Biomedical subjects
Publications and source records attributed to R Lauwerys.
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Chowdhury and Louria [1] reported that cadmium could reduce in vitro the concentration and the trypsin inhibitory capacity of plasma alpha 1-antitrypsin. They suggested that this could explain the emphysema observed in some workers exposed to cadmium. Using the same experimental approach as these authors, we could not reproduce their observations. Furthermore, in vivo results obtained on workers excessively exposed to cadmium during more than 20 years and exhibiting obvious signs of chronic cadmium intoxication did not reveal a decrease in the concentration and the activity of plasma alpha 1-antitrypsin.
Following oral administration of lead a difference in free erythrocyte protoporphyrin (FEP) increase was found between adult male, adult female and suckling rats: young animals are more susceptible than adult female rats which in turn exhibit a greater FEP increase than adult male animals. This observation parallels that made previously in humans. Possible difference in iron metabolism does not appear to explain the sex-linked difference in FEP response to lead. Sex hormones mainly progesterone, seem to play a role but their interaction with lead on the FEP response is restricted to female rats and apparently is not mediated through changes in delta-aminolevulinic acid synthetase activity.
Recently we have reported that the proteinuria developed by workers exposed to cadmium was characterized by an increased excretion of high and low molecular weight proteins. These observations were confirmed experimentally. Female rats which were injected intraperitoneally with CdCl2 (1 mg Cd2+/kg) 5 times a week developed after 2 months of treatment a proteinuria qualitatively similar to that observed in workers exposed to cadmium. The analysis of this proteinuria by electrophoresis and gel filtration revealed an increased excretion of low and high molecular weight proteins. This animal study, which confirms previous observations on man, strengthens our hypothesis that the cadmium-induced proteinuria, classically considered as a tubular type proteinuria, is in fact a mixed type proteinuria, involving not only the tubule but also the glomerulus.
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A method for the determination of manganese in blood and urine is described. A chelate fo manganese with cupferron is extracted with methylisobutylketone and determined by flameless atomic absorption spectrophotometry. The method is directly applicable to urine but the determination of manganese in blood required a preliminary digestion step. With the use of internal standards, this technique allows the determination of manganese concentrations of the order of 1 mug/1 of urine or 1 mug/100 ml whole blood.
Lead was administered to male and female rats in drinking water for 3 and 6 weeks at the following doses: 0, 10, 100, 1000, 5000 ppm and for 6 months at 10 ppm only. Various parameters of blood - lead concentration (Pb-B), hematocrit (Htc), hemoglobin (Hb), free erythrocyte porphyrins (FEB), delta-aminolevulinate dehydratase (ALAD), reticulocytes - and tissue - ALAD, free tissue porphyrins (FTP), lead concentration (Pb-T) - were determined. Pb-B increases with dose but reaches rapidly a plateau despite continuous Pb administration. Concentration of Pb in kidney, liver and brain correlates with Pb-B. Pb does not accumulate in heart. Kidney is the main site of Pb deposition and kidney ALAD is the parameter most susceptible to lead, since reduction is observed in all treated groups after 3 weeks of exposure. However, kidney ALAD inhibition is transitory since after 6 weeks it is only observed in the 5000 ppm group. At 10 ppm lead prevents also the increase in blood ALAD activity normally associated with the reticulocytosis of repetitive bleeding. The next parameters affected by lead are: ALAD in blood which is inhibited after 6 weeks of treatment with 100 ppm lead, and FEP, delta-aminolevulinic acid plus other pyrrole-forming substances in urine (ALA-U), and FTP in kidney which are increased after 3 or 6 weeks of treatment with 1000 and 5000 ppm lead.
Lead was administred to adult female rats in drinking water (0;0.1:1 and 10 ppm) for 3 weeks before mating, during pregnancy and during 3 weeks after delivery. On day 21 after delivery the mothers and their newborns were sacrified and various parameters of blood -- lead concentration on (Pb-B), hematocrit (Htc), hemoglobin (Hb), free erythrocyte porphyrins (FEP), delta0aminolevulinate dehydratase (ALAD) -- and tissue -- ALAD, free tissue porphyrins (FTP), lead concentration (Pb-T) -- were determined. In mothers a significant increase in Pb-B and Pb concentration in kidney was found in the 10 ppm group, but this increase in lead concentration was not associated with any statistically significant modification of the biochemical parameters. In newborns, lead concentration in blood and in kidney was also significantly increased in the 10 ppm group and this lead exposure was associated with a decrease of the ALAD activity in blood and an increase of FTP in kidney. On the basis of the biochemical parameters investigated one can therefore conclude that the developing organism is more susceptible to the biological action of lead than the organism of adult animals and that the "no-effect" level of lead administered during pregnancy and in the neonatal period is around 1 ppm.
Two esterases previously identified in seminal plasma, on the basis of their electrophoretic mobility, immunogenicity and sensitivity to organophosphorus esters were detected in various human external secretions and leucocyte extracts. alpha-Esterase was found to be abundant in urine and milk whereas this enzyme occurred in a low concentration in seminal plasma, leucocyte extract, cervical mucus and sweat. The concentration of betagamma-esterase was high in seminal plasma and leucocyte extract. The enzyme was present in small amounts in urine, milk, gastric juice, saliva, sputum, tears, cervical mucus and sweat.
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Sixty-six European laboratories participated in an intercomparison program of lead, mercury, and cadmium analysis in blood, urine, and aqueous solutions. The experimental protocol was designed in such a way that the effect of precision, experience, and analytical method could be evaluated. For all the analyses, the scatter of the reported results is important. The major factor influencing the variability of the results is the intralaboratory variation. Analytical methods and degree of experience do not seem to have a significant influence. However, with the exception of mercury determination in urine, a satisfactory intralaboratory precision is not sufficient to make the interlaboratory variation acceptable. It appears that systematic errors are responsible for the high interlaboratory variation observed between "precise" laboratories.