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Biomedical subjects

J K Lin

Publications and source records attributed to J K Lin.

At least 217 records · Page 12Linked to original sources
PubMed1980

Determination of urinary amino acids by liquid chromatography with "dabsyl chloride".

We describe a "high-performance" liquid-chromatographic procedure for measuring amino acids in 0.5 mL of urine. The procedure includes direct derivatization of amino acids in urine samples with "dabsyl chloride" (4-dimethylaminoazobenzene-4'-sulfonyl chloride). An aliquot of this dabsylated amino acid solution is analyzed on a muBondapak C18 column with ethanol/sodium acetate (20 mmol/L, pH 4.0) 4/6 (by vol.), as mobile phase. Dabsylated amino acids are detected by their absorbance at 425 nm and quantitated by measuring peak heights. The procedure allows for the reliable analysis of amino acids in urine at concentrations near 16 mg/L. The sensitivity of this analysis on column approaches 5 ng/sample. Higher urinary tryptophan concentrations were found in the urines of some cancer patients, whereas we saw no significant difference in urinary glycine between cancer patients and control subjects. The present method was shown to be a straightforward procedure for detecting phenylalanine in phenylketonuric urine. Extension of this procedure to screening for other inborn errors of aminoaciduria is recommended.

Amino Acids↗
PubMed1979

Detection by antihapten antibodies of liver-bound compounds related to azocarcinogens or their metabolites.

The localization of known azocarcinogens and metabolites such as p-aminoazobenzene and N-methyl-p-aminoazobenzene bound to components of liver cells of rats fed single or multiple doses of 3'-methyl-p-dimethylaminoazobenzene has been determined with the use of antibodies raised against p'-azo-p-aminoazobenzene and p'-azo-N-monomethyl-p-aminoazobenzene in the indirect fluorescent antibody procedure. These 2 antisera reacted with liver cells of rats fed 3'-methyl-p-dimethylaminoazobenzene, p'-amino-p-aminoazobenzene, p'-amino-N-monomethyl-p-aminoazobenzene and N-methyl-p-aminoazobenzene. The results obtained in this study suggest that both major and minor metabolites of azocarcinogens have common antigenic determinants.

Animals↗
PubMed1978

Reduced nicotinamide adenine dinucleotide phosphate-dependent formation of 2,3-dihydro-2,3-dihydroxyaflatoxin B1 from aflatoxin B1 by hepatic microsomes.

2,3-Dihydro-2,3-dihydroxyaflatoxin B1 (dihydrodiol) was formed as a major metabolite in the incubation of aflatoxin B1 with rat and hamster liver microsomes. The yield of the dihydrodiol was maximal at pH 6.5, was reduced nicotinmide adenine dinucleotide phosphate- and cytochrome P-450-dependent, and was increased 2- to 4-fold by pretreatment of the animals with phenobarbital; pretreatment with 3-methylcholanthrene did not alter the activity of rat hepatic microsomes. Inhibitors of epoxide hydrase did not lower the yield of the dihydrodiol in these systems. Negligible yields of the dihydrodiol were formed from aflatoxin B1 and rat liver microsomes in the presence of DNA. Little or no formation of the dihydrodiol was noted with microsomes from rat intestinal mucosa, kidney, or lung. These results further support the formation of aflatoxin B1 2,3-oxide as a major electrophilic metabolite of aflatoxin B1 in rat and hamster liver microsomal systems, since this highly reactive epoxide would be expected to hydrolyze readily to form the dihydrodiol.

Aflatoxins↗
PubMed1977

Aflatoxin B1-2,3-oxide as a probable intermediate in the covalent binding of aflatoxins B1 and B2 to rat liver DNA and ribosomal RNA in vivo.

Administration of[3H]aflatoxin B2 (2,3-dihydroaflatoxin B1)(AFB2) to male rats resulted in levels of hepatic DNA- and ribosomal(r)RNA-aflatoxin adducts that were about 1% of those for rats given [3H]aflatoxin B1(AFB1). The levels of hepatic protein-aflatoxin adducts were 35 to 70% as great for AFB2-treated as compared to AFB1-treated rats...

Aflatoxins↗
PubMed1975

N-substitution of carbon 8 in guanosine and deoxyguanosine by the carcinogen N-benzoyloxy-N-methyl-4-aminoazobenzene in vitro.

The major reaction products of the carcinogenic electrophile N-benzoyloxy-N-methyl-4-aminoazobenzene with guanosine or deoxyguanosine were characterized as N-(guanosin-8-yl)- and N-(DEOXYGUANOSIN-8-YL)-N-methyl-4-aminoazobenzene from the following chemical, radiochemical, and spectroscopic studies: (a) the presence of equimolar amounts of both N-methyl-4-aminoazobenzene (MAB) and guanosine or deoxyguanosine residues was shown by the 3H:14C ratios of the products from the reaction of (prime ring-3H)-N-benzoyloxy-N-methyl-4-aminoazobenzene with (8-14C)guanosine or (8-14C)deoxyguanosine and by the molecular weights of the trimethylsilyl derivatives of both products: (b) substitution of the dye residue on its amino nitrogen was indicated by the retention in the products of the 3H:14C ration of (CH2-3H + 14CH3)-N-BENZOYLOXY-N-methyl-4-aminoazobenzene and by the release of MAB on treatment of the nucleoside-dye derivatives with strong alkali in air; (c) substitution of the guanine residues in positon 7 or 8 was demonstrated by loss of 3H from (8-3H)guanosine or (8-3H)deoxyguanosine in the formation of the nucleoside-dye derivatives; (d) the stability of the products to mild alkali (as contrasted to the lability of 7-alkylguanosines) provided strong evidence that the substitution was in position 8 of the guanine residue; (e) direct evidence of 8-substitution came from the acid hydrolysis of guanosinyl- and deoxyguanosinyl-N-methyl-4-aminoazo benzene to N-(guan-8-yl)-N-methyl-4-aminoazobenze in up to 50% yield; (f) comparisons of the proton or 13C nuclear magnetic resonance spectra or both of N-(guan-8-yl)- N-methyl-4-aminoazobenzene, MAB, N-(guanosin-8-yl)-2-acetylaminofluorene, 2-acetylaminofluorene, guanosine, and 7 -methylguanosine with the spectra of the guanosine-MAB product further confirmed that substitution had occurred at position 8 of the guanosine residue. The new compound N-(guan-8-yl)-N-methyl-4-aminoazobenzene was synthesized. Attempts to devise an unambiguous synthesis of N-(GUANOSIN-8-YL)-N-methyl-4-aminoazobenzene were not successful.

Amines↗
PubMed1975

Structures of hepatic nucleic acid-bound dyes in rats given the carcinogen N-methyl-4-aminoazobenzene.

Rats were given the hepatocarcinogenic dye N-methyl-4-aminoazobenzene labeled in the prime ring with tritium. The hepatic ribosomal RNA and DNA from these rats were hydrolyzed to uoe;d imce;psode-dye products. The major nucleoside-dye derivatives cochromatographed with synthetic N-(guanosin-8-yl)-and N-(deoxyguanosin-8-yl)-N-(methyl-4-aminoazobenzene, respectively, on cellulose and silica gel thin layers in several solvent systems. Additional evidence for the characterization of the hepatic RNA-nucleoside derivative was obtained through its degradation by alkali in air to N-methyl-4-aminoazobenzene and -4-aminoazobenzene, as previously described for N-(guanosin-8-yl)-N-methyl-4-aminoazobenzene. The same nucleoside derivatives were also derived from ribosomal RNA and DNA reacted in vitro with the carcinogenic electrophilic derivative N-benzoyloxy-N-methyl-4-aminoazobenzene, esterification of the N-hydroxy derivative, and reaction of the resultant electrophilic esters with DNA and RNA.

Amines↗