Residues of persistent chlorinated hydrocarbons in human tissues as studied by neutron activation analysis and gas chromatography.
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Biomedical subjects
Publications and source records attributed to E Dybing.
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Nitrovin, a nitrofuran feed additive, is shown to be directly mutagenic in Salmonella typhimurium TA 98 and TA 100 between 0.1 and 2.5 microgram per plate (0.09--2.3 micrometer). Addition of a rat-liver homogenate reduces the mutation rates. Nitrovin inhibits growth of the same bacteria in suspension cultures at concentrations above 0.09 micrometer.
Cells from a rat hepatoma grown in culture were found to activate methyldopa to intermediates which are bound irreversibly to cellular proteins. The binding reaction was not inhibited by superoxide dismutase or allopurinol, but was strongly inhibited by ascorbic acid and glutathione. Methyldopa, paracetamol and furosemide were not mutagenic in the Salmonella/mammalian-microsome mutagenicity test.
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Hexachlorobenzene (HCB)-pretreatment of rats leads to an increase in liver microsomal 2,4-diaminoanisole activation to a mutagen after a dose of 10 mg/kg intraperitoneally and to an increase in ethylmorphine N-demethylase after a dose of 50 mg/kg intraperitoneally. 2,4-Diaminoanisole mutagenicity was increased 24 hrs after HCB-pretreatment, whereas ethylmorphine N-demethylase first increased after 48 hrs. There is a sex difference in the inducing effects of HCB on ethylmorphine N-demethylase, but not on 2,4-diaminoanisole mutagenicity. HCB-pretreatment also leads to increases in 2,4-diaminoansiole mutagenicity in the kidneys, but not in the lings or in foetal liver.
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Glucuronidation of p-aminophenol, p-nitrophenol and bilirubin has been investigated in cultures of human skin epithelial cells (HE cells) and human skin fibroblasts (FB) and in homogenates from the same cells. HE cells in culture glucoronidated p-aminophenol and p-nitrophenol at rates of about 5 and 10 nmol/mg cell protein per h respectively. Bilirubin was not conjugated by HE cells. In homogenates from HE cells supplemented with UDP glucuronic acid (UDPGA) both p-aminophenol and p-nitrophenol were glucuronidated at about the same rate as by living cells in culture. Assuming that the transferase activity is the same in the whole cells compared to the homogenates, transferase activity and not UDPGA production may be the limiting factor in glucuronidation of p-aminophenol and p-nitrophenol in these cells. The glucuronidation rate of HE cells was not increased by benzpyrene or benzanthrazene. FB did not glucuronidate p-aminophenol, p-nitrophenol or bilirubin.
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