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Biomedical subjects

L Vodicková

Publications and source records attributed to L Vodicková.

At least 19 recordsLinked to original sources
PubMed2006

["Unknown" cause of the onset and recurrence of venous thromboembolism].

We reported the case of 61 years old man with the first episode of massive pulmonary embolism at the age of 54 without the proper explanation of the cause. Thrombocythaemia was manifested after the dismissal from the hospital but the origin of this condition was not clarified. Essential thrombocythaemia was diagnosed after the recurrence of venous thromboembolism and that is the explanation for thrombophilic condition in this patient. The patient is without problems and signs of recurrent venous thromboembolism after the achievement of the complete remission of myeloproliferative disease and well-managed of anticoagulation therapy.

Humans↗
PubMed2004

[The occurrence of occult malignancy in patients less than 50 years of age with venous thromboembolism: which diagnostic screening methods to use?].

Trousseau was the first who describe an association of venous thromboembolism (VTE) with malignancy. The prevalence of occult cancer in patients with secondary VTE is comparable with the prevalence of cancer in general population (2-3%), while the prevalence of occult cancer in patients with idiopathic VTE is 4-10%. It has been demonstrated that the frequency of malignancy is higher in the first 6 to 12 months after diagnosis of VTE. 113 consecutive patients (50 males, 63 females) with first or recurrent VTE before the age 50, mean age (mean age 34.1 at time of VTE diagnosis) were followed retrospectively. Patients with known cancer were excluded for follow-up. The presence of known malignancy and concomitant cancer at the time of diagnosis of VTE and during follow-up (average 29 months) was investigated. The use of routine or extensive screening detection of occult cancer was also assessed. Extensive screening was performed in 61% of patients and compared with 39 % of routine screening. Overall of occult cancer was 1.8 %. The incidence of occult cancer was 1.2% during one year follow-up, and the prevalence at the time of diagnosis of VTE was 0.9%. The authors confirmed the low prevalence of occult cancer in cohort of consecutive young patients with VTE under the age of 50. It seems that only routine investigation with careful history taking, physical examination and simple laboratory tests are sufficient to detect of occult cancer in this age population. The authors recommend the follow-up of these patients, mainly those with idiopathic VTE. Inherited thrombophilia much more prevails in this young thrombophilia patients but risk of occult malignancy exists as well.

Adolescent↗
PubMed2003

Effects of 1,2-dibromoethane on haematopoiesis in the chick embryo.

1. Chick embryo in ovo was used to investigate the effects of 1,2-dibromoethane (DBE) on haematopoiesis at a developmental stage where the primitive erythroid cells divide and differentiate in circulation. 2. Early after DBE treatment on embryonic day 3, annexin V/propidium iodide labelling showed acute cell death of erythroid elements, which was subsequently compensated for by the release of immature cells into the circulation. Simultaneously, the comet assay indicated increased DNA damage in DBE-exposed blood cells when compared with controls. 3. After embryonic day 5, there was no indication for ongoing prominent cell death in the DBE-treated group. However, the DNA damage assessed by the comet assay persisted until embryonic day 10 in the peripheral blood cells, and for even longer in cells from thymus and bursa. 4. The kinetics of DNA fragmentation in both erythroid and lymphoid cells implied genotoxic damage by DBE to the stem cells of the definitive elements and transmission of this damage through the successive cell generations. 5. The early chick embryo provides a suitable alternative to mammalian models for investigation of long-term effects of xenobiotics on haematopoiesis.

Animals↗
PubMed2001

Kinetics of formation of specific styrene oxide adducts in double-stranded DNA.

The possible carcinogenicity of styrene is believed to be related to the DNA-binding properties of styrene 7,8-oxide (SO). In order to compare the intrinsic reactivity of the different nucleophilic sites in DNA towards SO and to evaluate the candidates for human biomonitoring we have determined the second-order rate constants and stabilities of several SO-adducts in double-stranded DNA. These include alpha- and beta-isomers of N7-substituted and alphaN(2)-substituted guanines, alpha- and betaN3-substituted and alphaN(6)-substituted adenines as well as betaN3- and alphaN(4)-substituted cytosines. The highest rate constants were found for the spontaneously depurinating N7-guanines being ca. 3-15-fold higher than those for the stable adducts. When the relative proportions of different alkylation products were determined in course of time, after a single addition of SO, the labile N7-guanines and N3-adenines were the major products at early time points. After 144 h of incubation at 37 degrees C, alphaN(6)-SO-adenine and alphaN(2)-SO-guanine as well as betaN3-SO-uracil were the major adducts. Regarding human biomonitoring, the N7-substituted guanines should be one of the main targets because of the high reactivity of the N7-atom of guanine. However, in the case of chronic styrene exposures the chemically more stable DNA adducts may become important.

Alkylation↗
PubMed2001

DNA adducts, strand breaks and micronuclei in mice exposed to styrene by inhalation.

Genotoxic and clastogenic effects of styrene were studied in mice. Male NMRI mice were exposed by inhalation to styrene in concentrations of 750 and 1500 mg/m3 for 21, 7, 3 and 1 days (6 h/day, 7 days/week). Followed parameters included styrene in blood, specific styrene oxide (SO) induced DNA adducts, DNA strand breaks and micronuclei. The formation of SO induced 7-SO-guanines and 1-SO-adenines in DNA was analysed from lung tissues by two versions of the 32P-postlabeling technique. In lungs after 21 days of exposure to 1500 mg/m3 the level of 7-SO-guanine was 23.0+/-11.9 adducts/10(8) normal nucleotides, while 1-SO-adenine was detected at the levels of 0.6+/-0.2 adducts/10(8) normal nucleotides. Both 7-SO-guanines and 1-SO-adenines strongly correlated with exposure parameters, particularly with styrene concentration in blood (r=0.875, P=0.0002 and r=0.793, P=0.002, respectively). DNA breaks were measured in peripheral lymphocytes, bone marrow cells and liver cells using comet assay. To discern oxidative damage and abasic sites, endonuclease III was used. In bone marrow of exposed mice slight increase of strand breaks can be detected after 7 days of inhalation. A significant increase was revealed in the endonuclease III-sensitive sites after 21 days of inhalation in bone marrow. In the liver cells inhalation exposure to both concentrations of styrene did not virtually affect either levels of DNA single-strand breaks or endonuclease III-sensitive sites. The inhalation of 1500 mg/m3 of styrene induced significant increase of micronuclei after 7 days of exposure (10.4+/-2.5/1000 cells, i.e. twice higher micronuclei frequency than in controls). After 21 days of inhalation no significant difference between the control group and the two exposed groups was observed. Whether the decrease of micronuclei after 21 days of inhalation was due to the inhibition of cell proliferation caused by styrene or due to the natural elimination of chromatide fragments, remains to be clarified. An interesting link has been found between DNA single-strand breaks in bone marrow and frequencies of micronuclei (r=0.721, P=0.028).

Administration, Inhalation↗
PubMed1999

An evaluation of styrene genotoxicity using several biomarkers in a 3-year follow-up study of hand-lamination workers.

A study employing several biomarkers of styrene exposure and genotoxicity was carried out in a group of lamination (reinforced plastic) workers and controls, who had been repeatedly sampled during a 3-year period. Special attention will be paid to the last sampling (S.VI), reported here for the first time. Styrene concentration in the breathing zone, monitored by personal dosimeters, and urinary mandelic acid (MA) were measured as indicators of external exposure. Blood samples were assayed for styrene-specific O6-guanine adducts in DNA, N-terminal valine adducts of styrene in haemoglobin, DNA single-strand breaks (SSB), determined by use of the single cell gel electrophoresis (Comet) assay), and hypoxanthine guanine phosphoribosyl transferase (HPRT) mutant frequencies (MF) in T-lymphocytes. O6-styrene guanine adduct levels were significantly higher in the exposed group (5.9 +/- 4.9 adducts/10(8) dNp) as compared to laboratory controls (0.7 +/- 0.8 adducts/10(8) dNp; P = 0.001). DNA adduct levels significantly correlated with haemoglobin adducts, SSB parameters and years of employment. Styrene-induced N-terminal valine adducts were detected in the lamination workers (1.7 +/- 1.1 pmol/g globin), but not in the control group (detection limit 0.1 pmol/g globin). N-terminal valine adducts correlated strongly with external exposure indicators, DNA adducts and HPRT MF. No significant correlation was found with SSB parameters. A statistically significant difference in HPRT MF was observed between the laminators (22.3 +/- 10.6/10(6)) and laboratory controls (14.2 +/- 6.5/10(6), P = 0.039). HPRT MF in the laminators significantly correlated with styrene concentration in air, MA and haemoglobin adducts, as well as with years of employment and age of the employees. No significant difference (P = 0.450) in MF between the laminators and the factory controls was observed. Surprisingly, we detected differences in MF between sexes. When data from all measurements were combined, women showed higher MF (geometric mean 15.4 vs. 11.2 in men, P = 0.020). The styrene-exposed group exhibited significantly higher SSB parameters (tail moment (TM), tail length (TL) and the percentage of DNA in the tail (TP)) than the control group (P < 0.001). SSB parameters correlated with indicators of external exposure and with O6-styrene guanine adducts. No significant correlation was found between SSB parameters and haemoglobin adducts or HPRT MF. The data encompassing biomarkers from repeated measurements of the same population over a 3-year period are discussed with respect to the mechanisms of genotoxic effects of styrene and the interrelationship of individual biomarkers.

Adult↗
PubMed1999

Biomonitoring of occupational exposure to styrene in a plastics lamination plant.

A comprehensive approach to biological monitoring of 44 workers occupationally exposed to styrene in a hand lamination plant was performed by using several end-points: styrene in workplace air, styrene in exhaled air, styrene in blood, DNA strand breaks (SBs) and oxidised bases in mononuclear leukocytes, chromosomal aberrations in lymphocytes, immune parameters and genotyping of polymorphic genes of some xenobiotic-metabolizing enzymes (CYP 1A1, EPHX, GSTM1 and GSTP1). We found a significantly higher number of DNA SBs, measured by a modified comet assay, in mononuclear leukocytes of the styrene-exposed workers compared with results from 19 unexposed controls (P<0.001). A fairly strong correlation was observed between SBs and years of exposure (P<0.001, r=0.545). The styrene-exposed workers also showed a significantly increased frequency of chromosomal aberrations (P<0.0001 for highly exposed group, P<0.004 for medium-exposed group, and P=0.0001 for low-exposed group). The proliferative response of T-lymphocytes stimulated with concanavalin A was significantly suppressed in people exposed to styrene (P<0.05). We recorded a significant increase of the percentage of monocytes in differential white blood cell counts in the exposed group (P<0.05). Using flow cytometry, we found an increased expression of adhesion molecules CD62L, CD18, CD11a, CD11b, CD49d and CD54 in the exposed workers as compared with the control group (P<0.05).

Adult↗
PubMed1996

Biotransformation of acrolein in rat: excretion of mercapturic acids after inhalation and intraperitoneal injection.

Biotransformation of acrolein (ACR) was studied in vivo in the rat following inhalation and ip administration. The major and minor urinary metabolites were 3-hydroxypropylmercapturic acid (HPMA) and 2-carboxyethylmercapturic acid (CEMA), respectively. Male Wistar rats were exposed to ACR, 23, 42, 77 and 126 mg/m3, for 1 hr. The sum of mercapturic acids HPMA and CEMA excreted within 24 hr after the exposure amounted to 0.87 +/- 0.12, 1.34 +/- 0.5, 2.81 +/- 1.15, and 7.13 +/- 1.56 mumol/kg, i.e., 10.9 +/- 1.5, 13.3 +/- 5.0, 16.7 +/- 6.9, and 21.5 +/- 4.8% of the estimated absorbed dose, respectively. The dose estimate was based on reported values of minute respiratory volume and respiratory tract retention and was corrected for the ACR-induced changes in minute respiratory volume. In the relevant dose range (8.9 to 35.7 mumol/kg) the portion of mercapturic acids excreted was nearly constant for ip exposed rats. The sum of HPMA and CEMA amounted to 29.1 +/- 6.5% of the dose. These results indicate that the deficiency in rat lung metabolism of ACR to acrylic acid previously observed is not compensated by the other detoxication pathway in vivo, mercapturic acid formation. The health hazard arising from inhalation of ACR is likely to be higher than that from other routes of exposure.

Acetylcysteine↗
PubMed1996

Oxidative phenotype polymorphism (P450 2D6) and metabolism of toluene.

Oxidative phenotype P-450 2D6 was examined using sparteine test in 3 groups of persons to determine if there is a coincidence in the defect of the oxidative biotransformation of sparteine and impaired oxidation of toluene, which could explain interindividual differences in the amounts of hippuric acid in the urine in exposed persons. The following groups of persons were examined: 30 rotogravure printers exposed to toluene vapors at concentrations of 8-307 ppm; 20 workers, 2 months after the cessation of the long-term exposure to toluene at concentrations of 104-1,170 ppm; 48 healthy volunteers with no exposure to toluene. Among the 98 persons 5 poor metabolizers (PMs) of sparteine were found, none in the group of printers exposed to toluene. In the experimental exposure chamber 5 PMs and 6 extensive metabolizers (EMs) were exposed to toluene concentration of 245 ppm for 5 hours. Hippuric acid and o-cresol in the urine, and toluene both in blood and in alveolar air were measured. However, no significant differences were found in either of these parameters between the PM and EM groups. Thus, the sparteine test does not appear to be applicable in the identification of persons with higher risk arising from toluene exposure.

Adult↗
PubMed1996

Pattern of inhalation exposure: blood levels and acute subnarcotic effects of toluene and acetone in rats.

Solvent blood concentrations and subnarcotic effects (inhibition of electrically evoked seizures) were measured in rats exposed to constant or fluctuating air concentrations of toluene or acetone. A 4 hour exposure of resting rats to toluene at an air concentration of 1 and 2 mg/l, or to acetone at 4 and 10 mg/l, led to blood levels of 6.7 and 12.8 mg/l of toluene, or 183 and 520 mg/l of acetone: seizure inhibition amounted to 18% and 40+, or 10% and 50%, respectively. Blood level and effect attained 1/2 of the final values after 40 min and 60 min of exposure to 2 mg/l toluene, respectively, and dropped to 1/2 70 min and 90 min after exposure cessation: respective values for acetone 10 mg/l were 80 and 120 min, and more than 4 hours. A steep rise and a rapid drop was characteristic also for the course of blood level and effect during an exposure to fluctuating concentrations of toluene: ten minute fivefold jump in the air concentration induced a shortlasting seizure inhibition by more than 80%; the curves for acetone were flat.

Acetone↗
PubMed1995

Biomarkers of styrene exposure in lamination workers: levels of O6-guanine DNA adducts, DNA strand breaks and mutant frequencies in the hypoxanthine guanine phosphoribosyltransferase gene in T-lymphocytes.

Occupational exposure to styrene was studied in nine workers of a hand lamination plant in Bohemia. Personal dosimeters were used to monitor the styrene workplace exposure, and the levels of styrene in blood and mandelic acid in urine were measured. Blood samples were taken at four occasions during a 7 month period to determine styrene-specific O6-guanine DNA adducts in lymphocytes and granulocytes, DNA strand breaks and hypoxanthine guanine phosphoribosyltransferase (HPRT) mutant frequency in T-lymphocytes. Seven administrative employees in the same factory (factory controls) and eight persons in a research laboratory (laboratory controls) were used as referents. DNA adduct levels determined by the 32P-postlabelling method in lymphocytes of laminators were remarkably constant and significantly higher (P < 0.0001) than in factory controls at all four sampling times. HPRT mutant frequencies (MF) measured by the T-cell cloning assay were higher in the laminators (17.5 x 10(-6), group mean) than in the factory controls (15.7 x 10(-6), group mean) at three of the four sampling times, but the differences were not statistically significant. However, a statistically significant (P = 0.021) difference between MF in the laminators (18.0 x 10(-6), group mean) and laboratory controls (11.8 x 10(-6), group mean) was observed at sampling time 4 (the only sampling time when this latter group was studied). This result indicates that styrene exposure may induce gene mutation in T-cells in vivo. DNA strand breaks were studied by the 'Comet assay' at the fourth sampling time. The laminators were found to have significantly higher levels of DNA strand breaks than the factory controls (P = 0.032 for tail length, TL; P = 0.007 for percentage of DNA in tail, T%; and P = 0.020 for tail moment, TM). A statistically significant correlation was also found between the levels of lymphocyte DNA adducts and all three DNA strand break parameters (TL P = 0.046; T% P = 0.026 and TM P = 0.034). On the contrary, no significant correlations were found between DNA adduct levels and the HPRT mutant frequencies or between the mutant frequencies and DNA strand breaks. Taken together, these results add further support to the genotoxic and possibly mutagenic effects of styrene exposure in vivo. However, no simple quantitative relationship seems to exist between the levels of styrene-induced DNA damage and frequency of HPRT mutation in T-lymphocytes.

Adult↗
PubMed1995

Neutrotropic effects and blood levels of solvents at combined exposures: binary mixtures of toluene, o-xylene and acetone in rats and mice.

Male rats and female mice were exposed to vapours of toluene, o-xylene and acetone in basic or double concentrations or to binary combinations of basic concentrations, for 4 and 2 hours, respectively. Basic air concentrations were for rats and mice (in ppm): toluene 270 and 380, o-xylene 230 and 320, acetone 1700 and 1530, respectively. The CNS effect-inhibition of electrically evoked seizure discharge-was measured immediately after exposure and blood levels of solvents were monitored during the desaturation phase. The effect of all binary mixtures was lower than that of double concentrations of each single component, the difference being significant only in mice, and lower than the additive effects predicted on the basis of regressions of the effect on air or on blood concentrations of individual components. On the target site in the neuronal membrane, the effects of mixtures were substantially less than additive. Blood concentrations of solvents immediately after the exposure to a mixture were generally higher in aromatics and lower in acetone than after exposure to individual solvents. The decline of blood toluene and even more so that of xylene after exposure was slowed down by acetone. Presumption of additivity seems to protect safely from acute neurotropic effects of solvents at realistic exposure levels. On the other hand, substantially protracted late phases of desaturation of aromatic solvents in the presence of slowly eliminated polar solvent points to a possible underestimation of exposure by biological exposure tests.

Acetone↗
PubMed1994

Persistence of O6-guanine DNA adducts in styrene-exposed lamination workers determined by 32P-postlabelling.

A modified 32P-postlabelling method was used for the detection of styrene-specific DNA adducts in lamination workers. The persistence of O6-styrene DNA adducts was studied in DNA from lymphocytes and granulocytes of an exposed and a control group. We compared O6-adduct levels obtained from a sampling prior to vacation, after 2 weeks of vacation and after an additional 1 month of work. In granulocytes, there was no significant difference in adduct levels between the control and the exposed groups in any individual samplings. In lymphocytes of laminators the detected adduct levels were significantly higher (5.4 adducts/10(8) nucleotides) than those in the controls (1.0 adduct/10(8) nucleotides). The 2 week interruption of exposure did not influence the total O6-adduct level (4.9 adducts/10(8) nucleotides in the first sampling versus 5.1 adducts/10(8) nucleotides in the second), indicating very slow removal of the specific O6-styrene adducts from DNA.

Adult↗
PubMed1990

Changes in the activity of thrombocytes by smoking.

Platelet function was investigated in 11 healthy non-smokers, 11 medium smokers (less than 10 cigarette/day) and 11 heavy smokers (greater than 20 cigarette daily). Cigarette consumption was in medium smokers 6.2 cigarette/day, and in heavy smokers 30.7 cigarette/day. Erythrocyte count, platelet count, plasma levels of cholesterol and triglycerides, and circulating platelet aggregates showed no significant difference between smokers and non-smokers. Thromboxane B2 level in plasma was higher in heavy smokers (20.1 +/- 17.3 pg/0.1 ml) than in non-smokers (58.8 +/- 37.1 pg/0.1 ml) and medium smokers (65.4 +/- 32.1 pg/0.1 ml) (P less than 0.01). Platelet factor 4 level was high in non smokers prior to smoking 1 cigarette and normal in medium and heavy smokers. Plasma concentration of beta thromboglobulin and 6-ketoprostaglandin F1 alpha showed no significant changes between non-smokers and heavy smokers. No dependence on smoking 1 cigarette was found in any group. The data suggest that long term cigarette smoking increases platelet activity manifested by an increased activity of thromboxane A2. Cigarette smoking contributes to the development of coronary artery disease also by means of activation of platelet functions.

Adult↗
PubMed1990

[Screening for venous thrombosis and pulmonary embolisms in patients with stroke using an adaptive classifier].

The use of adaptive linear neuron is referred to in recognizing veinous thromboses and lung embolism in a total of 88 acute palsies. As the input signs, the accessible clinical and laboratory data were used. Both training and adaptation of neuron have been performed in a part of total [35 patients], and 53 patients were submitted to the classification of patients with unknown distribution. In classified group with present complications, the screened diseases have been recognized in 16/20 patients. In 29 from 33 patients without thromboembolic states, the distribution by classificator appeared as correct one. The level of correct resolution was as high as 88% in all.

Cerebrovascular Disorders↗