Biological effects of molybdenum(IV) sulfide nanoparticles and microparticles in the rat after repeated intratracheal administration.

In this study, molybdenum(IV) sulfide (MoS2 ) nanoparticles (97 ± 32 nm) and microparticles (1.92 ± 0.64 µm) stabilized with poly (vinylpolypyrrolidone) (PVP) were administered intratracheally to male and female rats (dose of 1.5 or 5 mg/kg bw), every 14 days for 90 days (seven administrations in total). Blood parameters were assessed during and at the end of the study (hematology, biochemistry including glucose, albumins, uric acid, urea, high density lipoprotein HDL, total cholesterol, triglycerides, aspartate transaminase, and alanine transaminase ALT). Bronchoalveolar lavage fluid (BALF) analyses included cell viability, biochemistry (total protein concentration, lactate dehydrogenase, and glutathione peroxidase activity), and cytokine levels (tumor necrosis factor α, TNF-α, macrophage inflammatory protein 2-alpha, MIP-2, and cytokine-induced neutrophil chemoattractant-2, CINC-2). Tissues were subjected to routine histopathological and electron microscopy (STEM) examinations. No overt signs of chronic toxicity were observed. Differential cell counts in BALF revealed no significant differences between the animal groups. An increase in MIP-2 and a decrease in TNF-α were observed in BALF in the exposed males. The histopathological changes in the lung evaluated according to a developed classification system (based on severity of inflammation, range 0-4, with 4 indicating the most severe changes) showed average histopathological score of 1.33 for animals exposed to nanoparticles and microparticles at the lower dose, 1.72 after exposure to nanoparticles at the higher dose, and 2.83 for animals exposed to microparticles at the higher dose. In summary, it was shown that nanosized and microsized MoS2 can trigger dose-dependent inflammatory reactions in the lungs of rats after multiple intratracheal instillation irrespective of the animal sex. Some evidence indicates a higher lung pro-inflammatory potential of the microform.

Assessment of acute toxicological effects of molybdenum(IV) disulfide nano- and microparticles after single intratracheal administration in rats.

Despite growing applications of molybdenum(IV) sulfide (MoS2) nano- and microparticles in their capacity as lubricants, data available on their safety are scarce. In this study the effect of MoS2 nano- and microparticles after single intratracheal instillation in rats has been analyzed. MoS2 suspensions were administered at the dose of 1.5 or 5 mg MoS2/kg body weight. The analysis after 24 h and 7 days included: blood biochemical parameters, hematological parameters, bronchoalveolar lavage fluid (BALF) parameters with selected cytokines, a comet assay and histopathological examination. In the BALF cells isolated from animals exposed to both forms, numerous macrophages loaded with particles were observed. The hematological and biochemical parameters analyzed 24 h or 7 days after the exposure to both forms did not show any biologically meaningful changes. Comet assay results showed no genotoxic effect. The histopathological analysis of the lungs revealed inflammatory changes in the respiratory system of the treated animals, slightly stronger for the microsized form. The deposits of particles observed in the lung tissue up to 7 days after the instillation indicate their easy penetration through the epithelium and prolonged clearance. Concluding, no meaningful acute systemic effects were observed, however some pathological changes were noted in the lung tissue.

Early life environmental exposure in relation to new onset and remission of allergic diseases in school children: Polish Mother and Child Cohort Study.

Background: This study was based on data from the Polish Mother and Child Cohort Study. Objective: The aim was to study associations between home environment factors and allergic diseases at 1 year of life and new onset and remission of children's allergy diagnosis at ages 7-9 years. Methods: Children's health status was assessed at ∼12 months of age and then at ages between 7-9 years by using a questionnaire administered to the mothers. Children were assessed by pediatrician/allergists. The patients, who were 7-9 years old, underwent skin-prick tests. Exposure to tobacco smoke was evaluated with a questionnaire addressed to parents and/or caregivers and cotinine measurements were taken of mother's saliva during pregnancy and in children's urine at ages 7-9 years. Incidence and remission were calculated by comparing symptoms in the first year of life with symptoms at 7-9 years. We studied the associations among demographic data, home environment, and new onset and remission of food allergy, atopic dermatitis, and asthma and allergic rhinitis in logistic regression analysis. All associations were adjusted for independent risk factors of dependent variables. Results: Data from 211 participants were included in the analysis. During the first year of life, food allergy was the most common symptom (39%), followed by atopic dermatitis (35%) and asthma (12%). When comparing diagnoses at ages 7-9 years with the first year of life, food allergy had decreased by as much as 18.6%, atopic dermatitis decreased by as much as 23.8%, and asthma decreased by as much as 8%, whereas asthma and allergic rhinitis had increased from 6% to 14.8%. More frequent house cleaning negatively correlated with the new onset of atopic dermatitis and of asthma and allergic rhinitis. Hypersensitivity to seasonal allergens and mites and to any other allergen positively correlated with new onset of food allergy, atopic dermatitis, and asthma and allergic rhinitis. Parental atopy positively correlated with the new onset of asthma and negatively correlated with asthma remission. Conclusion: Analysis of our findings indicated that new onset and/or remission of allergic diseases was linked with hypersensitivity to house-dust mites in children who were polysensitized and with parental atopy. In addition, children who had food allergy, allergic rhinitis, or atopic dermatitis at the age of 1 year had more of a chance developing other atopic disease (except asthma) at ages 7-9 years and less of a chance of having a remission of the disease.

DNA damage and oxidative stress response to selenium yeast in the non-smoking individuals: a short-term supplementation trial with respect to GPX1 and SEPP1 polymorphism.

PURPOSE: Selenium, both essential and toxic element, is considered to protect against cancer, though human supplementation trials have generated many inconsistent data. Genetic background may partially explain a great variability of the studies related to selenium and human health. The aim of this study was to assess whether functional polymorphisms within two selenoprotein-encoding genes modify the response to selenium at the level of oxidative stress, DNA damage, and mRNA expression, especially in the individuals with a relatively low selenium status. METHODS: The trial involved 95 non-smoking individuals, stratified according to GPX1 rs1050450 and SEPP1 rs3877899 genotypes, and supplemented with selenium yeast (200 µg) for 6 weeks. Blood was collected at four time points, including 4 weeks of washout. RESULTS: After genotype stratification, the effect of GPX1 rs1050450 on lower GPx1 activity responsiveness was confirmed; however, in terms of DNA damage, we failed to indicate that individuals homozygous for variant allele may especially benefit from the increased selenium intake. Surprisingly, considering gene and time interaction, GPX1 polymorphism was observed to modify the level of DNA strand breaks during washout, showing a significant increase in GPX1 wild-type homozygotes. Regardless of the genotype, selenium supplementation was associated with a selectively suppressed selenoprotein mRNA expression and inconsistent changes in oxidative stress response, indicating for overlapped, antioxidant, and prooxidant effects. Intriguingly, DNA damage was not influenced by supplementation, but it was significantly increased during washout. CONCLUSIONS: These results point to an unclear relationship between selenium, genotype, and DNA damage.

MMP, VEGF and TIMP as prognostic factors in recurring bladder cancer.

OBJECTIVES: To investigate the clinical correlates and prognostic utility of MMP, VEGF and TIMP genes expression in bladder cancer (BCa) recurrence. METHODS: Expression of MMP1, MMP2, MMP9, VEGFA and TIMP1, TIMP3 was analyzed by qRT-PCR using SYBR Green in peripheral blood leukocytes (PBLs) of BCa patients at two time points (diagnosis (n=40), and first recurrence (n=40)) and an age-matched group of healthy controls (n=100). Plasma concentrations of MMP1 (pro- and active forms) were measured using ELISA in BCa patients. RESULTS: The expression of MMP1 mRNA was significantly lower in BCa patients with first recurrence compared to control (p=0.019). Expression of other genes did not differ significantly between the groups. MMP9 gene expression was associated with differentiation grade (p=0.043), with the highest expression in poorly differentiated tumors (G3) and was higher in smokers than in non-smokers (p=0.039) in BCa patients at diagnosis. The results at two time points showed that MMP9 and VEGFA genes expression was increased in patients with moderately differentiated BCa (p=0.029), and advanced pathologic stage (p=0.048), respectively. Moreover, gene expression of TIMP1 was increased for G3 (p=0.043), and was decreased for early recurrence (p=0.003). CONCLUSIONS: Our study suggests that the expression of MMP9 in PBLs of BCa patients at diagnosis is associated with the differentiation grade of the BCa, and smoking status. Genes expression of MMP9, VEGFA and TIMP1 in PBLs may play a pivotal role in regulation of progression of BCa. Additionally, TIMP1 gene expression may be important factor for early recurrence of BCa.

Cord serum 25-hydroxyvitamin D correlates with early childhood viral-induced wheezing.

BACKGROUND: There are investigations concluding that reduced vitamin D status in pregnancy, may be a risk factor for the development of allergic outcomes in offspring. However, studies on the relationship between cord levels of 25-hydroxyvitamin D (25[OH]D) and risk of early childhood wheezing and early-onset atopic dermatitis/food allergy are very limited. OBJECTIVE: To assess the associations between cord blood concentration of 25[OH]D and occurrence of the incidence of wheezing, atopic dermatitis, food allergy, during the first two years of life. METHODS: We evaluated 240 children by the age of 2 years from the Polish Mother and Child Cohort Study. Women were interviewed during pregnancy to collect demographic and socioeconomic data, the medical and reproductive history. At delivery, umbilical cord blood plasma was sampled. The child's health status were examined at approximately 2 years. In the analyses multivariable model was used. RESULTS: Data from 190 participants were included into the analysis. The median value and quartile range of 25[OH]D in cord blood [ng/ml] were as follows: 6.33, 4.16-8.53. 25[OH]D in cord blood below lower quartile increases the risk of multi-triggered wheezing (MTW) in children during first 2 years of life (OR: 2.81; 95% CI: 1.13-7.00). Higher cord serum level of 25[OH]D reduces the risk of viral induced wheezing (VIW). The cord serum level of 25[OH]D below median value (OR: 6.06; 95% CI: 1.3-28.3) or below lower quartile (OR: 5.43; 95% CI: 1.66-17.7) increases the risk of VIW. All above effects of vitamin D level in cord blood were corrected for the effects other independent risk factors of wheezing and VIW in this cohort. CONCLUSIONS: Cord serum 25[OH]D levels were inversely associated with the risk of multi-triggered wheezing, and especially viral-induced wheezing by the age of 2 years, but no association was found with food allergy, atopic dermatitis and frequencies of infections.

Expression of NRF2 and NRF2-modulated genes in peripheral blood leukocytes of bladder cancer males.

Nuclear factor (erythroid-derived 2)-like 2 (NRF2) is an oxidant-responsive transcription factor involved in induction of antioxidant genes. We assessed NRF2 and selected NRF2-modulated gene expression: glutathione S-transferase A1 and P1 (GSTA1 and GSTP1), mitochondrial superoxide dismutase (SOD2) in blood leukocytes of 51 bladder cancer patients and 90 control males. A significant up-regulation of SOD2 expression (P=0.002) was observed in leukocytes of patients. NRF2 expression was positively correlated with GSTP1 and with SOD2 mRNA level, both in patients and controls. These data suggest disturbances in SOD2 transcription in circulating blood leukocytes of males with bladder cancer. Moreover, concomitant constitutive expression of NRF2 and its target genes may suggest important role of NRF2 transcription factor in positive regulation of antioxidant genes, resulted in enhanced cytoprotection in human peripheral blood leukocytes.

Genetic polymorphism of matrix metalloproteinases in breast cancer.

The family of human matrix metalloproteinases (MMPs) consists of 24 zinc- and calcium-dependent proteolytic enzymes. MMPs are divided into six subgroups, in terms of differences in the substrate specificity with structural domain architecture. These enzymes are involved in many physiological processes, such as skeletal development, wound healing, scar formation, as well as carcinogenesis. MMPs, fulfilling its function of degradation of extracellular matrix components, are involved in one of the stages of angiogenesis enabling the development, growth and spread of the primary tumor. Therefore, the search for the common polymorphic variants of MMPs, new genetic markers as prognostic factors in breast cancer progress seems to be understandable.The minireview presents the results of 19 case-control or prospective studies concerning the association of SNPs of genes encoding nine MMPs: MMP-1, -2, -3, -7, -8, -9, -12, -13, -21 with the breast cancer risk, progression and survival.

Polymorphisms in metabolizing enzymes and the risk of head and neck squamous cell carcinoma in the Slavic population of the central Europe.

The question of susceptibility to squamous cell carcinoma of head and neck (SCCHN) in the environmental context was addressed by analysis of functional polymorphisms in enzymes metabolizing smoke constituents and/or alcohol (CYP2A13, CYP1B1, EPHX1, NQO1, GSTM1, GSTP1, GSTT1, ADH1B and ADH1C). Case-control study of 122 age- and sex-matched pairs of subjects was performed using so far unexplored Central European Slavic population with high level of tobacco and alcohol abuse. Age-, gender-, smoking- and alcohol-adjusted logistic regression failed to demonstrate any significant association of the analyzed polymorphisms with the SCCHN risk. When interactions between potential modifiers of effect, i.e. smoking and alcohol were tested, drinkers seemed to be at lower risk than nondrinkers when carrying the heterozygous genotype Ile/Val in codon 432 of CYP1B1 (OR=0.42; 95% CI=0.21-0.83; p=0.013 vs. OR=1.02; 95% CI=0.34-2.94; p=0.977). Similarly, drinkers were at lower risk than nondrinkers when carrying the heterozygous genotype Pro/Ser in codon 187 of NQO1 (OR=0.41; 95% CI=0.19-0.88; p=0.022 vs. OR=0.96; 95% CI=0.29-3.12; p=0.948). More interestingly, drinkers carrying the rare homozygous genotype Val/Val in codon 350 of ADH1C were at significantly higher risk than nondrinkers carrying this genotype (OR=4.01; 95% CI=1.61-10.01; p=0.003 vs. OR=0.93; 95% CI=0.25-3.57; p=0.919). This result confirmed findings of previously published studies. Smoking did not significantly modify the effect of genotypes. Our data thus demonstrate that genetic susceptibility to SCCHN shall be further followed on populations with different genetic background and lifestyle.

Association between GPx1 Pro198Leu polymorphism, GPx1 activity and plasma selenium concentration in humans.

BACKGROUND: Glutathione peroxidase 1 (GPx1) is an antioxidant selenoenzyme that protects the cells against reactive oxygen species. Its activity depends on the concentration of selenium (Se) which is present in the active centre of the enzyme. The genetic polymorphism of GPx1 encoding gene (GPx1) associated with the proline (Pro) to leucine (Leu) change at codon 198 is supposed to be functional. An in vitro study performed on human breast carcinoma cell line showed that GPx1Leu allele was associated with a lower responsiveness of the enzyme to Se added to the culture medium. Some authors observed a decrease in GPx1 activity associated with GPx1 Leu allele in humans; however, there were no findings on how GPx1 activity changes with Se concentration in individuals with different GPx1 genotypes. AIM OF THE STUDY: To assess whether GPx1 activity that depends on the Se status may be influenced by GPx1 polymorphism through studying this relationship in the blood of healthy individuals. METHODS: The association between the Se status, GPx1 activity and GPx1 genotype was assessed in 405 individuals of Polish origin. GPx1 activity in red blood cells was measured by the spectrophotometric method by Paglia and Valentine, using t-butylhydroperoxide as the substrate. Plasma Se concentration was measured using graphite furnace atomic absorption spectrometry. GPx1 Pro198Leu polymorphism was determined with the Molecular Beacon Real-Time PCR assay. RESULTS: In the subjects examined, the mean plasma Se concentration was 54.4 +/- 14.2 mcg/L. The mean GPx1 activity was 15.1 +/- 4.7 U/g Hb. No difference regarding both the parameters was found between individuals with different GPx1 genotype. However, the association between GPx1 activity and Se concentration, analyzed separately for each genotype group, was not the same. The correlation coefficients amounted to r = 0.44 (p < 0.001) for Pro/Pro, r = 0.35 (p < 0.001) for Pro/Leu and r = 0.25 (p = 0.45) for Leu/Leu group, which indicates that the correlation strength was as follows: Pro/Pro > Pro/Leu > Leu/Leu. Notably, statistically significant difference in this relationship (analyzed as difference between correlation coefficients for linear trends) was found between genotypes Pro/Pro and Leu/Leu (p = 0.034). CONCLUSIONS: The findings of the present study provide evidence for the hypothesis based on in vitro studies which assumes that GPx1 Pro198Leu polymorphism has a functional significance for the human organism and that this functionality is associated with a different response of GPx1 activity to Se. They also point to the importance of the genetic background in the assessment of the Se status with the use of selenoprotein biomarkers such as GPx1 activity.

Lung permeability, antioxidant status, and NO2 inhalation: a selenium supplementation study in rats.

Little is known about antioxidant status, selenium status in particular, and lung response to NO2, which acts as a proinflammatory air pollutant. The effects of a low selenium diet (1.3 microg Se/d) with or without selenium supplementation were therefore studied in 128 Wistar rats, 2 mo old, male exposed to either acute (50 ppm, 30 min), intermittent subacute (5 ppm, 6 h/d, 5 d), intermittent long-term NO2 (1 ppm, 10 ppm, 6 h/d, 5 d/wk, 28 d), or normal atmospheric air (controls). Following sacrifice, measurements of lipid peroxidation (thiobarbituric acid-reactive substances, chemiluminescence), antioxidative protective enzymes (glutathione peroxidase [GPx], superoxide dismutase [SOD], glutathione S-transferase [GST], ceruloplasmin), lung damage (lactate dehydrogenase, alkaline and acid phosphatases), lung permeability (total protein, albumin), and inflammation (cell populations), along with the determination of new biomarkers such as CC16 (Clara-cell protein), were performed in serum and bronchoalveolar lavage fluid (BALF). While selenium-supplemented animals had increased GPx activity in serum prior to inhalation experiments, they also had decreased BALF CC16, blood SOD, and GST levels. Nevertheless, the protective role of normal selenium status with respect to NO2 lung toxicity was evident both for long-term and acute exposures, as the increase in BALF total proteins and corresponding decrease in serum (indicating increased lung permeability) was significantly more pronounced in selenium-deficient animals. During the various inhalation experiments, serum CC16 demonstrated its key role as an early marker of increased lung permeability. These findings corroborate the important role of selenium status in NO2 oxidative damage modulation, but also indicate, in view of its negative impact on CC16, a natural anti-inflammatory and immunosuppressor, that caution should be used prior to advocating selenium supplementation.

Serum clara-cell protein and beta2-microglobulin as early markers of occupational exposure to nitric oxides.

Biochemical effects of NOx on 60 workers (both genders) of nitric acid production were studied. The control group consisted of 61 nonexposed people employed elsewhere in the plant. Although the actual threshold limit valuetime weighted averages (TLV-TWA) were not exceeded in the specific conditions of our study, the subjects were exposed to NO2 and NO during several exposure episodes with peak maximal concentrations of 140 ppm and 515 ppm, respectively. Additional cross-week evaluation of several biochemical biomarkers in 15 NOx-exposed workers from one shift was performed. The objective of the study was to evaluate the value of serum Clara-cell protein (CC16) as a marker of bronchoalveolar epithelium activity. Antioxidant status was assessed by measuring activity of enzymes: glutathione peroxidase (GSH-Px), ceruloplasmin (Cp) in plasma, or superoxide dismutase (SOD), gluthatione S-transferase (GST), and nonenzymatic alpha-tocopherol in erythrocytes and thiobarbituric acid-reactive substances (TBARS) in plasma. Serum hyaluronic acid (HA) determining the connective tissue matrix status of airways, and beta2-microglobulin in serum (beta2M-S) and urine (beta2M-U) as a marker of renal function in occupational exposure to NOx were also employed. Exposure to NOx initiates peroxidative chain depleting of lipoprotein pool (alpha-tocopherol) in blood. Serum CC16 levels in NOx-exposed workers were found to be closely connected with alpha-tocopherol content. In NOx-exposed workers, the beta2M-S level was significantly higher than in the nonexposed ones, with the exception of smokers. Results of the cross-week study confirm cumulative systemic effects of NOx on several examined biomarkers. SOD and GST were found to be depleted. A transient higher level of HA after a 5-d shift significantly inversely correlated with CC16 level. The data imply that NOx-depleted levels of CC16 are detectable already after an 8-h shift. Our results demonstrate that even low NOx human exposure can cause characteristic changes in bronchiolar epithelium cells and renal effects. Serum CC16 level, although a nonspecific marker, was lowest in NOx-exposed subjects. The most sensitive parameters in exposed workers were beta2M-S and a-tocopherol. Spirometric assessment was not useful to describe low occupational exposure to NOx. In studying the effects of NOx on biomarkers, it is essential to carefully select suitable time of sampling. Screening of CC16, beta2M-S, and a-tocopherol can be successfully employed for biological monitoring of exposure to NOx.

Oxidative-stress markers in blood of lung cancer patients occupationally exposed to carcinogens.

The study covered 152 lung cancer patients and 210 controls. The results of the study indicated decreased selenium (Se) concentrations and lowered activity of erythrocyte antioxidant enzymes (glutathione peroxidase, superoxide dismutase, glutathione-S-transferase) in the blood of lung cancer patients, as well as significantly increased concentrations of vitamin E in erythrocytes and thiobarbituric acid reactive substances in the plasma of the study population. Low plasma Se concentrations (< 45.7 microg/L) enhance the estimated risk of lung cancer (odds ratio = 3.047, p < 0.001). A more precise exposure assessment is required to identify the association between lung cancer incidence and occupational exposure to carcinogens.

Selenium status of low-selenium area residents: Polish experience.

The concentration of selenium (Se) in human organism varies widely between geographical areas depending on its content in soil and plants, dietary Se intake, bioavailability and retention, mineral interactions and other factors. The study includes healthy inhabitants of different regions of Poland; pregnant women, lactating women, children from 0 to 15 years of age and adults. Systematic determinations allow us to observe changes of the concentration of Se in time, which may be significant for developing preventive action. The results obtained confirm our thesis that Se concentration in the blood of the inhabitants of Poland depends on the region of the country. In recent years, in a considerable number of Polish inhabitants, the concentration of Se in blood plasma has been relatively low-about 50-55 microg/l, and the calculated daily dietary intake about 30-40 microg/day. The low levels of the element in the blood and urine are probably due to its deficiency in the diet.

Selenium, zinc, and copper concentrations in the blood and milk of lactating women.

The aim of the study was to determine Se, Zn, and Cu concentrations in blood plasma and milk of lactating women from central Poland who were in different stages of lactation and to investigate the relationship between the content of trace elements in mothers' blood and concentrations of microelements in their milk. Se and Zn concentrations in blood plasma of mothers were the lowest and Cu was the highest on the first 4 d of lactation (colostrum, n = 43) and were found to be 34.9 +/- 11.8 microg/L, 0.51 +/- 0.13 mg/L, and 1.70 +/- 0.55 mg/L, respectively. The highest plasma level of Se and Zn and the lowest content of Cu could be observed between d 10 and 30 of lactation (mature milk, n = 41), and were found to be 54.3 +/- 14.6 microg/L for Se (p < 0.001), 0.76 +/- 0.20 mg/L for Zn (p < 0.001), and 1.03 +/- 0.30 mg/L (p < 0.001) for Cu. The results of Se, Zn, and Cu determination in breast milk samples demonstrate a pattern of decline in their concentration with advancing stages of lactation. We found out that Se, Zn, and Cu concentrations were the highest in colostrum (n = 43) and amounted to 24.8 +/- 10.1 microg/L, 8.2 +/- 2.8 mg/L, and 0.45 +/- 0.11 mg/L, respectively. The content of all determined microelements declined significantly during the time of lactation. Statistically significant linear correlation was found between concentrations of Zn in blood plasma and milk in the first stage of lactation. Weak but statistically significant linear correlations were also found between plasma Se content in plasma and in transitional and mature milk of breast-feeding women.

Blood concentration of essential trace elements and heavy metals in workers exposed to lead and cadmium.

The aim of the study was to determine blood concentration of essential trace elements (Se, Zn, Cu) and toxic metals (Pb, Cd), markers of antioxidant (activities of glutathione peroxidase (GPx), superoxidase dismutase and ceruloplasmin) and prooxidant processes (thiobarbituric acid reactive substances (TBARS)) in workers exposed to Pb and Cd. Forty three male workers of the lead-acid batteries department, aged 25-52 years, and twenty two workers, including 15 women, aged 36-51 years, exposed to Cd in the alkaline batteries department were examined. The reference group consisted of 52 healthy inhabitants of the same region. It was found that Se concentration and GPx activity in both erythrocytes and plasma of Cd exposed workers were significantly lower (p < 0.001) than in the reference group. We found an inverse linear correlation between blood Se and Cd concentrations in the workers exposed to Cd (r = -0.449; p < 0.01). Moreover, the activity of erythrocyte and plasma GPx was shown to be significantly lower in the study group of workers (p < 0.001). It was observed that TBARS concentration in plasma was significantly higher (p < 0.05) in the lead exposed workers than in the group without contact with Pb. Our results indicate that exposure to Pb and Cd affects the antioxidant potential of blood in workers exposed to heavy metals.

The role of reactive oxygen species in the development of malignancies.

Numerous studies on animal models and cell cultures confirm the role of free radicals/reactive oxygen species and oxidative damages in the process of the initiation and promotion of neoplastic diseases. Also epidemiological studies attribute an important role to disturbances in the pro- and antioxidative potential in the development of malignancies and highlight the essential function of antioxidants to protect the cells from the attack of free oxygen radicals. The current literature data on the parameters of the anti- and prooxidant status in patients with malignant diseases and their role in pathogenesis of the disease is reviewed in this article.

[Selenium nutritional status and the course of psoriasis]. / Stan odzywienia selenem a przebieg luszczycy.

A case-control study was conducted to evaluate the role of dietary selenium (Se) intake and the selenium nutritional status in the course of psoriasis. The cases studied were 30 psoriatic patients with a history of the disease no longer than 10 months and 29 psoriatics with the disease lasting at least 3 years, 24 other dermatological patients and 14 healthy subjects constituted 2 control groups matched to cases studied by sex and age. Se dietary intake was calculated from 24-hours dietary recall and Se status was assessed with plasma Se level as well as plasma and erythrocyte GSH-Px activity. Dietary Se intake was found to be correlated to erythrocyte GSH-Px (r = 0.50, p < 0.05). The selenium nutritional status seemed to be insufficient, especially in females with psoriasis of no longer than 10 months' duration and males with long-lasting psoriasis. In these males plasma and erythrocyte GSH-Px activity were inversely correlated to the severity of the disease (r = -0.64 and r = -0.41, p < 0.05, respectively). The results obtained suggest that Se dietary intake could be one of the contributing factors in the pathogenesis and course of psoriasis. Further studies are needed to explore this relationship.

Selenium levels, thiobarbituric acid-reactive substance concentrations and glutathione peroxidase activity in the blood of women with gestosis and imminent premature labour.

The aim of the study was to investigate antioxidant status, monitored by selenium and thiobarbituric acid-reactive substance concentrations in blood plasma, and glutathione peroxidase activity in erythrocytes and blood plasma in women with gestosis (n = 26), imminent premature labour (n = 48) and normal pregnancy (n = 23) during 19-38 weeks of pregnancy. Selenium concentrations in blood plasma were significantly higher in women with pathological pregnancies than in normal (45.5 +/- 10.5 micrograms l-1, p < 0.01 and 44.1 +/- 11.6 micrograms l-1, p < 0.05 vs. 38.6 +/- 8.3 micrograms l-1, respectively). In all groups of pregnant women Se concentrations were extremely low as compared with non-pregnant females. Glutathione peroxidase (GSH-Px) activity in blood plasma was significantly higher in complicated pregnancies than in healthy ones. There were no significant differences in thiobarbituric acid-reactive substance concentrations between all groups of pregnant women. Statistically significant correlations were found between blood plasma Se concentrations and GSH-Px activity in healthy pregnant (r = 0.53, p < 0.01), imminent premature labour (r = 0.39, p < 0.01), and non-pregnant females (r = 0.56, p < 0.001).

Glutathione and glutathione metabolizing enzymes in tissues and blood of breast cancer patients.

Many reports indicate that glutathione and enzymes cooperating with it are important in neoplastic processes. Glutathione (GSH) concentrations and glutathione S-transferase (GSH STr) and glutathione peroxidase (GSH-Px) activities were determined in breast cancer tissue and adjacent healthy tissues, as well as in blood of 28 patients. There were considerable differences in the investigated parameters among individual patients. Therefore we analyzed the paired samples of normal and cancerous tissues from the same individual. In 68% of the patients the activities of GSH-Px and in 85% patients those of GSH STr were found to be higher in the tumor than in the normal tissue. GSH concentration in 48% tumor samples were higher and in 44% lower than in corresponding normal tissues. Statistically significant correlation was found between GSH-Px and GSH STr in normal (r = 0.51, p < 0.005) and in cancer tissues (r = 0.64, p = 0.001). Correlation coefficient between GSH Px activity in normal and corresponding cancer tissues was r = 0.71 (p < 0.001), however this correlation in the case of GSH STr was much lower but still significant (r = 0.38, p < 0.05). No significant correlation in the determined parameters was found between erythrocytes or plasma and normal or cancer tissues.