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Biomedical subjects

A Zitting

Publications and source records attributed to A Zitting.

At least 55 records · Page 3Linked to original sources
PubMed1982

Effects of nitroglycerin and ethylene glycol dinitrate mixture (blasting oil) on rat brain, liver and kidney.

Rats were injected intraperitoneally (150 mg/kg) with a mixture of nitroglycerin and ethylene glycol dinitrate (1:3). Treatment caused a transient small increase in methemoglobin contents in blood and diminished contents of reduced glutathione in liver and brain. Hepatic cytochrome P-450 concentration and ethoxycoumarin deethylase activity decreased shortly after exposure but later the effect disappeared. Succinate dehydrogenase activity decreased in liver, kidney and brain. In brain, activity of creatine kinase increased significantly and slight increase in hepatic UDPglucuronosyltransferase and epoxide hydrolase activity was observed. Renal ethoxycoumarin activity increased transiently. The results point to interaction of hydrolytically released nitrite with hemoproteins.

Animals↗
PubMed1981

Acute effects of 2-nitropropane on rat liver and brain.

Intraperitoneal injection (50 mg/kg) of 2-nitropropane (2-NP) induced lipid accumulation, centrilobular necrosis, degranulation of rough endoplasmic reticulum, proliferation of smooth endoplasmic reticulum and mitochondrial abnormalities in rat liver 24 h after exposure. These pathological changes were accompanied by elevated serum alanine aminotransferase (ALAT) levels. Hepatic glutathione content increased rapidly in exposed rats. 2-NP depressed markedly hepatic cytochrome P-450 and microsomal monooxygenase activity while the enzyme, epoxide hydratase, UDP-glucuronosyltransferase and cytosolic glutathione peroxidase were enhanced. 2-NP caused an increase of acetylcholine esterase activity in the brain. This effect was also detected in synaptosomes isolated from exposed rats. The results suggest peroxidative damage in the cells.

Alkanes↗
PubMed1980

Effects of single and repeated exposures to thermo-oxidative degradation products of poly(acrylonitrile-butadiene-styrene) (ABS) on rat lung, liver, kidney, and brain.

Male Wistar rats were exposed to thermo-oxidative degradation products of heated poly(acrylonitrile-butadiene-styrene) (ABS). The exposures were conducted once, three times or ten times (5 nights/week, 6 h/night) in the nighttime. The degradation products included styrene, various nitriles, aldehydes, acids, and a significant aerosol fraction. The oxygen concentration in the exposure chamber was constantly above 20%. The shortest exposures caused a significant reduction of the 0-deethylation activity in lung and kidney but not in liver, as well as a decrease in tissue reduced glutathione concentration in liver and kidney but not in lung. These effects well-nigh disappeared during the two-week exposure. In these rats the cerebral glutathione was below the control range. Superoxide dismutase activity increased in liver and brain during the three-day exposure. In liver the activity reached the control value after the two-week exposure but the cerebral activity was significantly lower than in controls. The complex mixture of noxious compounds in the ABS fumes does not readily allow identification of causative agents. Nitrile-dependent histotoxic, peroxidative and reactive metabolite mediated mechanisms may be involved.

Acrylic Resins↗
PubMed1980

Mutagenicity of aerosols from the oxidative thermal decomposition of rigid polyurethane foam.

The aerosol fraction of the oxidative thermal decomposition products (700 degrees C) of rigid polyurethane foam was collected on glass fiber filters and fractionated into either-soluble neutral, acidic, and basic fractions and water-soluble compounds. The fractions showed mutagenic activity in a bacterial fluctuation test with Salmonella typhimurium TA98 or Escherichia coli CM891 as the tester strains. All the fractions induced mutations in both strains after metabolic activation with rat liver S-9 mix. The basic and the water-soluble fractions were mutagenic for S. typhimurium TA 98 even without activation. Thin-layer chromatography showed the presence of several primary aromatic amines in the aerosol. Polycyclic aromatic hydrocarbons were not detected by glass capillary gas chromatogaphy.

Aerosols↗
PubMed1980

Glutathione depletion in isolated rat heaptocytes caused by styrene and the thermal degradation products of polystyrene.

Depletion of reduced glutathione (GSH) was induced in isolated rat hepatocytes incubated with styrene or exposed for 120 min to products from oxidative thermal degradation of polystyrene. The depletion depended on the concentrations of styrene and on the degradation temperature. Styrene (1 mM) or products from degradation of polystyrene at 200 degrees C (concentration of styrene in exposure atmosphere 0.7 ppm) had no detectable effect on glutathione levels in isolated hepatocytes. At higher degradation temperatures (250 degrees C and 300 degrees C, with styrene concentrations of 2.5 and 25 ppm, respectively) a rapid depletion was detected as well as with 3 mM styrene in incubation mixture. The latency of lactate dehydrogenase was affected neither by the polystyrene degradation products nor by the styrene added to the incubation mixture.

Animals↗
PubMed1980

Decrease of reduced glutathione in isolated rat hepatocytes caused by acrolein, acrylonitrile, and the thermal degradation products of styrene copolymers.

Decrease of reduced glutathione (GSH) was induced in isolated rat hepatocytes by incubation with acrolein or acrylonitrile for 120 min or exposure to the products of oxidative thermal degradation of acrylonitrile-butadiene-styrene copolymer (ABS), styrene-acrylonitrile copolymer (SAN), and high impact polystyrene (SB). The decrease of GSH by acrolein was rapid but the cells soon recovered at acrolein concentrations of 0.025--0.25 mM. 0.5 mM acrolein depleted the cells of GSH and they were uncapable of further GSH synthesis. At concentrations of 0.25--0.5 mM concomitant lipid peroxidation impaired the integrity of the cell membranes. Also acrylonitrile induced a dose dependent GSH decrease at concentrations of 0.05--1 mM. Neither membrane damage nor lipid peroxidation was detected during 120-min incubations at these acrylonitrile concentrations. The thermal degradation products of ABS, SAN and SB caused a decrease of GSH in hepatocytes. The extent of the decrease depended on the degradation temperature and the type of the plastic. The membrane integrity was impaired in the cases where GSH was depleted almost completely; ABS degraded at 350 degrees C and SB at 250 degrees C. The measurements of lipid peroxidation by the thiobarbituric acid and the diene conjugation methods were impossible because the degradation products contained compounds which interfered with these tests.

Acrolein↗
PubMed1980

Biochemical effects of subacute formic acid vapor exposure.

Male Wister rats were exposed to 20 ppm of formic acid vapor for three and eight days, 6 h daily. Analyses for neurochemical effects and effects on drug-metabolizing enzymes in liver and in kidneys revealed significant changes. Cerebral glutathione increased initially above the control range and decreased at eight days while lysosomal acid proteinase increased at the same time. Liver ethoxycoumarin deethylase increased somewhat above the control level at the end of the exposures while hepatic glutathione decreased. Kidney cytochrome P-450 was below the control range at all times as was its glutathione content. Formic acid is an end-product of methanol metabolism as well as a thermal degradation product of polyethylene plastics, and therefore, its metabolic effects may play a role in methanol or polyethylene fume exposures.

Animals↗
PubMed1980

The effects of the fumes from heated rosin (colophony) on tissue glutathione and xenobiotic metabolism in rat lung and liver.

Rats were exposed to the fumes from heated (360 degrees C) rosin for two weeks. The particulate concentration of the fumes was 220 mg/m3. Hepatic reduced glutathione (GSH) levels were decreased by 13% while no effect on GSH in the lungs was detected. In the liver the ethoxycoumarin O-deethylation and NADPH-cytochrome c reduction were enhanced 20% by the fumes. Hepatic cytochrome P-450 and aryl hydrocarbon hydroxylase were unaffected. An inhibition of pulmonary ethoxycoumarin O-deethylation (24%) and hepatic p-nitroanisole demethylation (29%) was noted in exposed rats.

Animals↗
PubMed1979

Allergy to coriander. A case report.

After 3 years of occupational exposure to powdered coriander - a spice - a woman developed respiratory symptoms of immediate hypersensitivity. Skin tests, nasal and bronchial challenge tests and the RAST were positive to coriander. Column chromatography, enzymatic digestion of the fractions and skin testing suggested that the allergen is a protein.

Allergens↗
PubMed1979

Carbon disulphide induced activation of liver UDP glucuronosyltransferase in rats pretreated with phenobarbitone.

Carbon disulphide (CS2) exposure has been shown to activate the UDP glucuronosyltransferase of liver microsomes in rats pretreated with phenobarbitone. Now the nature of CS2 induced activation of the enzymes has been studied further. Phenobarbitone pretreated rats were exposed to 0.15% CS2 for 2 hrs on two successive days. The activity of UDP glucuronosyltransferase was measured from the liver microsomes after the enzymes was activated by incubation of the microsomes with various concentrations of the detergents Triton X-100, digitonin and cetylpyridinium chloride. The exposed animals showed an increased enzyme activity at all applied concentrations of the detergents; therefore in addition to membrane destruction by CS2 exposure, some other mechanism must also be involved in the CS2 induced activation of liver microsomal UDP glucuronosyltransferase. The changes in membrane lipid-protein interactions with l-anilino-8-naphthalene sulphonate (ANS) were also probed. The CS2 exposed animals had more high-affinity binding sites for ANS in their liver microsomal membranes, and in addition the quantum yield of ANS fluorescence was enhanced by CS2. The changes differed from those found after carbon tetrachloride exposure and suggest that, even if the two drugs have some common effects on microsomes, e.g. UDP glucuronosyltransferase activation, P-450 destruction and lipid peroxidation induction, the changes they cause in the microsomal micro-environment differ.

Animals↗
PubMed1978

Radiographic and physiological findings in patients with asbestosis.

Radiographic and respiratory functional findings are reported for a series of 133 Finnish patients with asbestosis. Of these patients, 65 (49%) were found to have radiographically mild diffuse pulmonary fibrosis (profusion 0/1, 1/0 or 1/1), 48 (36%) moderate fibrosis (1/2, 2/1 or 2/2) and 20 (15%) diffuse fibrosis in an advanced stage (2/3 or more). The type of fibrosis was mostly irregular (110 = 83%). Fibrosis was typically the most advanced in the lower zones of the lungs. Of the 133 patients, 88 (66%) showed pleural changes and 78 (59%) pleural calcifications. The more severe the fibrosis, as seen in the radiographs, the greater the decrease in vital capacity (VC) and expiratory volume in 1 s (FEV1.0). Transfer factor was generally impaired only in advanced cases of asbestosis (fibrosis 2/3 or more). In general, obstruction was not observed in this series. Pleural changes seemed to decrease VC and FEV1.0 when the fibrosis was mild (0/1, 1/0 or 1/1). They had no effect on diffusion capacity (TLco).

Adult↗
PubMed1978

Thermal degradation products of homopolymer polystyrene in air.

Polystyrene without additional compounds was treated in a laboratory oven at elevated temperatures (200 degrees, 350 degrees, 500 degrees C) under slight air flow (0.7 l/min). The thermal degradation products appearing in different phases (gases, vapors, aerosols) were collected and analyzed by methods of chromatography. Thermogravimetric analysis showed the thermal degradation of the polymer to begin at 270 degrees C in air and stop at 425 degrees C. The main groups of vaporized compounds generated were monoalkyl-substituted aromatic hydrocarbons and their oxidized products, of which styrene monomer and benzaldehyde were the most abundant. Only trace amounts of carbon monoxide and aliphatic compounds (hydrocarbons, aldehydes, and acids) were produced. The aerosol produced, the amount of which increased as the temperature rose, contained mainly fragments of the polymer chain (e.g., dimers and trimers of styrene). The traces of styrene, cumene, and ethylbenzene that appeared at 200 degrees could represent residual compounds in the initial polymer and indicate the beginning of the thermal degradation. If proportional concentrations are kept as a criterion, the important products, from the point of view of industrial hygiene, were styrene, benzaldehyde, styrene oxide, acetophenone, and l-phenylethanol. The large amount of aerosol that appeared may also be of practical importance.

Acids↗
PubMed1978

Interaction of styrene and acetone with drug biotransformation enzymes in rat liver.

In the presence of hepatic microsomes, styrene produced a type I difference spectrum, which demonstrates that styrene binds to the catalytic site of ferricytochrome P-450. A comparison of the binding parameters for the interaction of styrene with noninduced, phenobarbital-induced, and 3-methylcholanthrene-induced microsomes indicated that styrene is predominantly bound by cytochrome P-450 and not by cytochrome P-448. Inhalation exposure to a mixture of acetone (1,000 ppm, 6 h/d) and styrene (300 ppm, 6 h/d) for 5 d caused a distinct decrease in hepatic free nonprotein sulfhydryl groups. This decrease could be observed both with and without phenobarbital treatment. Acetone inhalation alone also enhanced ethoxycoumarin O-deethylase activity in rats without pretreatments. Acetone inhalation also increased the cytochrome P-450 content of liver microsomes, but it had no effect on NADPH cytochrome c reductase or epoxide hydratase activity. Combined exposure to styrene and acetone enhanced NADPH cytochrome c reductase activity in nonphenobarbital-treated rats, but no effect was seen in the phenobarbital-treated animals. Phenobarbital treatment of animals can greatly modify the biotransformation and toxicity of styrene, phenobarbital inducible P-450 hemoprotein playing a predominant role in its metabolism. Simultaneous inhalation exposure to acetone also interacts with the metabolism of styrene.

Acetone↗