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Biomedical subjects

H Vainio

Publications and source records attributed to H Vainio.

At least 253 records · Page 14Linked to original sources
PubMed1982

Subacute toxicity of vinyltoluene vapour: effects on the hepatic and renal drug biotransformation and the urinary excretion of thioether.

Male rats were exposed by inhalation to vinyltoluene at concentrations of 50, 100, or 300 p.p.m. for 8, 12 or 15 weeks. Vinyltoluene was found to be metabolized to glutathione conjugates via the formation of electrophilic intermediates. This metabolic pathway was suggested by the decreased hepatic non-protein sulfhydryl content, with a concomitant increase in the urinary excretion of thioethers. The excretion of thioethers showed no saturation phenomena, suggesting that the formation of electrophilic intermediates capable of conjugating with glutathione is fairly linear, at least with exposure to vinyltoluene vapour up to 300 p.p.m. The slight increase in the activities of hepatic drug biotransformation enzymes (7-ethoxycoumarin 0-deethylase. UDPglucuronosyltransferase) observed after 8 weeks of exposure to vinyltoluene vapour disappeared by week 15 irrespective of the continued intermittent inhalation of vinyltoluene. Histological study revealed that cell size had decreased in the rats exposed to vinyltoluene.

Animals↗
PubMed1982

Identification of mutagen exposures in the rubber industry by the sister chromatid exchange method.

The rubber industry is known to use a large and expanding array of chemicals, some of which are experimentally proven mutagens or carcinogens. An association with cancer risk has been shown in several epidemiological studies carried out in the rubber industry. Sister chromatid exchanges were studied in blood lymphocytes of 54 workers from various job categories in two rubber plants and 34 control subjects mainly from office jobs. The highest numbers of SCEs were observed among rubber workers who smoked, but smokers in the control group also differed significantly from non-smokers by their incidence of SCEs. In both rubber plants the highest incidence of SCEs was observed among workers employed in the mixing operations of the rubber chemicals.

Adult↗
PubMed1982

Inhalation anesthetics, anticancer drugs and sterilants as chemical hazards in hospitals.

In recent years, there has been a considerable increase in the use of chemicals (chemical sterilants and antimicrobial agents, antineoplastic drugs, and anesthetic gases) in hospitals. The possible existence of occupational health hazards has often been overlooked in light of the great advantages provided by the use of chemical agents. It appears that certain hospital sectors, such as anesthesia units, sterilizing units and oncology units, require different degrees of caution and protective measures with respect to the handling of chemicals. The scientific evidence on which recommendations should be based is, in most cases, fairly meager; until more is known about the hazards, it would be prudent to minimize the occupational exposure to chemicals in hospitals.

Abnormalities, Drug-Induced↗
PubMed1982

Phenoxy acid herbicides cause peroxisome proliferation in Chinese hamsters.

An increase in either the size or amount of peroxisomes was obtained in the liver cells of Chinese hamsters after the animals were exposed to the phenoxy herbicides 2,4-dichlorophenoxyacetic acid (2,4-D) or 4-chloro-2-methylphenoxyacetic acid (MCPA). At the dose level studied, 2,4-D was found to be more potent than MCPA in increasing the number of peroxisomes. A phenoxy acid derivative, clofibrate, one of the peroxisome proliferators known to possess carcinogenic properties in rodents, appeared to be still more potent in inducing peroxisome proliferation than either of the herbicides studied. Further investigations are warranted to clarify the significance of peroxisome proliferation to the toxicity of phenoxy herbicides.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1982

Application of the chicken embryo in testing for embryotoxicity: thiurams.

A test protocol was developed for the testing of chemicals for toxicity on the chicken embryo. The protocol called for a continuous monitoring of the developing embryo for those that died before maceration. The eggs were injected on day 3, and the test was continued up to day 14 of incubation. The following parameters of embryotoxicity were used: early deaths (spanning the first 2 d after injection), late deaths with malformed embryos, late deaths with nonmalformed embryos, and malformed survivors. The order of embryotoxic potency, in descending order, among the thiurams was tetramethylthiuramdisulfide, tetramethylthiurammonosulfide, tetraethylthiuramdisulfide. It was found that late deaths were seen in 70% of the cases with malformations. The most common types of malformations were eye defects and open coeloms. Dead embryos frequently had multiple malformations. In lethal cases, embryonic development terminated at stages 25/26 and 29 on the Hamburger-Hamilton scale.

Abnormalities, Drug-Induced↗
PubMed1982

Possibilities for identifying genotoxic risks in the rubber industry: use of the urinary mutagenicity assay and sister chromatid exchange.

Two approaches have been used for biological monitoring of exposure to genotoxins in the rubber industry: (1) assay of mutagenic activity in urine with the bacterial fluctuation test; and (2) analysis of sister chromatid exchange frequencies in peripheral blood lymphocytes. Workers in the rubber industry have significantly more mutagenic activity in their urine than nonexposed controls. Mutagenic activity was tested with Escherichia coli WP2 uvrA as indicator bacteria was significantly higher in urine of workers after a normal work week than in urine samples from the same individuals after a holiday. The mean frequency of sister chromatid exchange in rubber workers who smoked was significantly higher (p less than 0.01) than that in unexposed smokers. The only job categories in which workers who smoked had statistically significantly higher mean frequencies than others were mixing and weighing. People in these jobs generally also had high mutagenic activity in their urine.

Female↗
PubMed1981

Metabolism and genotoxicity of styrene.

An overview on the metabolism and genotoxicity of styrene is given in this article. The mutagenic potency of styrene has been confirmed in a number of test systems providing the metabolic activation of styrene. Styrene is converted to styrene-7,8-oxide as catalyzed by cytochrome P-450 cored enzyme complex. Styrene-7,8-oxide is mutagenic in prokaryotic and eukaryotic test systems without metabolic activation. It reacts with nucleic acid bases, especially with deoxyguanosine producing 7-alkylguanine and deoxycytidine producing N-3 alkylcytosine. Quite recently, styrene-7,8-oxide has been found to be a potent carcinogen in rats. In human whole blood cultures, styrene is metabolized into styrene-7,8-oxide. Styrene is able to induce both SCEs and chromosomal aberrations in cultured lymphocytes. The clastogenic action of styrene can be explained by the metabolism of styrene into styrene-7,8-oxide in cultured human blood cells. Although also an arene oxide, styrene-3,4-oxide, has been suggested in the biotransformation of styrene, the evidence so far supports the view that the vinyl group oxidation and oxirane formation plays a predominant role in the genotoxicity of styrene.

Animals↗
PubMed1981

Alkylation of guanosine and 4-(p-nitrobenzyl)-pyridine by styrene oxide analogues in vitro.

In vitro alkylation activity of styrene oxide (SO) and three of its analogues, 4-vinyltoluene oxide (VTO), 3,5-dimethylstyrene oxide (DMSO), and 4-nitrostyrene oxide (NSO) was assayed using 4-(p-nitrobenzyl)pyridine (NBP) and guanosine as nucleophiles. Hydrolysis rates were also determined. The half-lives of VTO, DMSO, SO, and NSO were 8, 11, 40, and 60 h, respectively in aqueous solution. The rate of NBP alkylation correlated with the rate of hydrolysis. By contrast, the rates of guanosine alkylation were quite different: SO greater than VTO greater than DMSO. NSO did not react with guanosine. Fluorescence an ultraviolet spectroscopic data on the guanosine adducts indicated that SO, VTO, and DMSO formed main alkyl products at N-7.

Alkylation↗
PubMed1981

Dichloromethane and carbon monoxide inhalation: carboxyhemoglobin addition, and drug metabolizing enzymes in rat.

Male Wistar rats were exposed for 3 h to 100 ppm Co, 1,000 ppm dichloromethane, or to their combination. Exposure to dichloromethane alone or in combination with CO double the ethoxycoumarin O-deethylase activity in the kidney microsomes but not in the liver. An additive effect on blood COHb concentration by simultaneous exposure to CO and dichloromethane was observed. The mechanism of the additive effect is discussed.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1981

Dose-dependent toxicity of ethylene glycol monomethyl ether vapour in the rat.

Wistar male rats were exposed by inhalation to 50, 100 or 400 ppm of ethylene glycol monomethyl ether (EGME) for 1 to 2 weeks. The overall hepatic drug oxidation reactions, O-deethylation of 7-ethoxycoumarin and 7-ethoxyresorufin and cytochrome P-450 content were only slightly affected by the EGME exposures. NADPH cytochrome c reductase activity showed a tendency toward a dose-dependent decrease in liver, the activity being 73% and 64% of that in the controls after one and two weeks of exposure, at 400 ppm respectively. UDP glucuronosyl transferase activity exhibited a dose-dependent enhancement in liver microsomes after exposure for two weeks to EGME. The enhancement was 1.3- 1.7- and 3.0 fold with exposure to 50, 100 and 400 ppm of EGME respectively. After exposure for one week the UDPglucuronosyltransferase activity in kidney microsomes was similarly enhanced. A dose-related increase in measurable UDPglucuronosyltransferase activity was also obtained in Triton X-100 treated hepatic microsomes. GSH levels of the liver and kidneys in EGME treated animals showed a tendency towards a dose-dependent increase. The activities of low-Km and high-Km aldehyde dehydrogenases in liver were decreased 6 - 14% of that in the controls with exposure to 400 ppm of EGME when glycolaldehyde was used as a substrate. Serum alanine aminotransferase activity was not influenced by inhalation exposures to EGME.

Animals↗
PubMed1981

Interactions of styrene and styrene oxide with partially purified cytochrome P-450 and P-448 from rat liver microsomes.

Styrene and styrene 7,8-oxide were able to bind both to partially purified cytochrome P-450 isolated from phenobarbital (PB)-treated rat liver and to cytochrome P-448 from liver microsomes of 3-methylcholanthrene (3-MC)-treated rats. In the presence of either purified preparation or "fresh" microsomes from PB- or 3-MC-treated animals, styrene produced a characteristic Type I difference spectrum as did styrene 7,8-oxide with "fresh" microsomes from PB rats. In other experiments, the addition of styrene oxide produced spectra which resembled Type I spectra but were somewhat shifted to longer wavelengths. A comparison of the binding parameters for the interaction of styrene or styrene 7,8-oxide with partially purified preparations and "fresh" microsomes indicated that the binding is catalyzed by more than one type of P-450 hemoprotein and that the binding affinity is slightly reduced by the purification procedure. The addition of phosphatidylcholine was unable to restore the binding parameters.

Animals↗