcinogenesis.

Aflatoxin B1↗
PubMed1993

Epinephrine stimulates Na-K pump by mediation of alpha-and beta-adrenoceptors in canine cardiac Purkinje fibers.

The effects of epinephrine on the twitch tension, intracellular Na+ activity (aiNa), and action potential were simultaneously investigated in an electrically driven canine Purkinje fiber. Epinephrine (0.3 microM) increased the twitch tension, duration of action potential (APD), and plateau height with a fall in aiNa. The twitch force increased during exposure and decreased during recovery. Propranolol (3 microM) or lidocaine (10 microM) decreased the twitch tension, APD, and aiNa when added to the bathing solution alone. They partially inhibited the effects of epinephrine (0.3 microM) on the development of the twitch tension and action potential and on the decrease of aiNa. Phentolamine (2 microM) reduced the twitch tension and plateau height of the action potential but failed to eliminate the action of epinephrine on the fibers. The combined action of phentolamine and epinephrine abbreviated the APD. The effect of epinephrine on the decrease of aiNa was entirely suppressed when the fiber was pretreated with propranolol (1 microM) and phentolamine (1 microM) or in a potassium-depleted solution. The results indicate that epinephrine exerts effects on the canine Purkinje fiber by the mediation of alpha-and beta-adrenoceptors. Adrenoceptor stimulation of both types is involved in the positive inotropic effect and the activation of the sarcolemmal Na-K pump.

Animals↗
PubMed1992

Mutagenicity of azo dyes: structure-activity relationships.

Azo dyes are extensively used in textile, printing, leather, paper making, drug and food industries. Following oral exposure, azo dyes are metabolized to aromatic amines by intestinal microflora or liver azoreductases. Aromatic amines are further metabolized to genotoxic compounds by mammalian microsomal enzymes. Many of these aromatic amines are mutagenic in the Ames Salmonella/microsomal assay system. The chemical structure of many mutagenic azo dyes was reviewed, and we found that the biologically active dyes are mainly limited to those compounds containing p-phenylenediamine and benzidine moieties. It was found that for the phenylenediamine moiety, methylation or substitution of a nitro group for an amino group does not decrease mutagenicity. However, sulfonation, carboxylation, deamination, or substitution of an ethyl alcohol or an acetyl group for the hydrogen in the amino groups leads to a decrease in the mutagenic activity. For the benzidine moiety, methylation, methoxylation, halogenation or substitution of an acetyl group for hydrogen in the amino group does not affect mutagenicity, but complexation with copper ions diminishes mutagenicity. The mutagenicity of benzidine or its derivatives is also decreased when in the form of a hydrochloride salt with only one exception. Mutagenicity of azo dyes can, therefore, be predicted by these structure-activity relationships.

Aniline Compounds↗
PubMed1992

The reduction of azo dyes by the intestinal microflora.

Azo dyes are widely used in the textile, printing, paper manufacturing, pharmaceutical, and food industries and also in research laboratories. When these compounds either inadvertently or by design enter the body through ingestion, they are metabolized to aromatic amines by intestinal microorganisms. Reductive enzymes in the liver can also catalyze the reductive cleavage of the azo linkage to produce aromatic amines. However, evidence indicates that the intestinal microbial azoreductase may be more important than the liver enzymes in azo reduction. In this article, we examine the significance of the capacity of intestinal bacteria to reduce azo dyes and the conditions of azo reduction. Many azo dyes, such as Acid Yellow, Amaranth, Azodisalicylate, Chicago Sky Blue, Congo Red, Direct Black 38, Direct Blue 6, Direct Blue 15, Direct Brown 95, Fast Yellow, Lithol Red, Methyl Orange, Methyl Red, Methyl Yellow, Naphthalene Fast Orange 2G, Neoprontosil, New Coccine, Orange II, Phenylazo-2-naphthol, Ponceau 3R, Ponceau SX, Red 2G, Red 10B, Salicylazosulphapyridine, Sunset Yellow, Tartrazine, and Trypan Blue, are included in this article. A wide variety of anaerobic bacteria isolated from caecal or fecal contents from experimental animals and humans have the ability to cleave the azo linkage(s) to produce aromatic amines. Azoreductase(s) catalyze these reactions and have been found to be oxygen sensitive and to require flavins for optimal activity. The azoreductase activity in a variety of intestinal preparations was affected by various dietary factors such as cellulose, proteins, fibers, antibiotics, or supplementation with live cultures of lactobacilli.

Animals↗
PubMed1991

Mutagenicity studies of kojic acid.

Kojic acid, a fungal metabolite produced by some species of Aspergillus and Penicillium, was found to induce sister chromatid exchanges and chromosomal aberrations in Chinese hamster ovary cells in the presence or absence of the rat liver S9 mix. Furthermore, this compound was demonstrated to induce mutations in Salmonella typhimurium strains TA98 and TA100 using both plate-incorporation and preincubation methods.

Animals↗
PubMed1990

Growth inhibition of selected food-borne bacteria, particularly Listeria monocytogenes, by plant extracts.

Six extracts from Chinese medicinal plants: Tin Men Chu, Sey Lau Pai, Siu Mao Heung, Bak Tao Yung, Kam Chin Chiu and Liao Ya, were tested for their inhibitory effect on selected food-borne bacteria by the well assay technique. Among them, Tin Men Chu, Siu Mao Heung and Sey Lau Pai inhibited the growth of Staphylococcus aureus, Klebsiella pneumonia, Escherichia coli, Shigella flexneri, Streptococcus faecalis, Salmonella paratyphi, Salm. enteritidis, Enterobacter aerogenes, Pseudomonas fluorescens, Proteus vulgaris, Alcaligenes faecalis, and three strains of Listeria monocytogenes. Two of these three extracts, Tin Men Chu and Siu Mao Heung, suppressed the growth of L. monocytogenes Scott A in cabbage juice. This inhibition was prevented by the addition of protein but not sodium chloride. Plant extracts show potential to control the growth of food-borne bacteria.

Bacteria↗
PubMed1990

Survival of Aeromonas hydrophila and Escherichia coli in aquatic environments.

Survival of Aeromonas hydrophila and Escherichia coli in distilled water, pond water and effluents of anaerobic digesters were examined. Survival capabilities of A. hydrophila in various aquatic systems were similar to E. coli except in the raw effluents of anaerobic digesters, where A. hydrophila survived significantly better than E. coli for 6 days. Pathogens such as Staphylococcus aureus, Salmonella enteritidis and Vibrio cholerae were readily killed in the raw effluents of the anaerobic digester. Results explain why A. hydrophila were so numerous in many fish ponds examined in Taiwan. A. hydrophila may also be recommended as a supplemental index of fecal pollution of water supplies.

Aeromonas↗
PubMed1989

Effects of nisin on growth of bacteria attached to meat.

Nisin had an inhibitory effect on gram-positive bacteria (Listeria monocytogenes, Staphylococcus aureus, and Streptococcus lactis) but did not have an inhibitory effect on gram-negative bacteria (Serratia marcescens, Salmonella typhimurium, and Pseudomonas aeruginosa) attached to meat. Nisin delayed bacterial growth on meats which were artificially inoculated with L. monocytogenes or Staphylococcus aureus for at least 1 day at room temperature. If the incubation temperature was 5 degrees C, growth of L. monocytogenes was delayed for more than 2 weeks, and growth of Staphylococcus aureus did not occur. We also found that the extractable activity of nisin decreased rapidly when the meats were incubated at ambient temperatures and that this decrease was inversely related to the observed inhibitory effect. These findings disclosed that nisin delays the growth of some gram-positive bacteria attached to meat. However, nisin alone may not be sufficient to prevent meat spoilage because of the presence of gram-negative and other nisin-resistant gram-positive bacteria.

Animals↗
PubMed1989

Detection of lactobacilli and their interaction with clostridia in human gastrointestinal tracts and in vitro.

Culture counts of aerobic lactobacilli in the feces of vegetarians ([8.1 +/- 0.7] of log10 bacteria per gram dry weight) were higher than those of meat consumers ([5.2 +/- 0.1] of log10 bacteria per gram dry weight). Co-culture of Lactobacillus acidophilus and Clostridium perfringens in various media revealed that an interaction between these two species. The pH was the most important factor controlling their relative growth, which might explain the relative abundance of lactobacilli in feces of men and animals on vegetarian diets. Lactobacilli but not clostridia were detected in feces of newborn infants. These findings are discussed in relation to health.

Clostridium perfringens↗
PubMed1983

The significance of azo-reduction in the mutagenesis and carcinogenesis of azo dyes.

Azo dyes are widely used in textile, printing, cosmetic, drug and food-processing industries. They are also used extensively in laboratories as either biological stains or pH indicators. The extent of such use is related to the degree of industrialization. Since intestinal cancer is more common in highly industrialized countries, a possible connection may exist between the increase in the number of cancer cases and the use of azo dyes. Azo dyes can be reduced to aromatic amines by the intestinal microflora. The mutagenicity of a number of azo dyes is reviewed in this paper. They include Trypan Blue, Ponceau 3R, Pinceau 2R, Methyl Red, Methyl Yellow, Methyl Orange, Lithol Red, Orange I, Orange II, 4-Phenylazo-Naphthylamine, Sudan I, Sudan IV, Acid Alizarin Violet N, Fast Garnet GBC, Allura Red, Ponceau SX, Sunset Yellow, Tartrazine, Citrus Red No. 2, Orange B, Yellow AB, Carmoisine, Mercury Orange, Ponceau S, Versatint Blue, Phenylazophenol, Evan's Blue and their degraded aromatic amines. The significance of azo reduction in the mutagenesis and carcinogenesis of azo dyes is discussed.

Animals↗
PubMed1982

An association of carcinogenesis and decrease of cellular NAD concentration.

It is postulated that a decrease in nicotinamide adenine dinucleotide (NAD) concentration has a primary association with carcinogenesis. The following observations are presented as evidence: (1) NAD and adenosine triphosphate (ATP) concentrations are lower in cancer cells; (2) chemical carcinogens and radiation can cause a lowering of NAD concentration in precancerous cells: (3) biosynthesis of NAD in Ehrlich ascites tumor cells is altered; and (4) NAD is involved in regulating deoxyribonucleic acid (DNA) synthesis. The lowering of NAD concentration would lead to the expression of oncogene and/or virogene according to the protovirus hypothesis, and the cellular characteristics of cancer cells can also be explained through the lowering of cellular NAD concentration. Experimental approaches are also proposed.

Adenosine Triphosphate↗
PubMed1981

Mutagenicity testing of some commonly used dyes.

Seventeen commonly used dyes and 16 of their metabolites or derivatives were tested in the Salmonella-mammalian microsome mutagenicity test. Mutagens active with and without added Aroclor-induced rat liver microsome preparations (S9) were 3-aminopyrene, lithol red, methylene blue (USP), methyl yellow, neutral red, and phenol red. Those mutagenic only with S9 activation were 4-aminopyrazolone, 2,4-dimethylaniline, N,N-dimethyl-p-phenylenediamine, methyl red, and 4-phenyl-azo-1-naphthylamine. Orange II was mutagenic only without added S9. Nonmutagenic azo dyes were allura red, amaranth, ponceau R, ponceau SX, sunset yellow, and tartrazine. Miscellaneous dyes not mutagenic were methyl green, methyl violet 2B, and nigrosin. Metabolites of the azo dyes that were not mutagenic were 1-amino-2-naphthol hydrochloride, aniline, anthranilic acid, cresidine salt, pyrazolone T,R-amino salt (1-amino-2-naphthol-3,6-disulfonic disodium salt), R-salt, Schaeffer's salt (2-naphthol-6-sulfonic acid, sodium salt), sodium naphthionate, sulfanilamide, and sulfanilic acid. 4-Amino-1-naphthalenesulfonic acid sodium salt was also not mutagenic. Fusobacterium sp. 2 could reductively cleave methyl yellow to N,N-dimethyl-p-phenylenediamine which was then activated to a mutagen.

Coloring Agents↗