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Biomedical subjects

M Náray

Publications and source records attributed to M Náray.

At least 19 recordsLinked to original sources
PubMed2001

Lead accumulation in human ovarian follicular fluid, and in vitro effect of lead on progesterone production by cultured human ovarian granulosa cells.

Lead content of ovarian follicular fluid obtained from 23 women was determined by atomic absorption spectrophotometry. In an in vitro experiment the direct effect of lead on the morphology and on progesterone (P) production by cultured granulosa cells of six women was investigated. Follicular fluid and granulosa cells were obtained from follicular aspirates of women undergoing in vitro fertilization (IVF) and embryo transfer (ET). Granulosa cells were cultured for 48 h to form monolayers in the presence or absence of lead acetate (100-1,600 microM). The effect of the metal proved to be concentration dependent. While 100-400 microM lead had no effect on the integrity of the monolayer, concentrations as high as 800 microM or higher inhibited cell adhesion and induced detachment of cells. The lead levels found in follicular fluid were 11.29 +/- 1.38 microg/L (0.056 +/- 0.007 microM). With lead in vitro at 1,600 microM (331.5 mg/L) there resulted a significant decrease in P production by granulosa cells. This concentration is very much higher than that measured in follicular fluid of IVF/ET patients, specifically nonexposed to lead, and even higher than mean blood levels reported by others in high exposure groups. In conclusion, lead seems not to exert a specific effect on the steroidogenesis by cultured human granulosa cells. Therefore, the lead levels measured in the ovarian follicular fluid seem not to pose a hazard with respect to progesterone secretion by the ovary.

Adult↗
PubMed2001

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↗
PubMed2001

The effect of prenatal indium chloride exposure on chondrogenic ossification.

Daily indium chloride doses of control (0) or 400 mg/kg were administered orally to pregnant Sprague-Dawley (SD) rats by gavage, on d 20 of gestation. Indium concentration was determined in the maternal and fetal blood, livers, kidneys, skulls, and femurs by atomic absorption spectrometry. Further groups of pregnant rats were treated with control (0) or 400 mg/kg indium chloride orally, during the whole gestation period. The fetuses were examined on d 21 of gestation, using histological and histochemical methods. Four hours after the administration indium concentration was found to be significant in the blood, liver, and kidneys of the dams. Twenty-four hours later it increased in the blood but not in the liver and kidney. Fetal indium concentrations were 40-50% of the maternal levels due to a barrier of the placenta. In the skull and the femur, indium was already detectable at 4 h after the administration, and by the end of 24 h, metal concentration was several times higher than that at 4 h, indicating accumulation. Furthermore, it was found that the birefringency of collagen detectable by picrosirius red staining in polarized light around the chondrocytes disappeared and became irregular. In the matrix of the epiphyseal cartilage, the regular, birefringent network demonstrable by Rivanol reaction became irregular and hardly recognizable. In the cytoplasm of the chondrocytes, the diffuse, evenly distributed positive Ricinus communis agglutinin reaction became irregular or disappeared. Similar but much weaker changes were observed with concanavalin A and wheat germ agglutinin stainings. It was concluded that the missing femur and micromelia diagnosed by alizarin staining is the consequence of a specific toxic effect of indium that inhibits chondrogenic ossification. No similar histochemical changes were observed in the bones of the skull developing by desmogenic ossification, despite the presence of indium. Data indicate that the mechanisms of the effects of indium causing retardation and/or malformation differ in the bones developing through desmogenic or chondrogenic ossification.

Animals↗
PubMed2001

Future need for development of occupational exposure databases in Hungary.

The data on the occupational exposure measured by the hygienic network laboratories in Hungary were collected during the last 20 years. The data refer to the air pollutant chemicals and to the biological monitoring. The structure of the database of occupational exposure that has been used in the last decade is intended to be changed according to the guideline of the European Working Group on Exposure Registers in Europe. The current databases on the occupational exposure contain data only related to the substances responsible for air pollution. It would be desirable to complement the database with data from the biological monitoring, which also characterize the occupational exposure. It would then be possible to harmonize two distinct databases, and the risk assessment of the employees would become more thorough. This practice would require close cooperation of several organizations. It is desirable to set minimum requirements against the measurement techniques, thus, giving results that are accepted in the exposure database. It is necessary to encourage the use of direct reading instruments in collecting the exposure data and to complement the requirements of the strategies of data collection and the system of evaluation.

Databases, Factual↗
PubMed2000

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↗
PubMed1998

[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↗
PubMed1998

[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↗
PubMed1998

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↗
PubMed1997

[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↗
PubMed1997

[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↗
PubMed1996

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↗
PubMed1995

Haemodynamic effect of nickel chloride in pregnant rats.

Non-pregnant and pregnant CFY rats were given 3 mg/kg nickel chloride or physiological saline by gavage daily for eight days during days 7-14 of organogenesis. The haemodynamic investigations were carried out using 113Sn labelled microspheres. Nickel concentrations in maternal and fetal blood, as well as in amniotic fluid were determined by atomic absorption spectrophotometry. It was found, that nickel crossed the placenta, appeared in the fetal blood and amniotic fluid, where its concentration depended on the dose given to the pregnant animal and the nickel concentration of the maternal blood. Nickel chloride influenced neither the systemic haemodynamic parameters (arterial blood pressure, total peripheral resistance--TPR, cardiac index) nor the values of the organ (including the placenta) circulation indices, neither in the pregnant nor in the non-pregnant animals. It is concluded that in the pathomechanism of embryotoxicity (causing weight gain retardation) and teratogenicity (causing major anomalies of the uropoietic apparatus) of nickel, demonstrated earlier, the assumed effects of nickel on maternal and placental circulation probably do not play role (as such effects could not be detected). The direct embryo-damaging effect of nickel crossing the placenta (direct cytotoxic effect) may be held responsible for the embryotoxicity and teratogenicity of nickel.

Amniotic Fluid↗
PubMed1994

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↗
PubMed1992

[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↗
PubMed1992

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↗
PubMed1992

Altered ovarian progesterone secretion induced by cadmium fails to interfere with embryo transport in the oviduct of the rat.

The effect of Cadmium (Cd) on embryo transport through the oviduct and on ovarian progesterone (P) secretion were studied in the rat. Animals were given 2.5, 5, 10 mg/kg CdCl2 or 1.0 mL/kg NaCl sc on day 1 of pregnancy. On days 1, 2, 3, 4, and 5, they were anesthetized with pentobarbital, cannulae were inserted in one of the utero-ovarian veins, and 5-minute blood samples were taken from the ovary. Ovarian venous outflow was recorded, P was determined from the blood fractions, and secretion rates were calculated. P levels were determined in peripheral blood. Body weights and the wet weight of adrenals, ovaries, and oviducts were checked; oviducts and uterine horns were flushed; and number, location, and developmental stage of embryos were observed. Cd content of the oviducts was measured. Cd accumulated dose and time dependently in oviducts and induced a dose-dependent depression and delay in the rise of ovarian P secretion during days 1 through 5 of pregnancy. In the peripheral blood, P levels also failed to rise until day 4 of pregnancy in Cd-treated rats. In embryo transfer, however, no alteration could be observed. It is hypothesized that lack of vascular contact in the oviduct makes it possible for the preimplantation embryos to escape toxic effects of Cd.

Animals↗