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Biomedical subjects

H Vainio

Publications and source records attributed to H Vainio.

At least 217 records · Page 12Linked to original sources
PubMed1984

Bacterial urinary assay in monitoring exposure to mutagens and carcinogens.

The bacterial bioassay procedure provides a sensitive test for the presence of mutagenic activity in urine. Its sensitivity for detecting the presence of individual chemicals may not be as high as that of specific analytical methods, but it has the following advantages: (1) many substances and metabolites may be active in a single assay, making it possible to detect mutagenic activity from unanticipated sources; (2) biological activity is demonstrated, rather than simply the presence of substances; or (3) the assay may also reflect the 'integrated' effect of multiple substances, although this capability has not been well characterized and (4) the assay can be easily coupled with a chemical analysis. The chief disadvantages of the test system are lack of sensitivity for certain specific substances, as compared to chemical techniques, and possible interference from substances normally present in urine (such as amino acids). The urinary mutagenicity assay is most useful when exposure to carcinogens and mutagens is suspected but when the specific chemical is unknown, when chemical analytical techniques are not available or when exposure is to undefined complex mixtures.

Antineoplastic Agents↗
PubMed1984

Human exposure to potentially carcinogenic compounds.

Average exposures to suspected carcinogens were surveyed for the population in Finland. Alcohol, food and tobacco constitute the largest sources of exposure. Occupational populations may be more exposed than the population at large, by many orders of magnitude. For example, occupational exposure to airborne asbestos and trichloroethylene may be 10 000 times higher than exposure outside workplaces. Application of exposure data to health surveillance and epidemiological research is discussed.

Air Pollutants↗
PubMed1983

Hypolipidemia and peroxisome proliferation induced by phenoxyacetic acid herbicides in rats.

Male Wistar rats were treated daily by gavage with two phenoxy herbicides, 2,4-dichlorophenoxyacetic acid (2,4-D)(100-200 mg/kg body wt) and 4-chloro-2-methylphenoxyacetic acid (MCPA) (100-200 mg/kg body wt), and with the chemically different glyphosate N-phosphonomethyl glycine (300 mg/kg body wt) 5 days per week for 2 weeks. A hypolipidemic drug, clofibrate [ethyl-2-(4-chlorophenoxy)-2-methylpropionate], which is structurally related to phenoxy acids, was used as a positive control (200 mg/kg body wt). 2,4-D and MCPA had several effects similar to those of clofibrate: all three compounds induced proliferation of hepatic peroxisomes, decreased serum lipid levels, and increased hepatic carnitine acetyltransferase and catalase activities. 2,4-D and MCPA, but not clofibrate, decreased lipoprotein lipase activity in the adipose tissue to about a third of the control value but did not change the lipoprotein lipase activity in the heart muscle. The data suggest that these compounds cause hypolipidemia not by enhancing the storage of peripheral lipids in adipose tissue but by preferentially increasing lipid utilization in the liver. Glyphosate caused no peroxisome proliferation or hypolipidemia, suggesting that these effects are associated with the structural similarity between phenoxy acid herbicides and clofibrate.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1983

Embryotoxicity of industrial chemicals on the chicken embryo: dithiocarbamates.

Seven dithiocarbamates and three acetates were tested for teratogenicity and lethality in three-day chicken embryos. These included: cadmium diethyldithiocarbamate (CdDE), zinc diethyldithiocarbamate (ZnDE), zinc ethylphenyldithiocarbamate (ZnEP), zinc dibutyldithiocarbamate (ZnDB), copper dimethyldithiocarbamate (CuDM), tellurium diethyldithiocarbamate (TeDE), and piperidine pentamethylenedithiocarbamate (PPM), cadmium acetate (CdAC), copper-(II)acetate (CuAC), and zinc acetate (ZnAC). The parameters measured were early deaths, recorded within two days of injection, late deaths of malformed embryos, late deaths of nonmalformed embryos, and malformed survivors. The order of embryotoxicity decreased as follows: CdAC greater than CdDE greater than ZnDE greater than or equal to ZnEP greater than or equal to ZnDB greater than CuDM greater than TeDE greater than CuAC greater than PPM greater than ZnAC. The only exception to this order was the relatively weak teratogenicity of the metal acetates as compared to dithiocarbamates. Cadmium and zinc dithiocarbamates were potent embryotoxic agents eliciting lethality and malformations at doses of 1 to 10 nmole per egg. Most embryonic deaths occurred at stages 29 to 31, and most of the dead embryos were malformed.

Acetates↗
PubMed1983

Embryotoxicity of sixteen industrial amines to the chicken embryo.

Sixteen amine compounds that are used in the rubber industry, and sodium nitrite, were tested on three-day chicken embryos for embryotoxicity. The parameters measured were: early deaths recorded within two days of injection, late deaths of malformed embryos, late deaths of non-malformed embryos and malformed survivors. The most embryotoxic chemicals were N-phenyl-N'-isopropyl-p-phenylenediamine, N,N,N-triethylethylenediamine, N,N'-dicyclohexyl-p-phenyleneamine and triethylamine, with total effect ED50 values, including deaths and malformations, between 0.11 and 0.90 mumol per egg. The ED50 values for triethylenetetramine, N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine, triethanolamine, N-phenyl-2-naphtylamine, aniline and N-nitrosodiphenylamine ranged from 1.1 to 7.0 mumol per egg. Sodium nitrite was the least potent, with an ED50 of 22 mumol per egg. Six chemicals produced no effects. They probably did not reach the embryo. The four most potent chemicals, together with aniline, caused the highest frequencies of malformations.

Amines↗
PubMed1983

Effects of methyl methacrylate on non-protein thiols and drug metabolizing enzymes in rat liver and kidneys.

Male Wistar rats received methyl methacrylate monomer (MMA) i.p. in olive oil 1.0 g/kg body weight on 3 successive days. The weight of the livers and kidneys, and the body weights did not differ from their controls. On the fifth day after treatment, hepatic NADPH-cytochrome c reductase, 7-ethoxycoumarin 0-deethylase and the 2,5-diphenyloxazole hydroxylase exhibited maximal decreases in activity (25%, 58%, 36%, respectively) without any coincident effect on the total amount of cytochrome P-450 hemoprotein itself. One week later these activities had returned to control levels. The enzymatic changes in the kidneys were smaller in magnitude, and they were also reversed sooner. A single i.p. dose of MMA (2 g/kg body weight) caused elevation of serum alanine aminotransferase activity. A tenfold increase of the excretion rate of urinary thioethers was also discovered. The hepatic reduced glutathione (GSH) was depleted in 3 h to 20% and the GSSG to half of the value in controls. In kidneys, the GSH was decreased to 48% in 3 h before an apparent phase of overrecovery. At the end of the 24 h observation period, cytochrome P-450 concentrations were somewhat decreased in the liver. The GSH contents showed dose and time-dependent reversible decreases in isolated hepatocytes when incubated for 2 h in a medium containing MMA at the nominal concentrations of 0, 2, 5, or 10 mM. None of the treatments affected either the content of cytochrome P-450 or the viability of the liver cells.

Animals↗
PubMed1983

Urinary excretion of thioethers among low-tar and medium-tar cigarette smokers.

The urinary excretion of thioethers was studied among smokers of medium-tar cigarettes (16.3 mg/cig.) and low-tar cigarettes (5.4 mg/cig.). The test persons (26 smokers and 11 nonsmokers) were healthy young men in the military service. The smokers had an increased excretion of thioethers into the urine (P = 0.002 with Mann-Whitney U-test) when compared with the nonsmokers. No differences in the amount of urinary thioethers were detected between the low-tar and medium-tar cigarette smokers. The smokers (varying from 2.0 to 8.5 mmol/mol creatinine) had more individual variation than the nonsmokers (varying from 1.5 to 4.5 mmol/mol creatinine). Furthermore, the individual variation in the group of low-tar cigarette smokers did not markedly differ from the individual variation of medium-tar cigarette smokers.

Adult↗
PubMed1983

Induction of sister-chromatid exchanges by styrene analogues in cultured human lymphocytes.

Styrene and 11 styrene analogues were tested for their ability to induce sister-chromatid exchanges (SCEs) by a 48-h treatment in human whole-blood lymphocyte cultures (72 h). Styrene, its methyl-substituted derivatives (substituted at 2-, 3-, 4-, 3,5- or beta-position) and two styrene oxides (3,5-dimethylstyrene-7,8-oxide and 4-nitrostyrene-7,8-oxide) induced a distinct dose-dependent increase in SCEs. Also, 4-methylstyrene-7,8-oxide and alpha-methylstyrene showed a positive effect, but were not able to double the mean number of SCEs/cell at the concentration ranges available. Ethylbenzene had a marginal effect on SCEs at the highest dose tested. 2-Phenylethanol did not increase SCEs. The results indicate that styrene and methylstyrenes are converted into reactive metabolites in the whole-blood lymphocyte cultures. The negative or weak effects of styrene analogues without a double bond in the side-chain (ethylbenzene and 2-phenylethanol) suggest that the reactive metabolites are derived from the conversion of the vinyl group and are styrene-7,8-oxides.

Cell Cycle↗
PubMed1983

Styrene oxidation to styrene oxide coupled with arachidonic acid oxidation by soybean lipoxygenase.

Styrene was co-oxidated to styrene oxide during soybean lipoxygenase catalyzed formation of arachidonic acid lipid peroxides. Styrene oxidation showed linear dependence on the amount of enzyme and on arachidonic acid concentration, and saturation kinetics with styrene concentration. Styrene oxide formation was dependent on the lipid substrate used and was inhibited by antioxidants. Lipid peroxides appear to be able to support styrene oxidation when produced from rat liver microsomes.

Animals↗
PubMed1983

Effects of phenoxyherbicides and glyphosate on the hepatic and intestinal biotransformation activities in the rat.

The effects of phenoxyacid herbicides 2,4-D (2,4-dichlorophenoxyacetic acid) and MCPA (4-chloro-2-methylphenoxyacetic acid), clofibrate, and glyphosate on hepatic and intestinal drug metabolizing enzyme activities were studied in rats intragastrically exposed for 2 weeks. The hepatic ethoxycoumarin O-deethylase activity increased about 2-fold with MCPA. Both 2,4-D and MCPA increased the hepatic epoxide hydrolase activity and decreased the hepatic glutathione S-transferase activity. MCPA also increased the intestinal activities of ethoxycoumarin O-deethylase and epoxide hydrolase. Glyphosate decreased the hepatic level of cytochrome P-450 and monooxygenase activities and the intestinal activity of aryl hydrocarbon hydroxylase. Clofibrate decreased the hepatic activities of UDPglucuronosyltransferase with p-nitrophenol or methylumbelliferone as the substrate. Also 2,4-D decreased the hepatic activity of UDPglucuronosyltransferase with p-nitrophenol as the substrate. MCPA decreased the intestinal activities of UDPglucuronosyltransferase with either p-nitrophenol or methylumbelliferone as the substrate. The results indicate that phenoxyacetic acids, especially MCPA, may have potent effects on the metabolism of xenobiotics. Glyphosate, not chemically related to phenoxyacids, seems to inhibit monooxygenases. Whether these changes are related to the toxicity of these xenobiotics remains to be clarified in further experiments.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1983

N,N-Dimethylformamide-induced effects on hepatic and renal xenobiotic enzymes with emphasis on aldehyde metabolism in the rat.

Male Wistar rats were dosed with N,N-dimethylformamide (DMF) in drinking water at four concentration levels (0,0.1,0.5 or 1.0 g/l) for 2 or 7 weeks. Upon evaluation of the effects in the liver increased values were found for the following parameters: liver/body weight-ratio, GSH content, ethoxycoumarin O-deethylase and UDPglucuronosyltransferase activities. The GSH content, deethylase activity and, transiently, the glucuronidation activity were slightly increased also in the kidneys. Oxidative N-demethylation of DMF by hepatic microsomes in vitro was not enhanced by oral treatment. No DMF-dependent formaldehyde liberation in vitro could be detected under conditions where formaldehyde liberation from N,N-dimethylnitrosamine could be demonstrated. However, the endogenous rate of formaldehyde generation by liver microsomes isolated from DMF-treated rats was enhanced with the highest oral dose of DMF. The daily intake of DMF lowered the activities of both formaldehyde and propionaldehyde dehydrogenases in the liver soluble fraction. No inhibition of these dehydrogenases was shown in vitro by DMF (less than or equal to 10 mM) or by its main urinary metabolite N-methylformamide (less than or equal to 10 mM). The observed impairment of aldehyde oxidation in liver and kidneys of the rat after the DMF intake could explain the mechanism behind the alcohol intolerance observed in man after DMF-exposure.

Alcohol Dehydrogenase↗
PubMed1983

Embryotoxic effects of acrolein, methacrylates, guanidines and resorcinol on three day chicken embryos.

Acrolein, four methacrylates, two guanidine compounds and resorcinol were tested for embryotoxicity on three day chicken embryos. The most potent chemical was acrolein, with the ED50 0.05 mumol per egg for the total effect, including deaths and malformations. The substances next in potency were N,N'-di-o-tolyl-guanidine and N,N-diphenylguanidine, with ED50 values 0.17 and 0.20 mumol per egg, respectively. Resorcinol and the methacrylates had ED50 values ranging from 2.4 to 22.0 mumol per egg. Acrolein, diphenylguanidine, tetrahydrofururylmethacrylate and trimethylolpropanetrimethacrylate caused the largest amounts of malformed embryos.

Acrolein↗