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Biomedical subjects

A Hudák

Publications and source records attributed to A Hudák.

At least 19 recordsLinked to original sources

Effects of cobalt sulfate on prenatal development of mice, rats, and rabbits, and on early postnatal development of rats.

The effects of cobalt sulfate administered to pregnant C57BI mice, OFA-SD rats, and New Zealand rabbits was studied on fetal and postnatal offspring. Cobalt concentration in the maternal blood was increased in proportion to the administered doses. Cobalt crossed the placenta and appeared in the fetal blood and amniotic fluid. Regardless of the administered dose of cobalt sulfate, cobalt concentration in the blood peaked 2 h after administration. Cobalt produced dose-dependent maternal toxicity and was found to be embryotoxic in all three species, as evidenced by elevated frequency of fetuses with body weight or skeletal retardation and embryolethality. Cobalt increased the frequency of major anomalies significantly in mice and rats, with anomalies of the eyes, kidneys, skull, spine, and sternum in mice, and anomalies of the urogenital system in rats. Cobalt sulfate was not teratogenic in rabbits. Intra-amnial administration of cobalt sulfate produced a dose-dependent increase of the frequency of dead fetuses, and weight retardation of the live fetuses. The direct cytotoxic effect probably plays a role in the embryotoxic and teratogenic effects of cobalt. The postnatal examinations revealed a decrease of the perinatal index in the treated group. The body weight of the pups in the treated group was lower during wk 1 of life, but no difference was found between the control and treated by the end of wk 2. Eye opening was completed in the usual time period in both groups, while time of appearance of the teeth, descending of the testes, shaping of ears, and development of hearing was delayed in the treated group. The development of muscle strength and of the locomotor system was delayed. All the functions studied (forward movement, swimming, righting reflex) normalized by postnatal d 21, with the exception of muscle strength. It was concluded that cobalt sulfate exposure decreases the perinatal viability of the fetuses, but the functions of the surviving fetuses with perinatal retardation become compensated by postnatal wk 2-3. The development of fetuses is undisturbed thereafter.

Abnormalities, Drug-Induced↗

Effects of sodium diethyldithiocarbamate on type II pulmonary epithelial cells in vitro.

Dithiocarbamates (DDTC) are chemicals widely used in the form of pesticides, therapeutic and chelating agents, and scavengers. Since DDTC interfere with SH, Cu, and Zn enzymes due to chelating properties, it was of interest to clarify, in primary culture of type II alveolar pneumocytes, the effect of this compound upon enzymes of glutathione cycle, Cu, Zn-superoxide dismutase, and the membrane structure of cells. DDTC significantly inhibited the activity of superoxide dismutase and the activity of gamma-glutamyl transpeptidase, glutathione reductase, and alkaline phosphatase, whereas an increase in the activity of glutathione peroxidase was found. The membranes of pneumocytes type II were injured. Data show that DDTC adversely affected type II pneumocyte function and structure.

Acetylgalactosamine↗

Embryotoxic and teratogenic effects of indium chloride in rats and rabbits.

Daily indium chloride doses of control (0), 50, 100, 200, or 400 mg/kg were administered orally to Sprague-Dawley rats by gavage, on d 6-15 of gestation, and daily metal doses of control (0), 50, 100, or 200 mg/kg were administered to New Zealand rabbits on d 6-20 of gestation. Further groups of pregnant rats were treated with control (0) or 400 mg/kg indium chloride orally on one of d 8, 9, 10, 11, 12, 13, 14, or 15 of gestation. The dams and fetuses were examined on d 21 (rats) and 30 (rabbits) of gestation, using standard teratological methods. Indium concentration was determined in the maternal and fetal blood, as well as in the amniotic fluid, by atomic absorption spectrometry. Indium was found to cross the placenta and appeared in fetal blood in proportion to the metal concentration of the maternal blood. In the amniotic fluid, indium concentrations remained below the detection limit. In rats, indium chloride produced dose-dependent maternal toxic effects, with a dose of 400 mg/kg inducing embryotoxicity (embryolethality) and teratogenicity. Doses of 200 and 100 mg/kg were embryotoxic (retarding) and teratogenic, causing skeletal and visceral anomalies in addition to external anomalies (rudimentary or missing tail, syndactylia, clubfoot, exencephalia) in rats. In rabbits, 200 mg/kg indium chloride was lethal for the dams and the embryos (some of the animals died, and the number of abortions and full resorptions increased). This dose was found to be teratogenic (caused gross renal anomalies) and increased the frequency of fetuses with skeletal retardation. In rats, the effects of indium chloride causing fetal retardation was found to be independent of exposure time. The teratogenic effects were the highest on d 11 and 12 of gestation, when indium chloride caused gross external malformations. Data suggest that the teratogenic effects of indium chloride can be attributed primarily to a direct cytotoxic action of indium resulting from placental transfer, but the effect is not a selective one, as it appears only in the presence of maternal toxic effects.

Abnormalities, Drug-Induced↗

[Lead poisoning caused by lead-glazed ceramic household article, initially assumed to be of occupational origin].

The authors observed serious lead intoxication of a 18 year old female ceramic apprentice caused by tea with lemon stored in a glazed ceramic teapot made by the patient herself. The case history suggests: 1. the need of warning people to avoid the use of ceramic tablewares made by insufficient technology for alimentary purposes. 2. Patient with lead exposure can have also alimentary intoxication. 3. It seems advisable to perform screening tests of the ceramic apprentices who use lead glazes in order to detect the eventual increased absorption of lead in time.

Adolescent↗

[Severe lead poisoning caused by an ingested fishing weight].

Authors describe the case-history of a 17 year old male who accidentally ingested a fishing weight that was retained in the stomach and caused a serious lead poisoning. It is worth mentioning that beside the wellknown symptoms and signs of lead intoxication also the liver was seriously affected. The histologically verified toxic lesion of the liver presumably can be attributed to the large quantities of lead absorbed within a short period. This also explains the appearance of symptoms and signs indicating to encephalopathy beside the young age of the patient. The foreign body could not be removed by means of gastroscopy, therefore a gastrotomy was carried out followed by chelating treatment with i.v. CaNa2EDTA that resulted in complete clinical and laboratory recovery. The case history draws the attention to the importance of the quick removal of the retained lead containing objects out of the gastrointestinal tract.

Adolescent↗

Follow-up biological and genotoxicological monitoring of acrylonitrile- and dimethylformamide-exposed viscose rayon plant workers.

In order to investigate the genotoxic effects of occupational acrylonitrile (ACN) and dimethylformamide (DMF) exposures, clinical serum and urine parameters and genotoxicological endpoints such as chromosome aberration (CA), sister chromatid exchange (SCE), high frequency SCE (HFC), cell cycle kinetics, and UV-induced unscheduled DNA synthesis (UDS) were followed up three times during a 20-month period in peripheral blood lymphocytes (PBL) of 26 workers (13 maintainers and 13 fiber producers) occupationally exposed to ANC and/or DMF in a viscose rayon plant, 26 matched control subjects, and six industrial controls (all males). Six of the 26 exposed subjects were hospitalized because of liver dysfunction that had developed due to inhalative DMF exposure. The rate of smoking was estimated on the basis of serum thiocyanate (SCN) levels. Average peak air ACN and DMF concentrations were over the maximum concentration limits at the time of both investigations. Urine ACN and monomethyl-formamide (MMF) excretions of the exposed subjects were almost doubled after work shifts. An increase in lymphocyte count (in months 0 and 7), and severe alterations in the liver function were observed in the exposed subjects. In PBLs the proliferative rate index (PRI) was already increased in month 0 compared with the controls. In each study, significant increases in CA and SCE frequencies, as well as increases in UDS were found in PBLs of the exposed subjects. The frequencies of chromatid breaks and acentric fragments further increased in month 7 and remained constantly elevated in month 20. Increased yields of both chromatid and chromosome-type exchange aberrations first appeared in month 20, when HFCs were 2.72 times more frequent in fiber producers than in maintainers. The role of some important biological confounding factors (age, white blood cell count, and hematocrit) and lifestyle confounding factors (smoking and drinking habits) were subjected to an analysis of variance during the second study. Increased CA, SCE, and UDS were found both in control and exposed smokers when current smoking was established on the basis of the serum SCN levels. The cytogenetic data suggest that occupational exposures to ACN and DMF induce considerable genotoxic consequences and may increase the cancer risk in the exposed human populations.

Acrylonitrile↗

[Microenvironmental lead poisoning].

Authors describe two cases of lead poisoning of unusual origin. A 43 year old male patient bought some waste metal in order to build a fence around his new house for saving money. He removed the old corroded coat of paint using a grinder without any protection. Consequently, he had got grave lead intoxication with colic and anemia. Another 34 year old unemployed male person moulded leaded chessmen in his own kitchen. This activity resulted in serious intoxication of the patient and highly increased lead absorption of the family members. In addition to the exploration of professional exposure the authors stress also the significance of the clearing up of occasional lead-related hobbies and home activities in case of lead intoxication of unknown origin.

Adult↗

[The favorable effect of humic acid based complex micro-element preparations in cadmium exposure].

The authors have studied the effect of consumption of a humic acid based complex microelement preparation (potassium, magnesium, iron, zinc, manganese, copper, vanadium, cobalt, molibden, selenium bound to humic acids) for six weeks (10 ml daily) on the biological exposure indices (blood and urine cadmium levels) and clinical laboratory parameters (liver and kidney tests, blood picture) of men (n = 18; 39.7 +/- 10.4 years of age;) working in cadmium exposure for 8.3 +/- 5.0 years. The initial mean blood and urine cadmium levels of the non-smoking subjects was twice higher than that of the non-smoking male controls living in the same urban area (n = 35), and significantly correlated with the length of exposure. Their mean serum alanin-aminotransferase, gamma-glutamyl-transferase, creatinine, uric acid and urinary N-acetyl-beta-D-glucosaminidase levels were significantly higher than that of the controls. After the six-week treatment blood cadmium level, activity of serum alanin-aminotransferase, serum uric acid and urinary protein concentrations decreased significantly, the abnormal serum iron levels normalized. According to this results, the absorption of cadmium decreased on the effect of the complex microelement supplementation and the adverse laboratory changes attributable partly to cadmium exposure improved. Therefore humic acid based complex microelement supplementation is recommended as an effective tool for prevention and health protection in occupational cadmium exposure as well as for smokers known to be considerably burdened by cadmium.

Cadmium↗

Lead intoxication epidemic caused by ingestion of contaminated ground paprika.

OBJECTIVE: Report of a lead intoxication epidemic caused by ingestion of contaminated ground paprika. DESIGN: Retrospective study of case histories. SETTING: Institutional, toxicological and medical referral center for ambulatory and hospitalized care. PATIENTS: One hundred forty-one adults consumed paprika contaminated with lead tetroxide (red lead). INTERVENTIONS: Intravenous calcium disodium versenate (edetic acid). MAIN OUTCOME MEASURES: Measurement of zinc protoporphyrin:heme ratio of whole blood and the blood lead level. EDTA mobilization test. RESULTS: Fifty-three patients had symptoms and signs of lead poisoning. The most common clinical signs were colic and/or anemia. Twenty-six persons showed increased lead absorption without clinical symptoms and signs. Chelation therapy with calcium disodium versenate resulted in complete clinical recovery. CONCLUSION: Lead-contaminated ground paprika, not previously described as a cause of alimentary lead intoxication, may cause symptomatic poisoning.

Adult↗

Evaluation of delta-aminolaevulinic acid excretion in random urine samples of children.

Urinary delta-aminolaevulinic acid (delta-ALA) excretion was evaluated in random urine samples of 191 healthy children, aged 2-14 years, with blood lead levels < 0.8 mumol/l (mean +/- SD: 0.34 +/- 0.13), erythrocyte zinc-protoporphyrin < 70 mumol/mol haem (mean +/- SD: 50.4 +/- 8.0) and blood haemoglobin > 6.8 mmol/l (mean +/- SD: 8.2 +/- 0.5). It was found that uncorrected delta-ALA concentration and delta-ALA/creatinine ratio are age-dependent, whereas the ratio of delta-ALA/logarithm of creatinine concentration (mean +/- SD: 55.3 +/- 13.5 mumol/log mmol) is independent of age and sex. The authors recommend the use of this parameter for the assessment of delta-ALA excretion in random urine samples in children.

Adolescent↗

[Erythrocyte zinc-protoporphyrin/hem ratio--screening test for the detection of iron deficiency and lead exposure. Experience with the Hemofluorometer in Hungary].

Increased zinc protoporphyrin/hem ratio (ZP) in erythrocytes caused by iron deficiency and/or lead exposure can be measured very simply and directly using a dedicated instrument, the Hematofluorometer. Clinical value of ZP test in detecting iron deficiency and lead exposure has been demonstrated by the authors in 465 females. Based on the literature and their own favourable experiences, the authors call attention to this useful screening method of preventive and diagnostic importance.

Anemia, Hypochromic↗

Clinical relevance of urinary delta-aminolevulinic acid/logarithm of creatinine ratio in screening for occupational lead exposure.

Using receiver operating characteristics (ROC) analysis, the clinical relevance of urinary delta-aminolevulinic acid concentration adjusted to the logarithm of creatinine concentration (ALA/log.Cn) proved to be better than that of uncorrected ALA or ALA/Cn ratio for the detection of blood lead levels (Pb-B) exceeding 2.5, 3.0, or 3.5 mumol/l in 483 men occupationally exposed to lead. Ala/log.Cn yielded validities of 1.63, 1.75, and 1.79 at Pb-B levels 2.5, 3.0, and 3.5 mumol/l, respectively. The same values for ALA/Cn were 1.59, 1.70, 1.78 and for ALA 1.52, 1.65, 1.72, respectively. The simple adjustment to log. Cn makes urinary ALA determination more efficient in biological monitoring of the effect of occupational lead exposure.

Adult↗

Improved method for the adjustment of urinary delta-aminolevulinic acid concentration.

The work was aimed at finding whether the ratio of delta-aminolevulinic acid (ALA) and creatinine (Cn) concentration (ALA/Cn), presently used in occupational health practice for evaluation of lead exposure gives a better assessment of ALA excretion than uncorrected ALA concentration itself, as well as at finding a better, but not complicated method for adjustment. ALA and Cn concentrations were measured in untimed urine samples of altogether 390 men and women (age: 18-60 years) not occupationally exposed to lead. In agreement with others, ALA/Cn was found to be an unsuitable method of adjustment for the differences in ALA concentration due to the different concentrations of samples. This can be explained by the different renal handling of ALA and Cn, proved by the literature data. The exponential relationship between ALA/Cn and Cn concentration raised the possibility of adjustment to the logarithm of Cn concentration (ALA/log.Cn). This simple method provided a more reliable index, the value of which was independent of the actual Cn concentration of urines within a wide range (2-32 mmol/liter). The recommended biological limit value (70 mumol/log.Cn mmol) separates equally well from normal values, both in dilute and concentrated urines. The evaluation of occupational lead exposure might be more reliable using this index, instead of uncorrected ALA concentration or the ALA/Cn ratio.

Adolescent↗

[Correlation between the fetotoxic effect of benzol inhalation in CFY rats and benzol concentration in the inhaled gas].

CFY rats from the 7th to the 14th days of pregnancy were given benzole to inhale during 24 hours a day in doses 150, 450, 1500 or 3000 mg/m3 (50, 150, 500 or 1000 ppm). It was established that benzole has no teratogenous effect in rats. Frequency of the obvious malformations of the scelet and soft tissues has not increase at any doses given. The concentration of benzole 150 mg/m3 has induced moderate, 450 mg/m3 marked maternal and foetal toxicity i.e. increase of the maternal mortality rate, damage to the circulation, decrease in the gain of the body weight and that of the placenta, increase of the foetal mortality rate (early and late) and retardation of the foetal development. Further increase of the concentration of the benzole was not followed by more severe toxical symptoms. Authors conclude, that women already before the onset of the planned pregnancy should avoid benzole exposition.

Abnormalities, Drug-Induced↗

Concentration dependence of the embryotoxic effects of benzene inhalation in CFY rats.

CFY rats were exposed to continuous benzene inhalation 24 h/day from day 7 to day 14 of gestation at 150, 450, 1500, or 3000 mg/m3 (50, 150, 500, or 1000 ppm) atmospheric concentrations. None of the benzene concentrations used proved to be teratogenic. There was no increase in the incidence of external, visceral, or skeletal malformations. Benzene inhalation at a 150 mg/m3 concentration brought about a slight toxic effect at a 450 mg/m3 concentration a more pronounced effect on both mothers and fetuses. The toxic effects were manifest as an increase in maternal mortality, circulatory damage, decreased gain in body weight, decrease in the weight of the placenta in the mothers and an increase in mortality (early and late), retardation of development (weight and skeleton) in the fetuses. No further change in the parameters was seen with further increases in benzene concentration. Avoidance of the risks of benzene exposure seems desirable before the commencement of planned pregnancy in the human.

Abnormalities, Drug-Induced↗