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Biomedical subjects

K Kurppa

Publications and source records attributed to K Kurppa.

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

Oral clefts and organic solvent exposure during pregnancy.

A cumulative case-referent study concerning selected exposures during pregnancy among mothers to children born with oral clefts has been in progress in Finland since December 1, 1977. The present study covering the initial 3.5 years' material can be regarded as a specific, more detailed extension of earlier retrospective studies concerning environmental factors in the causation of oral clefts, using material accumulated from the Finnish Register of Congenital Malformations. Information on exposures was gained by personal interviews with all the mothers. The analysis of different exposures and the classification of the material were performed blindly. Significantly more case-mothers than referent-mothers had been exposed to organic solvents during the first trimester of pregnancy (P less than 0.05).

Abnormalities, Drug-Induced↗
PubMed1982

Car painters' exposure to a mixture of organic solvents. Serum activities of liver enzymes.

The serum activities of liver enzymes of car painters (N = 102) exposed to a mixture of solvents [toluene, xylene, and other constituents; about half the threshold limit value recommended by the American Conference of Governmental Industrial Hygienists (ACGIH) in 1981] were compared with those of age-matched referents (N = 102). The activities of aspartate aminotransferase, alanine aminotransferase, ornithine carbamoyl transferase, and gamma glutamyl transferase did not differ between the exposed and the nonexposed groups. Simultaneous neurophysiological and ophthalmological examinations of the same car painters had distinguished subgroups of "solvent-affected" and "non-affected" car painters. The enzyme activities were not higher in the "affected" subgroups than in the "nonaffected" ones. The results suggest that car painters' exposure to organic solvents (at the overall level of half the threshold limit value of the ACGIH) does not increase liver enzyme activities in routine tests.

Adult↗
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

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

Marked lethality of rats in combined exposure to carbon monoxide and diethyldithiocarbamate.

Simultaneous exposure of rats to carbon monoxide (COHb 60%) and diethyldithiocarbamate (i.p. 0.5 g/kg), a superoxide dismutase inhibitor, for 2.5 h resulted in a death of sixteen out of twenty-three rats. No rats treated with saline and exposed to CO died (0/26). There were no fatalities among the group of rats injected with the diethyldithiocarbamate solution and exposed to ambient air (0/16).

Animals↗
PubMed1981

Effects of intermittent dichloromethane inhalation on blood carboxyhemoglobin concentration and drug metabolizing enzymes in rat.

Rats were exposed to dichloromethane vapor in concentrations of 500 ppm, 1000 ppm, or 1000 ppm as a time-weighted average. All of the exposures lasted for 6 h, five days a week for two weeks. Kidney microsomes displayed a dose-dependent enhancement of the ethoxy-coumarin O-deethylase activity. After the second week the enhancement was accompanied by an increase in the renal glutathione content. In the liver, the UDP-glucuronosyltransferase activity showed a dose-dependent increase and the NADPH-cytochrome c reductase activity decreased. The hepatic glutathione content remained unchanged. Dichloromethane exposure did not affect the hemoglobin concentration of the blood. An 8 to 9% COHb concentration was found after exposure in all of the study groups. The similarity of COHb concentrations suggest that, in the rat, the metabolic pathway converting dichloromethane to CO is saturated already at the lowest exposure level under study.

Animals↗
PubMed1980

Biochemical effects of carbon monoxide poisoning in rat brain with special reference to blood carboxyhemoglobin and cerebral cytochrome oxidase activity.

Male Wistar rats exposed to 1000 ppm carbon monoxide for 3 h showed a rapid removal of carbon monoxide from the blood, and a cerebral cytochrome oxidase activity within the control range immediately after the end of the exposure. The cytochrome oxidase activity decreased while carboxyhemoglobin concentration diminished during the reoxygenation period. The effect might have been caused through a loss of mitochondria by increased lipid peroxidation as cerebral glutathione concentration decreased and lysosomal acid proteinase activity increased in glial cell fractions. The present results seem to indicate that the cerebral cytochrome oxidase may not be specifically inhibited in non-lethal carbon monoxide poisoning despite its proven interactions in vitro.

Animals↗
PubMed1978

Angiotensin-converting enzyme and lysozyme in silicosis and asbestosis.

Serum angiotensin-converting enzyme (ACE) activity and lysozyme (LZM) concentration in 22 silicosis and 18 asbestosis patients were studied. These patients were compared with 57 untreated and 36 treated sarcoidosis patients. In all groups significantly raised ACE and LZM mean values were noted. Untreated sarcoidosis patients had the highest values. Raised ACE activity in silicosis and asbestosis has not been reported before, and weakens the differential diagnostic value of this enzyme determination for sarcoidosis. The similar patterns of increased ACE and LZM mean values in all three diseases suggest that these enzymes have a common source.

Adult↗
PubMed1977

Blood pressure and renin during treatment with pindolol.

Beta-receptor blocking drugs are known to decrease BP and plasma renin activity (PRA) in hypertensive patients. We treated 31 hypertensive patients with the beta-receptor blocking drug, pindolol, for 3 months. During the first month (mean daily dose 10 mg) and the second month (mean daily dose 14.2 mg) BP and PRA decreased. During the third month of pindolol therapy (mean daily dose 19.0 mg) 16 patients had an unexpected rise of BP towards control levels and PRA levels rose, too. The remaining 15 patients maintained a good antihypertensive drug effect and suppression of PRA. Pretreatment PRA was not related to BP reduction. The change in diastolic BP was not significantly related to that in PRA. The results indicate that low doses of pindolol,10-15 mg daily, will suffice in mild essential hypertension. An increasing frequency of partial drug resistance may be a result of unnecessarily high doses of pindolol.

Adult↗