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Biomedical subjects

R Lauwerys

Publications and source records attributed to R Lauwerys.

At least 109 records · Page 6Linked to original sources
PubMed1991

Depletion of sialic acid without changes in sialidase activity in glomeruli of uninephrectomized diabetic rats.

The role of sialidase in the depletion of glomerular sialic acid induced by diabetes has been investigated in uninephrectomized rats. Four months after streptozotocin administration, diabetic rats showed an enhanced urinary excretion of albumin and transferrin, which was associated with a decrease of sialic acid concentration in isolated glomeruli. Despite the sialic acid depletion, the glomerular sialidase activity was unchanged. These results indicate that the decreased glomerular sialic acid concentration observed in diabetic nephropathy might be caused by a disturbance of the sialylation of glomerular structures.

Albuminuria↗
PubMed1991

Does environmental exposure to cadmium represent a health risk? Conclusions from the Cadmibel study.

Cadmium is a very dispersive pollutant which has progressively accumulated in the environment mainly in the areas where nonferrous smelters have been in operation. An important toxicological feature of cadmium is its exceptionally long biological half-life in the human body. For the general population mainly exposed to cadmium by the diet and smoking, the kidney is the main target organ. Some studies have also suggested that cadmium might play a role in the pathogenesis of hypertension. A cross-sectional study (called Cadmibel) was undertaken to assess whether environmental pollution by cadmium in Belgium might represent a health risk. This paper does not present the detailed results of this study which are published elsewhere but simply report its main conclusions. A total number of 2327 subjects (stratified according to age and sex) was randomly sampled in two urban (Liège and Charleroi) and two rural (Hechtel-Eksel and Noorderkempen) areas, with different environmental pollution by cadmium. After allowing for the various factors known to influence cadmium accumulation, it was estimated that the cadmium body burden of the residents of the most polluted district (Noorderkempen) was 50 to 85% higher than in the less polluted areas. No statistical association was found between environmental exposure to cadmium and blood pressure elevation or the prevalence of cardiovascular diseases. However, the study has shown that the environmental exposure of the general population to cadmium may induce slight renal tubular dysfunction and may probably also affect cadmium homeostasis. The probability of tubular dysfunction (as assessed by sensitive tests) is about 10% when cadmium in urine reaches 2 micrograms/day. The morbidity associated with the changes in the renal proximal tubule and the calcium metabolism observed when the body burden of cadmium exceeds this value remains to be assessed.

Adult↗
PubMed1991

Biological responses of isolated macrophages to cobalt metal and tungsten carbide-cobalt powders.

A previous study from this laboratory, using morphological and biochemical (LDH release) parameters, has shown that tungsten carbide-cobalt dust exhibits a greater cytotoxicity toward isolated macrophages than cobalt metal powder alone. The present study extends this comparison by examining additional biological parameters. Glucose uptake and superoxide anion production by isolated macrophages were significantly more depressed by the tungsten carbide-cobalt mixture (WC-Co) than by cobalt alone (Co) while pure tungsten carbide (WC) had no effect or even stimulated the cells. For glucose-6-phosphate dehydrogenase and cell-associated plasminogen activator (PA) activities, no difference between Co and WC-Co dusts was observed. These observations add further evidence to our previous findings regarding the different biological reactivity of cobalt metal alone or mixed with tungsten carbide.

Animals↗
PubMed1991

Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony.

Unlike inorganic arsenic, inorganic trivalent antimony (Sb) is not methylated in vivo. It is excreted in the bile after conjugation with glutathione and also in urine. A significant proportion of that excreted in bile undergoes an enterohepatic circulation. In workers exposed to pentavalent Sb, the urinary Sb excretion is related to the intensity of exposure. It has been estimated that after eight hours exposure to 500 micrograms Sb/m3, the increase of urinary Sb concentration at the end of the shift amounts on average to 35 micrograms/g creatinine.

Adult↗
PubMed1991

Importance of accurate employment histories of patients admitted to units of internal medicine.

A study was undertaken to assess the importance of systematically recording occupational histories of patients admitted to an internal medicine unit of a university hospital. Detailed information on current and past employment was obtained with questionnaires and in personal interviews from 200 inpatients over a 12-month period. Twenty-one patients (10.5%) were considered to have a "primary illness" (condition causing hospital admission) probably (4.5%) or possibly (6%) related to their current or previous occupation. From the 786 primary and secondary illness and medical antecedents diagnosed for the 200 patients examined, 70 illnesses of 55 patients were considered probably or possibly related to current or previous occupation. This pilot study emphasizes the need for accurate occupational records for patients in an internal medicine ward. This task is best performed by an appropriately trained occupational physician.

Adult↗
PubMed1990

Urinary proteins and red blood cell membrane negative charges in diabetes mellitus.

The nature and origin of proteinuria in diabetes mellitus have been investigated by measuring the urinary excretion of seven specific proteins of low (beta 2-microglobin, retinol-binding protein) or high molecular weight (albumin, transferrin, hemopexin and IgG). Using the Alcian Blue binding test, we also measured negative charges on red blood cell (RBC) membrane which according to recent studies might mirror the glomerular polyanion charge. A group of 190 diabetics was examined, including 90 patients with type I diabetes, 23 type II diabetics treated with diet and/or hypoglycaemic agents and 77 longstanding type II diabetics requiring insulin therapy. With the exception of beta 2-microglobulin all proteins measured were excreted in the urine of diabetics in significantly higher amounts than in controls. The assay of transferrin proved the most sensitive (58% positive) followed by albumin (49%), IgG (34%), hemopexin (28%) and retinol-binding protein (26%). Practically the same ranking was obtained when only type I diabetics were considered. RBC membrane negative charges were diminished in diabetics and negatively correlated with the urinary excretion of albumin (r = -0.61, n = 190). RBC charges were also negatively correlated with other urinary proteins of high molecular mass (r between - 0.5 and - 0.2) but presented no relation with urinary beta 2-microglobulin or retinol-binding protein. The loss of RBC charges in diabetics most likely reflects the concomitant depletion of the glomerular polyanion responsible for the increased glomerular leakage of high molecular mass plasma proteins. The preferential increase in transferrin excretion together with the progressive rise in the urinary excretion of IgG lead us to postulate that the loss of glomerular polyanion in diabetes is accompanied, from the early stage, by a progressive decrease in the size-selectivity of the glomerular filter. The urinary excretion of retinol-binding protein was weakly correlated with albuminuria (r = 0.26, n = 186). Eight % of diabetics showed an elevation of urinary retinol-binding protein without evidence of microalbuminuria, which clearly demonstrates that a proximal tubular impairment can occur independently of the glomerular alterations in the course of diabetic nephropathy.

Adult↗
PubMed1990

Renal effects of cadmium body burden of the general population.

In a cross-sectional population study to assess whether environmental exposure to cadmium is associated with renal dysfunction, 1699 subjects aged 20-80 years were studied as a random sample of four areas of Belgium with varying degrees of cadmium pollution. After standardisation for several possible confounding factors, five variables (urinary excretion of retinol-binding protein, N-acetyl-beta-glucosaminidase, beta 2-microglobulin, aminoacids, and calcium) were significantly associated with the urinary excretion of cadmium (as a marker of cadmium body burden), suggesting the presence of tubular dysfunction. There was a 10% probability of values of these variables being abnormal when cadmium excretion exceeded 2-4 micrograms/24 h. Excretion reached this threshold in 10% of non-smokers. There was also evidence that diabetic patients may be more susceptible to the toxic effect of cadmium on the renal proximal tubule.

Acetylglucosaminidase↗
PubMed1990

Plasminogen activator activity of normal and retinoic acid-treated post-implantation embryos.

Urokinase-type plasminogen activator (uPA) has been implicated in cellular migration accompanying different biological phenomena including organogenesis. An increase in uPA activity was observed in mouse post-implantation embryos during the early organogenesis period. Since we have previously shown that all-trans retinoic acid (RA) prevented the induction of uPA in mouse peritoneal macrophages, we have now assessed whether teratogenic doses of this agent could also interfere with uPA activity in mouse embryo in vitro and in vivo. Post-implantation embryos (8.5 days) were incubated for up to 24 hr with micromolar concentration of RA resulting in the occurrence of malformations. No significant difference in uPA activity was found between control and treated embryos. Likewise, uPA activity was not altered in embryos explanted on day 9.5 from dams treated 24 hr before with a teratogenic dose of RA. This study indicates that the teratogenic activity of RA is not caused by an inhibition of the induction of uPA in embryos.

Abnormalities, Drug-Induced↗
PubMed1990

Biological monitoring of exposure to monochlorobenzene.

We assessed the exposure to monochlorobenzene (MBC) of 44 male subjects performing maintenance work in a diphenylmethane-4-4'diisocyanate producing plant. In total, 251 whole shift personal air sampling measurements (passive diffusion) were carried out and at the end of the shift, during which the time-weighted average exposure (TWA) to MCB was determined, a urine sample was collected for the analysis of 4-chlorophenol and 4-chlorocatechol, the two main urinary metabolites of MCB in human. The MCB-TWA values were log normally distributed with a median of 1.2 ppm and a range from less than 0.05 to 106 ppm. The Pearson's correlation coefficient between the log MCB-TWA (ppm) and the log concentration (mg/g creatinine) of the metabolites in post shift-urine samples amounted to 0.65 (P less than 0.001) for 4-chlorophenol (log 4-chlorophenol = 0.22 + 0.43 log MCB-TWA) and 0.72 (P less than 0.001) for 4-chlorocatechol (log 4-chlorocatechol = 0.53 + 0.58 log MCB-TWA), respectively. On the average the workers excreted three times more 4-chlorocatechol than 4-chlorophenol. The follow up of 21 workers over several days did not show any tendency for the metabolite concentration in urine to increase during the workweek.

Adult↗
PubMed1990

Ventilatory function of workers exposed to cobalt and diamond containing dust.

The ventilatory function of 48 workers occupied on the average for six years in a plant producing diamond-cobalt circular saws was compared with that of 23 control subjects. The geometric mean airborne cobalt concentrations in the two main work areas amounted to 15.2 and 135.5 micrograms/m3 respectively. The spirometric changes found in the exposed workers were compatible with a moderate restrictive syndrome and were correlated with duration of exposure.

Carbon↗
PubMed1990

Mutagenicity, carcinogenicity and teratogenicity of cobalt metal and cobalt compounds.

Cobalt metal and cobalt compounds are extensively used for the production of high-temperature alloys, diamond tools, cemented carbides and hard metals, for the production of various salts used in electroplating and as catalysts, drying agents in paints, additives in animal feeds and pigments. Cobalt oxides are used not only in the enameling industry and for pigments, but also in catalytic applications. There is no indication that cobalt metal and cobalt compounds constitute a health risk for the general population. Allergic reactions (asthma, contact dermatitis) can be induced by certain cobalt compounds. Interstitial fibrosis has also been observed in workers exposed to high concentrations of dust containing cobalt, tungsten, iron, etc., mainly in the cemented carbides and the diamond-polishing industries. Several experiments have demonstrated that single or repeated injections of cobalt metal powder or some forms of cobalt salt and cobalt oxide may give rise to injection site sarcoma in rats and in rabbits but the human health significance of such data is questionable. Intratracheal administration of a high dose of one type of cobalt oxide induces lung tumors in rats but not in hamsters. In the latter long-term inhalation of cobalt oxide (10 mg/m3) did not increase the incidence of lung cancer. The human data are too limited to assess the potential carcinogenic risk for workers. Co2+ interacts with protein and nucleic acid synthesis and displays only weak mutagenic activity in microorganisms. Some cobalt salts have been reported to enhance morphological transformation of Syrian hamster embryo cells. Cobalt chloride displays some limited mutagenic activity in yeast and some cobalt compounds are able to produce numerical and structural chromosome aberrations in plant cells. Cobalt and its salts appear to be devoid of mutagenic and clastogenic activity in mammalian cells. Cobaltous acetate and cobaltous chloride have not been found to be teratogenic in hamsters and rats respectively.

Animals↗
PubMed1990

Inorganic arsenic methylation by rat tissue slices.

Rat liver, kidney and lung slices methylate trivalent inorganic arsenic (AsIII) to monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA); the liver has the greatest methylating capacity. AsIII enters the liver cells by a diffusion process followed by extensive binding to intracellular components which favors its extensive accumulation inside the cells. Reduced glutathione regulates AsIII metabolism through several mechanisms: facilitation of AsIII diffusion into the cells, stimulation of the first methylation reaction and increase of DMA excretion by the cells. An excess of AsIII inhibits DMA production by liver cells but this inhibition is reversible; mercuric ions inhibit both MMA and DMA production probably by decreasing inorganic arsenic (Asi) uptake and the second methylation reaction. DMA can be produced from MMA by rat liver slices and this methylation step is stimulated by GSH. In contrast to AsIII, AsV is not extensively taken up by the hepatocyte and is thus poorly methylated.

Animals↗
PubMed1990

In vitro cytotoxic effects of cobalt-containing dusts on mouse peritoneal and rat alveolar macrophages.

"Hard metal disease" is a chronic lung disease characterized by the presence of interstitial fibrosis; the role of cobalt in the development of this entity is still debated. Indeed, most cases have been observed in some workplaces (grinding) of the hard metal industry and in the diamond polishing industry whereas no similar cases have been reported from workers exposed to pure cobalt powders in cobalt refineries. This study was designed to assess the in vitro toxicity (LDH release, morphology) of different cobalt-containing dusts toward murine peritoneal and alveolar macrophages. The results clearly demonstrate that, both in terms of dust particle and cobalt concentrations, the reactivity of the tungsten carbide-cobalt mixture is quite different from that of cobalt metal powder. The ground tungsten carbide-cobalt mixture prepared by the hard metal industry is almost as toxic as crystalline silica whereas, when tested separately, tungsten carbide has no effect and pure cobalt metal powder slightly impairs cell viability. The uptake of cobalt by macrophages in the presence of tungsten carbide was found to be increased. These observations may have some practical implications in industrial hygiene; they suggest that the acceptable exposure level to cobalt metal should be different when handled alone or in association with other powders such as tungsten carbide.

Animals↗
PubMed1990

Poisoning by some insecticides, herbicides and fungicides.

To avoid accidental poisoning, pesticides must be handled according to prescribed rules. Furthermore, the exact composition of the pesticide formulation should be known. Cases of acute poisoning usually occur by ingestion and less frequently by the other routes. Symptoms may appear immediately but sometimes they can appear later and/or be more prolonged giving rise to delayed death and/or delayed morbidity. Acute poisoning by raticides and by organophosphate insecticides should deserve all our attention. Poisoning by herbicides containing chlorate salts, oxidative phosphorylation uncouplers or bipyridilium derivatives may be particularly dangerous. The ingestion of Paraquat, in particular, which is a veritable lesional poison, could be beyond all therapeutic resources.

Fungicides, Industrial↗
PubMed1990

Comparison of the effects of auranofin, heavy metals and retinoids on protein kinase C in vitro and on a protein kinase C mediated response in macrophages.

The effect of auranofin (AF), retinoic acid (RA), and three heavy metals reacting with thiol groups (Hg, Cd, Pb) has been compared on a PKC mediated response of intact macrophages (i.e. plasminogen activator (PA) induction) and on purified PKC activity. AF, cadmium chloride, and lead nitrate directly inhibit PKC and hence prevent the induction of PA activity in macrophages stimulated with PMA. In vitro, and in absence of chelators, mercuric chloride is also a potent inhibitor of PKC. However, at the cellular level, the PKC mediated response (PA induction) was not inhibited by non-cytotoxic concentrations of mercury possibly due to interference of the metal with additional cellular mechanisms such as calcium mobilisation. Direct inhibition of PKC is probably not the mechanism by which retinoids block the activation of macrophages.

Animals↗
PubMed1990

Assessment of urinary protein 1 and transferrin as early markers of cadmium nephrotoxicity.

Transferrin and protein 1, a sex linked alpha 2-microprotein, were assayed in urine from 58 workers exposed to cadmium (Cd) in a non-ferrous smelter and from 58 age matched referents. These two new markers of nephrotoxicity were compared with urinary beta 2-microglobulin (beta 2-m), retinol binding protein (RBP), albumin, and beta-N-acetyl-glucosaminidase (NAG). The response of protein 1 to Cd tubulotoxicity was similar to that of beta 2-m, RBP, and NAG. In Cd workers, protein 1 had a correlation with urinary Cd (r = 0.56) similar to beta 2-m (r = 0.48), RBP (r = 0.58), and NAG (r = 0.49). Values of these three low molecular weight proteins and of NAG were increased only in workers with urinary Cd higher than 10 micrograms/g creatinine. Urinary transferrin and albumin were similarly affected by exposure to Cd. Their response, however, was clearly more sensitive than that of low molecular weight proteins. Prevalences of positive values of these two high molecular weight proteins were not only higher but also tended to rise at lower concentrations of Cd in urine or blood. This finding suggests that in some subjects subtle defects in glomerular barrier function may precede the onset of proximal tubular impairment after chronic exposure to Cd. It remains to be assessed whether these subjects are more at risk of developing renal insufficiency.

Acetylglucosaminidase↗
PubMed1990

Health effects of environmental exposure to cadmium: objectives, design and organization of the Cadmibel Study: a cross-sectional morbidity study carried out in Belgium from 1985 to 1989.

Cadmium is a cumulative environmental pollutant. For the general population mainly exposed by the oral route and through tobacco smoke inhalation, the kidney is the critical organ. Belgium is the principal producer of cadmium in Europe, and certain areas of the country are polluted by cadmium mainly because of past emissions from nonferrous industries. Preliminary studies carried out in one polluted area have suggested that environmental pollution might lead to an increased uptake of cadmium by the human body and possibly to health effects. Thus, a large-scale morbidity study has been initiated to assess the validity of this hypothesis. The present paper describes the protocol of this study. Its main objectives are to determine to what extent environmental exposure to cadmium resulting from industrial emissions may lead to accumulation of the metal in the human organism; to establish whether or not environmental exposure may induce renal changes and/or influence blood pressure; and to assess the acceptable internal dose of cadmium for the general population. The study design takes advantage of the fact that biological indicators of exposure, body burden, and early nephrotoxic effects of cadmium are available, which increase the likelihood of detecting a cause-effect relationship.

Adult↗