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Biomedical subjects

K Pekari

Publications and source records attributed to K Pekari.

24 records · Page 2Linked to original sources
PubMed1984

Skin absorption as a source of error in biological monitoring.

Concentrations of toluene, tetrachloroethylene, and 1,1,1-trichloroethane were determined in blood collected from both forearms of subjects after one of their hands was soaked for 5 min in the corresponding solvent or in a thinner containing toluene, as a simulation of the washing of hands with solvent after work. The concentrations of toluene, tetrachloroethylene, and 1,1,1-trichloroethane on the soaked side were high, maximally 5.4, 9.0, and 4.0 mumol/l, respectively, and 20-, 130-, and 35-fold, respectively, compared to the contralateral side. Intraindividual differences were very marked, and dramatic changes were detected within a short period of time. It was not until after 3 h with toluene and 5 h with the chlorinated solvents that the difference between the two arms vanished. It is concluded that analyses of solvents in blood specimens drawn during or immediately after the workday may lead to markedly erroneous estimations of exposure.

Environmental Exposure↗
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↗
PubMed1979

Neurochemical and behavioural effects of extended exposure to isopropanol vapour with simultaneous ethanol intake.

Exposure of male Wistar rats to 12.3 mumol/l (300 ppm) isopropanol vapour for 5-21 weeks, 5 days a week for 6 h daily with a simultaneous ethanol administration in drinking water (5% v/v) caused a significant increase in isopropanol removal as assessed by blood isopropanol and acetone determinations. Ethanol treatment caused a marked synergistic effect during early exposure. Neurochemical studies revealed decreased superoxide dismutase and azoreductase activities at the end of the exposure whereas increased protein degradation was found in glial cells isolated from ethanol-fed rats throughout the experiment. Analyses of spinal cord axon lipid composition showed increases in cholesterol content in relation to lipid phosphorus in animals exposed to isopropanol or to the isopropanol and ethanol combination. Behavioural tests indicated minor effects on emotional reactivity from the 10th week onwards with isopropanol exposure whereas caffeine-stimulated activity was augmented only in rats ingesting ethanol. Co-exposure to isopropanol vapour abolished the increased excitability. The data indicate that marked metabolic and functional adaptation towards the small-molecular-weight alcohols takes place at moderate dose levels.

1-Propanol↗
PubMed1979

Neurochemical effects of peroral administration of technical pentachlorophenol.

Administration of technical pentachlorophenol in drinking water (20 mg/l) to male Wistar rats caused significant liver concentration of tetrachlorophenol which remained stable during the exposure of 14 weeks. Pentachlorophenol and tetrachlorophenol accumulated to some extent in the perirenal fat whereas only pentachlorophenol could be found in brain. A period of four weeks of chlorophenol-free diet was sufficiently long to allow removal of the major part of the chlorophenol burden. The neurochemical effects included increased acid proteinase activity at the 8th week of exposure. It levelled off while superoxide dismutase activity increased to twice the control level. Glial glutathione peroxidase activity did not change whereas glial glutathione concentration was below the control range at the 12th week of exposure. Cerebral diaphorase activity was below the control range initially, and its activity increased above the control level during the recovery period whereas other biochemical changes levelled off.

Adipose Tissue↗