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Biomedical subjects

P Pfäffli

Publications and source records attributed to P Pfäffli.

At least 55 records · Page 3Linked to original sources
PubMed1984

Burden and biochemical effects of extended tetrahydrofuran vapour inhalation of three concentration levels.

Adult male rats exposed to tetrahydrofuran vapour at 8.2 (200 p.p.m.), 41 (1,000 p.p.m.) or 82 mumol/l (2,000 p.p.m.) for 2 to 18 weeks, five days a week, 6 hrs daily, showed dose-dependent brain and perirenal fat solvent burden linearly correlated to each other. After two weeks of exposure, the body burden of tetrahydrofuran seems to decrease. This might have been caused by increased oxidative metabolism as enhanced 7-ethoxycoumarin O-deethylase activity was detected in liver and kidneys in the 2nd week and onwards. The exposure also caused inhibition of alcohol and formaldehyde dehydrogenase activities in liver at the highest dose. Biochemical effects in the cerebellum were not detected while gluteal muscle specimens showed increased succinate dehydrogenase activity in a dose-related manner. This points to effects on the energy metabolism. Muscle acetylcholine esterase activity was also increased showing possible effects on the myoneural junctions.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1984

Biochemical effects and decreased body burden of cyclopentanone by extended vapour inhalation.

Male Wistar rats exposed intermittently to cyclopentanone vapour at 50, 100 or 300 p.p.m. 6 hrs daily 5 days a week for 1 to 15 weeks showed brain and perirenal fat solvent concentrations which correlated to the exposure although they decreased at the later stages of the experiment. Cyclopentanone caused almost no effects on liver drug metabolizing enzymes or aldehyde dehydrogenase activities while an early increase in the kidney 7-ethoxycoumarin O-deethylase was found after 1 week without a concomitant increase in the cytochrome P-450 content. This effect was abolished later so that an enhancement was found only at the highest exposure level after 15 weeks. Postmitochondrial fractions isolated from liver of exposed animals metabolized cyclopentanone more actively than controls after 15 weeks.

Adipose Tissue↗
PubMed1984

Analytical, occupational and toxicologic aspects of the degradation products of polypropylene plastics.

Thermooxidative degradation of polypropylene (PP) at close to the industrial processing temperatures was studied with thermogravimetric analysis, infrared spectroscopy, and gas chromatography-mass spectrometry (GC-MS). GC-MS allowed identification of 47 volatile degradation products. Formaldehyde, acetaldehyde, alpha-methylacrolein, acetic acid, and acetone were the major products. Antioxidants markedly slowed down the degradation of polypropylene and the evolution of the degradation products. The relative amounts of the oxidized products were mostly independent of the degradation temperature or the type of antioxidant. Measurements in the plastics industry revealed low airborne concentrations of individual volatile products. The concentration of aerosols, which infrared analysis showed to resemble paraffin fumes, was significant and probably the most important hygienic hazard. The biochemical parameters (the consumption of protecting sulfhydryl groups and the effects on foreign compound metabolism) indicated that the degradation products are biologically reactive, affecting the balance of normal metabolism in exposed animals.

Air Pollutants, Occupational↗
PubMed1983

Neurotoxicity of furfuryl alcohol vapor in prolonged inhalation exposure.

Three-month-old male Wistar rats exposed intermittently (5 days weekly, 6 hr/day) to furfuryl alcohol vapor at 1 (25 ppm), 2 (50 ppm), or 4 mumol/liter (100 ppm) for 4 to 16 weeks were lighter than controls at the end of the experiment at the two higher concentration levels. Urinary furoic acid excretion was in a linear relationship to the exposure at the same time. Analysis for cerebellar creatine kinase showed increased activity in all groups throughout the experiment while succinate dehydrogenase activity decreased in a dose-dependent manner at later time points. Glial cell fractions isolated from cerebral hemispheres showed decreased succinate dehydrogenase activity while 2',3'-cyclic nucleotide 3'-phosphohydrolase activity increased at 4 mumol/liter for 16 weeks. This change was accompanied by decreased basic protein content of isolated myelin fractions. The results indicate that furfuryl alcohol, at fairly low vapor concentrations, may have significant mitochondrial effects in the brain which lead to glial cell degeneration and initiation of demyelination.

Air Pollutants↗
PubMed1982

Neurochemical effects of extended exposure to white spirit vapour at three concentration levels.

Male Wistar rats were exposed to 575 (100 ppm), 2875 (500 ppm) or 5750 mg/m3 (1000 ppm) white spirit vapour for 4-17 weeks 5 days a week, 6 h daily. Perirenal fat solvent concentration corresponded in composition and concentration to those of the vapour at all times. The neurochemical effects included a dose-dependent decrease in the cerebellar succinate dehydrogenase activity for 8 weeks while creatine kinase activity increased after 12 weeks. The specific creatine kinase activity in the glial cell fraction, a marker for astroglia, did not increase suggesting proliferation of astroglial cells in the homogenate. The serum creatine kinase activity originating mainly from striated muscle was below the control range at the two higher concentrations after 12 weeks. Simultaneous analyses for isolated muscle membrane sialic acid and uronic acid residues showed decreased concentrations in proportion to lipid phosphorus or total membrane protein. Thus, the white spirit mixture has neurochemical effects possibly caused by paraffins and the same components may have caused the muscle cell membrane effects. The lowest exposure concentration represents a virtual 'no effect' level for rats in the 17-week exposure.

Animals↗
PubMed1982

Metabolic interaction between m-xylene and ethanol.

Ingestion of a moderate dose of ethanol (0.8 g/kg) by volunteers prior to 4-h inhalation exposure to m-xylene (6.0 or 11.5 mmol/m3) caused marked alterations in xylene kinetics. After ethanol intake the blood xylene level rose about 1.5-2.0-fold and urinary methylhippuric acid excretion declined by about 50% suggesting that ethanol decreased the metabolic clearance of xylene by about one half during xylene inhalation. This effect was noticeable up until a few hours after completed xylene exposure. Urinary excretion of 2,4-xylenol, the minor m-xylene metabolite, was generally not decreased by ethanol and sometimes the reverse seemed to be the case. The disturbance of xylene kinetics can be hypothesized to be caused mainly by ethanol-mediated inhibition of microsomal metabolism. When four volunteers who ingested ethanol prior to m-xylene inhalation at the higher concentration were monitored for blood acetaldehyde, transiently raised levels were found without notable effects on ethanol elimination. This observation may explain why some individuals experienced dizziness and nausea during the combined ethanol-xylene exposure.

Acetaldehyde↗
PubMed1981

Dose-related effects of dichloromethane on rat brain in short-term inhalation exposure.

Male Wistar rats were exposed to 500, 1000 or 100 ppm as time-weighted average (t.w.a.) concentrations of dichloromethane vapour. The 1000 (t.w.a.) ppm exposure consisted of two 1-h peak concentrations (2800 ppm) on a basal exposure of 100 ppm. All exposures lasted for 6 h, 5 days weekly and for 2 weeks. The solvent burdens were analyzed in the perirenal fat samples which showed a relation to the dose with the highest values in the 1000 (t.w.a.) ppm exposures. The solvent concentrations increased in the perirenal fat between the two weeks of exposure. Blood carbon monoxide concentrations did not accurately reflect the body solvent burdens. Neurochemical effects also displayed a dose relationship, and included decreased succinate dehydrogenase activity in the cerebellum at the two higher doses and increased acid proteinase activity at 1000 ppm in the cerebrum. Withdrawal of the animals for 7 days from the 2-week exposure showed that the biochemical changes were largely abolished with the exception of decreased succinate dehydrogenase activity at 1000 ppm (t.w.a.).

Adipose Tissue↗
PubMed1981

Neurochemical effects of short-term inhalation exposure to vinyltoluene vapor.

Male rats were exposed to vinyltoluene vapor after pretreatment with polychlorinated biphenyl (PCB). Brain and body solvent burdens were in a linear relationship to the exposure level although it changed between the two weeks while the solvent accumulated in the perirenal fat. The pretreatment caused a significantly smaller burden in the fat samples. Lysosomal acid proteinase was above the control range in the brain homogenate in the highest exposure, while glutathione peroxidase and 2',3'-cyclic nucleotide 3'-phosphohydrolase showed a dose-dependent decrease in the homogenate during the first week. Acid proteinase activity in the glial cells increased above the control range only in the PCB-pretreated rats in the first week. Azoreductase increased in the glial cells above the control range only in the first week, and the pretreatment augmented the increase very significantly. All biochemical effects were largely abolished within two weeks of solvent-free period with the exception of an increase in the cerebral RNA at the highest dose level. Vinyltoluene can cause more pronounced neurochemical effects compared to styrene, xylene, or toluene at similar exposure levels.

Animals↗
PubMed1980

Neurochemical effects on rats of n-heptane inhalation exposure.

Inhalation exposure of male rats at three dose levels (4.2, 21, 62 mol/L) to n-heptane vapor caused a dose-dependent brain and body solvent burden, which increased during two weeks of exposure. Initial neurochemical effects included reduced RNA concentration and increased NADPH-diaphorase in brain at the lowest dose. Increased proteolysis was detected in the cerebral samples in the second week at all doses, and the NADPH-diaphorase returned to the control range. Brain RNA content tended to be larger than in the controls. All biochemical effects were abolished after two weeks of withdrawal from the two-week exposure, with the exception of reduced glutathione at the lowest dose. None of the rats presented clinical signs of neuropathy, which indicates that heptane and its metabolites do not share the specific neurotoxicity of hexane and its metabolites.

Adipose Tissue↗
PubMed1980

Dose-dependent neurochemical changes during short-term inhalation exposure to m-xylene.

Male Wistar were exposed to m-xylene vapor at concentrations of 2.0, 16.1, and 30.3 mumol/1 for 2 weeks (5 days a week, 6 h daily). Xylene concentrations in brain and perirenal fat increased between weeks 1 and 2 of exposure, in proportion to the exposure concentrations. Increase in brain NADPH-diaphorase and azoreductase activities was seen after week 2 at the two higher exposure levels, while superoxide dismutase activity decreased in a dose-related manner at the same time. Biochemical analyses on rats withdrawn from exposure for 2 weeks indicated that the biochemical effects were largely abolished within that time, although cerebral RNA was above the control value at the two higher exposure levels.

Adipose Tissue↗
PubMed1980

Burden and dose-related neurochemical effects of intermittent cyclohexane vapour inhalation in rats.

Intermittent daily inhalation exposure to 300, 1000 or 2000 ppm of cyclohexane vapour resulted in a dose-dependent solvent concentration in the perirenal fat in rats. The linear relationship changed between the first and second week of exposure as the body solvent burden decreased, despite the continued exposure: this was especially clear in the brain cyclohexane analyses. The salient feature in the brain was the reduction in the activity of azoreductase, while no change could be found in the RNA or glutathione content or in glutathione peroxidase activity. The azoreductase activity was somewhat below the control range after a 2-week withdrawal period, while no solvent could be found and other biochemical variables were within the control ranges.

Animals↗
PubMed1980

Dose-dependent neurochemical effects of 1,1,2-trichloro-1,2,2-trifluoroethane inhalation exposure in rats.

Male Wistar rats were exposed to 200, 1000 or 2000 ppm of 1,1,2-trichloro-1,2,2-trifluoroethane vapour for 2 weeks, 5 day/week, 6 h daily and showed a dose-dependent accumulation of the compound in perirenal fat and brain. In the first week increased NADPH-diaphorase activity was observed and there was decreased cerebral glutathione at the highest dose. During the second week these effects disappeared while RNA tended to increase, and glutathione peroxidase activity to decrease at the highest dose. After a withdrawal period of 7 days, no fluorohydrocarbon was detected and the neurochemical effects had disappeared except that brain RNA at the highest exposure was below the control range.

Animals↗
PubMed1980

Styrene and styrene oxide induce SCEs and are metabolised in human lymphocyte cultures.

Both styrene and its presumed active metabolite styrene oxide show dose response as potent inducers of sister chromatid exchanges (SCEs) in human lymphocyte cultures. The SCE inducing and clastogenic capacity of styrene in lymphocytes in vitro can be explained by gas chromatographically measurable increase of styrene oxide in styrene treated cultures.

Biotransformation↗
PubMed1980

The combined toxicity of technical grade xylene and ethanol in the rat.

1. Inhalation exposure to xylene of technical grade (300 p.p.m. in air, 6 h a day, 5 days a week, up to 18 weeks) enhanced the overall mono-oxygenation reactions (7-ethoxycoumarin O-deethylase and 2,5-diphenyloxazole hydroxylase( as well as the UDP-glucuronyltransferase activity in rat liver microsomes. 2. The simultaneous ingestion of aqueous 15-20% ethanol as drinking fluid increased the cytochrome P-450 concn. and the mono-oxygenation activity even more than the xylene exposure alone. 3. Xylene-ethanol treatment resulted in additive or less than additive effects on the measured hepatic enzyme activities. 4. Renal ethoxycoumarin deethylase activity was enhanced both by ethanol ingestion and by xylene inhalation, and the response was additive after the combined exposure. 5. Liver histology revealed that even though the xylene exposure alone did not produce detectable liver damage, the xylene-ethanol treatment produced more severe liver damage than did ethanol ingestion alone.

Animals↗