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Biomedical subjects

J L Theuws

Publications and source records attributed to J L Theuws.

28 records · Page 2Linked to original sources
PubMed1984

Genotoxic exposure of workers creosoting wood.

In a small wood preserving industry spot samples were taken from contaminated surfaces at several places and tested for mutagenicity. The results suggest that the application of a wipe test can give a first indication of occupational exposure to mutagenic and carcinogenic substances, particularly when exposure occurs more from skin contact than from inhalation. One of the pesticide chemicals used to preserve wood is the mutagenic creosote . It was found that mutagens appeared in the urine of rats after intraperitoneal administration of creosote . Despite these results, no increase in mutagenicity could be detected in the urine of creosote workers in relation to their work.

Animals↗
PubMed1984

Exposure to mutagenic aromatic hydrocarbons of workers creosoting wood.

Creosote P1 is mutagenic in the Salmonella microsome assay towards strains TA1537, TA1538, TA98 and TA100 in the presence of S9 mix. The mutagenic polycyclic aromatic hydrocarbons benzo[a]pyrene and benz[a]anthracene in this mixture are detected in concentrations of 0.18 and 1.1%, respectively. Spot samples taken from contaminated surfaces in several areas of a wood-preserving industry were tested for mutagenicity. The positive results suggest that a wipe test can give a first indication of occupational exposure to mutagenic substances, particularly when greater exposure occurs via skin contact than via inhalation. In urine of rats, mutagens appeared after treatment with creosote. However, no increase in mutagenicity could be detected in urine of creosote workers in relation to their work.

Animals↗
PubMed1983

Excretion of mutagens in human urine after passive smoking.

Eight non-smokers were experimentally exposed to cigarette smoke by staying in a poorly ventilated room together with heavy smokers for 6 h. Air samples were taken and the extract appeared to contain mutagenic substances. This is in accordance with the presence of carcinogens in tobacco smoke. Inhalation of the contaminated air by the passive-smokers resulted in an increase in the urinary excretion of products mutagenic in the Salmonella/microsome assay. This observation suggests that there is a causality in the association between increased cancer risk and passive-smoking, as was found by other investigators.

Adult↗
PubMed1982

Mutagenicity of urine from nurses handling cytostatic drugs, influence of smoking.

Mutagenicity towards Salmonella typhimurium TA 100 of urine from smoking nurses, who were occupationally involved in the treatment of patients with cytostatic drugs, was significantly increased in comparison with that of smoking control subjects. Mutagenicity towards Salmonella typhimurium TA 100 was not increased in exposed non-smokers when compared to control non-smokers. In smoking subjects urinary mutagenicity appeared increased towards Salmonella typhimurium TA 1538 in the presence of S-9 mix. Rats pretreated with Aroclor 1254 showed higher mutagenicity in their urine than untreated rats after cyclophosphamide administration. Therefore, the synergistic effect of smoking might be due in part to induction of enzymes involved in the mutagenic activation of cytostatic drugs. Further, the animal experiments showed that cyclophosphamide (the most frequently used mutagenic cytostatic drug) can be absorbed after oral or percutaneous administration. Therefore, it is not excluded that differences in working hygiene between smokers and non-smokers also play a role.

Animals↗
PubMed1981

Involvement of non-oxidative enzymes in mutagenic activation of urine from rats, given benzidine and some other aromatic amines.

Urinary metabolites of rats treated with benzidine and some other genotoxic aromatic amines became mutagenic in the Ames assay after activation with liver cytosol from rat, mouse and guinea pig. Most of the mutagenic metabolites appeared in urine as glucuronides. Strong evidence was found that N,O-acyltransferase is responsible for the mutagenic activation by rat liver cytosol. The inhibitory effect of paraoxon and sodium fluoride indicates that the activation by mouse liver cytosol is due to the action of deacetylase. Mutagenic activation by guinea pig liver cytosol seemed to be mediated in part by deacetylase. The metabolite activated by these enzymes most likely is a glucuronidated, N-acetylated, N-hydroxylated product.

Amines↗
PubMed1980

The appearance of mutagens in urine of rats after the administration of benzidine and some other aromatic amines.

The mutagenicity of urine from rats treated with benzidine or 5 other arylamines (0.25 mmol/kg; i.p.) was studied using the Ames-assay. It was found that samples of urine collected for 24 h after the administration of the carcinogens, benzidine, 4-aminobiphenyl and 2-aminonaphthalene, showed significantly mutagenic activity, whereas no mutagenicity was observed in urine after treatment with 3,3'-5,5'-tetramethylbenzidine, 2-aminobiphenyl and 1-aminonaphthalene. Mutagenic activities were dependent on the use of either hepatic S-9 Mix or cytosol as the activating enzyme preparation. The addition of beta-glucuronidase enhanced mutagenicity, except for 2-aminonaphthalene. The appearance of mutagens in urine was studied at varying doses of benzidine and at different time-intervals after the administration. The different excretion patterns found after the activation either with S-9 Mix or with cytosolic enzyme(s) suggest the presence in urine of different types of mutagenic products.

Amines↗