Circulating P-Selectin and Its Glycoprotein Ligand in Nondiabetic Obstructive Sleep Apnea Patients.

Selectins and their ligands play an important role in atherosclerosis. The role of these adhesion molecules in the pathogenesis of obstructive sleep apnea (OSA) may be of clinical relevance. Therefore, the aim of this study was to assess the serum content of platelet P-selectin (P-SEL) and P-selectin glycoprotein ligand 1 (PSGL-1) in different OSA stages. The study was performed in nondiabetic patients, aged 32-71, in whom OSA was verified by polysomnography. The apnea/hypopnea index (AHI) was used to stratify OSA stages: AHI <5, no sleep pathology (OSA-0); AHI 5-15, (OSA-1); AHI 16-30, (OSA-2); and AHI >30, (OSA-3). There were 16 patients in each group. P-SEL and PSGL-1 were assessed by ELISA kits. There were no appreciable differences in the patients' glucose or high-specificity C-reactive protein content. We found that P-SEL and PSGL-1 significantly increased from OSA-0 to OSA-3. There were the following positive associations in all OSA patients: P-SEL vs. AHI, PSGL-1 vs. AHI, and P-SEL vs. PSGL-1. In addition, the adhesion molecules are associated with the anthropometric parameters, oxygen saturation, and sleep architecture in the OSA-1 group. We conclude that the adhesion molecules consistently increase in the blood of nondiabetic OSA patients, along with progression of disorder severity.

Oxidative Stress Markers and Severity of Obstructive Sleep Apnea.

Oxidative stress underlies both obstructive sleep apnea (OSA) and atherosclerosis. The aim of the study was to assess the markers of oxidative stress in plasma at different stages of OSA in non-smoking obese Caucasian males aged 41-60, with normal oral glucose tolerance test. All patients were subjected to clinical and polysomnographic examinations. The stage of OSA severity was set according to the following criteria of the apnea-hypopnea index (AHI): AHI < 5/h - no disease (OSA-0; n = 26), AHI 5-15/h - mild disease (OSA-1; n = 26), AHI 16-30/h - moderate disease (OSA-2: n = 27), and AHI > 30/h obstructive episodes per hour - severe disease (OSA-3; n = 27). Plasma total antioxidant status (TAS) and thiobarbituric acid-reacting substances (TBARS), reflecting the level of lipid peroxides, were determined spectrophotometrically. We found that TAS decreased and TBARS increased significantly from OSA-0 to OSA-3. We conclude that the oxidative stress markers are conducive to setting the severity of OSA in normoglycemic patients.

Paraoxonase 1 Gene L55M Polymorphism and Paraoxonase 1 Activity in Obstructive Sleep Apnea Patients.

The antioxidant enzyme paraoxonase-1 (PON1) may limit oxidative stress in the development of cardiovascular diseases (CVD) and obstructive sleep apnea (OSA). The aim of the study was to determine PON1 gene L55M polymorphism in OSA-positive and OSA-negative subjects, along with paraoxonase activity of the enzyme (PON1-act). Caucasians aged 25-75, with BMI 19.0-53.0 kg/m2 and no acute or severe chronic disorder underwent polysomnography, and OSA-negative (n = 44) and OSA-positive (n = 57) groups were established. The following parameters were assessed: arterial blood pressure and serum glucose, lipids, C-reactive protein, and homocysteine. Genomic DNA was extracted and amplified, and automatic sequencing was used to confirm the LL, LM, MM genotypes. PON1-act was measured spectrophotometrically using paraoxon as a substrate. We found that frequency of polymorphisms differed significantly between the OSA-negative and OSA-positive patients (p < 0.05). Increased PON1-act was observed in the LL-genotype versus the LM + MM-genotype in the study population (p < 0.05). PON1-act was higher in the OSA-negative compared with OSA-positive patients (p < 0.001); in general and in the subgroups presenting the LL or LM genotype. In addition, there was an inverse relationship between PON1-act and LDL-cholesterol in the entire study population. The OSA-positive group presented an inverse relationship between PON1-act and fasting glucose. We conclude that patients could benefit from the LL genotype related with higher activity of PON1. OSA pathology might decrease the enzyme activity, despite the presence of L allele.

Fire Blight Symptomatic Shoots and the Presence of Erwinia amylovora in Asymptomatic Apple Budwood.

Erwinia amylovora, the causal agent of fire blight, causes considerable economic losses in young apple plantings in New York on a yearly basis. Nurseries make efforts to only use clean budwood for propagation, which is essential, but E. amylovora may be present in trees that appear to have no apparent fire blight symptoms at the time of collection. We hypothesized that the use of infected budwood, especially by commercial nursery operations, could be the cause, in part, of fire blight outbreaks that often occur in young apple plantings in New York. Our goal was to investigate the presence of E. amylovora in asymptomatic budwood from nursery source plantings as it relates to trees with fire blight symptoms. From 2012 to 2015, apple budwood was collected from two commercial budwood source plantings of 'Gala' and 'Topaz' at increasing distances from visually symptomatic trees. From these collections, internal contents of apple buds were analyzed for the presence of E. amylovora. E. amylovora was detected in asymptomatic budwood in trees more than 20 m from trees with fire blight symptoms. In some seasons, there were significant (P ≤ 0.05) differences in the incidence of E. amylovora in asymptomatic budwood collected from symptomatic trees and those up to 20 m from them. In 2014 and 2015, the mean E. amylovora CFU per gram recovered from budwood in both the Gala and Topaz plantings were significantly lower in budwood collected 20 m from symptomatic trees. Further investigation of individual bud dissections revealed that E. amylovora was within the tissue beneath the bud scales containing the meristem. Results from the study highlight the shortcomings of current budwood collection practices and the need to better understand the factors that lead to the presence of E. amylovora in bud tissues to ensure the production of pathogen-free apple trees.

Prevalence of Streptomycin-Resistant Erwinia amylovora in New York Apple Orchards.

Resistance to streptomycin in Erwinia amylovora was first observed in the United States in the 1970s but was not found in New York until 2002, when streptomycin-resistant (SmR) E. amylovora was isolated from orchards in Wayne County. From 2011 to 2014, in total, 591 fire blight samples representing shoot blight, blossom blight, and rootstock blight were collected from 80 apple orchards in New York. From these samples, 1,280 isolates of E. amylovora were obtained and assessed for streptomycin resistance. In all, 34 SmR E. amylovora isolates were obtained from 19 individual commercial orchards. The majority of the resistant isolates were collected from orchards in Wayne County, and the remaining were from other counties in western New York. Of the 34 resistant isolates, 32 contained the streptomycin resistance gene pair strA/strB in the transposon Tn5393 on the nonconjugative plasmid pEA29. This determinant of streptomycin resistance has only been found in SmR E. amylovora isolates from Michigan and the SmR E. amylovora isolates discovered in Wayne County, NY in 2002. Currently, our data indicate that SmR E. amylovora is restricted to counties in western New York and is concentrated in the county with the original outbreak. Because the resistance is primarily present on the nonconjugative plasmid, it is possible that SmR has been present in Wayne County since the introduction in 2002, and has spread within and out of Wayne County to additional commercial growers over the past decade. However, research is still needed to provide in-depth understanding of the origin and spread of the newly discovered SmR E. amylovora to reduce the spread of streptomycin resistance into other apple-growing regions, and address the sustainability of streptomycin use for fire blight management in New York.

Impulse oscillometry in the diagnosis of airway resistance in chronic obstructive pulmonary disease.

Spirometry is a standard lung function test for diagnosis and staging of chronic obstructive pulmonary disease (COPD). Impulse oscillometry (IOS) can be complementary to spirometry, especially in patients at advanced age and with physical or mental disorders who cannot be diagnosed through spirometry. The aim of this study was to compare IOS and spirometry in the assessment of airway obstruction in COPD. The study was conducted in 112 stable COPD patients, including 29 females and 83 males of the mean age of 69±11 years. The oscillometric evaluation included total (R5), peripheral (R5-R20), and negative reactance (X5), which were compared with the predicted forced expiratory volume in 1 s (FEV1%pred). The findings show a significantly negative correlation between FEV1%pred and the R5, R5-R20, and X5. COPD patients had increased R5, R5-R20, and X5. The severity of bronchial obstruction found by impulse oscillometry correlated well the spirometric assessment. IOS is a simple to perform test that may be helpful for functional examination of COPD patients.

Circulating CD3+56+ cell subset in pre-diabetes.

The CD3+56+ cells are a small but significant population of T lymphocytes encompassing NKT-like and NKT cells, which may play the essential role at the very early stages of atherosclerotic plaque development. The frequency and activity of CD3+56+ cells in atherosclerosis-inducing dysglycaemic disease (diabetes type 2 or pre-diabetes) is largely unknown.We analysed CD3+56+ cell count, granzyme, perforin and annexin V profiles in the peripheral blood from a group of patients with pre-diabetes, with diabetes type 2 and from non-dysglycaemic controls. Measurements were made of fasting glucose levels, HbA1c, 1,5-anhydroglucitol and lipid profile.The mean counts of CD3+56+ cells were significantly higher in patients with pre-diabetes compared to both patients with diabetes and to control group. There was an increase in the number of CD3+56+ cells producing granzyme and perforin in pre-diabetic patients compared to other groups, while there were no difference in annexin V+ populations within examined groups. It was confirmed that CD3+56+ cells count is modified by metabolic factors and their parameters, namely HbA1c and 1,5-anhydroglucitol values.It could be stated that the alterations of CD3+ 56+ cells count in peripheral blood of pre-diabetic and type 2 diabetic patients are related to different grades of carbohydrate deteriorations - postprandial hyperglycaemia and chronic hyperglycaemia.

Spinal epidural abscess: common symptoms of an emergency condition. A case report.

Spinal epidural abscess (SEA) is a severe pyogenic infection of the epidural space that leads to devastating neurological deficits and may be fatal. SEA is usually located in the thoracic and lumbar parts of the vertebral column and injures the spine by direct compression or local ischemia. Spinal injury may be prevented if surgical and medical interventions are implemented early. The diagnosis is difficult, because clinical symptoms are not specific and can mimic many benign conditions. The classical triad of symptoms includes back pain, fever and neurological deterioration. The gold standard in the diagnostic evaluation is magnetic resonance imaging with gadolinium enhancement, which determines the location and extent of the abscess. Increased awareness of the disease is essential for rapid recognition and immediate implementation of treatment. Here we describe the case of a 26-year-old woman with SEA with fever, back pain in the thoracic region and delayed symptoms of a transverse spinal cord injury.

Plasma selectins in patients with obstructive sleep apnea.

Obstructive sleep apnea (OSA) is an independent risk factor in the pathogenesis of -cardiovascular diseases. The aim of the study was to analyze three specific adhesion molecules involved in the development of an atherosclerotic plaque: E-selectin (endothelium), L-selectin (leukocyte surface), and P-selectin (from platelet), circulating in plasma in patients at different OSA severity. Eighty non-smoking male Caucasians aged 30-64 were enrolled into the study after clinical, biochemical, and polysomnographic examinations. The patients were divided into four groups based on the results of apnea/hypopnea index (AHI): OSA-0 with AHI 0-4.9 (n = 20), OSA-1 with AHI 5-15 (n = 21), OSA-2 with AHI 16-30 (n = 18), OSA-3 with AHI ≥ 31 (n = 21). Complete blood count, oral glucose tolerance test, fasting lipid profile, C-reactive protein and insulin, and plasma concentrations of soluble E-selectin, P-selectin and L-selectin were measured. We found a progressive increase in the concentrations of all three selectins with the severity of OSA. In conclusion, the level of plasma adhesion molecules may be indicative of OSA severity and may contribute to cardiovascular sequelae.

Lung impairment in scleroderma.

Scleroderma typically manifests as fibrosis of the skin, but may also involve other organs, particularly the lungs. Interstitial lung disease and functional abnormalities are observed in the majority of patients. The aim of this study was to evaluate radiological changes in the lungs and their correlation with functional disorders in scleroderma patients. The study was conducted in 37 scleroderma patients (F/M-31/6). High resolution computed tomography (HRCT), Warrick score system and spirometry, body plethysmography, and lung diffusion examinations (DLco) were performed. The HRCT showed septal and subpleural lines in 70%, ground-glass opacities in 51%, and honeycomb lungs in 30% of the cases. The DLco values were decreased in 92% of the patients. Total lung capacity (TLC) showed a restrictive pattern in 24% of the patients, and only in 11% of them obstruction predominated. The Warrick score correlated inversely with both DLco (r=0.36; p>0.05). Interstitial lung disease often coexists with scleroderma and is accompanied by functional lung abnormalities.

Endothelium-derived markers and antioxidant status in the blood of obstructive sleep apnea males.

OBJECTIVE: The relationship between obstructive sleep apnea (OSA) and cardiovascular disease is intensively discussed. Endothelial leukocyte adhesion molecule (E-selectin) is one of factors facilitating leukocyte migration to the subendothelial layer which could be considered proatherogenic. The aim of the study was to determine E-selectin levels and total plasma antioxidant status (TAS) in the blood of different stage OSA patients. METHODS: Non-smoking, OSA-suspected males, aged 30-63, were selected for the study. An EMBLA polysomnographic system was used to establish the severity of apneic episodes. The results of apnea/hypopnea index (AHI) allowed dividing patients into the following groups: OSA-0 with AHI 0-4.9 (n=14), OSA-1 with AHI 5-15 (n=14), OSA-2 with AHI 16-30 (n=13), OSA-3 with AHI > or =30 (n=13). Complete blood count (CBC), glycemia during oral glucose tolerance test, fasting plasma lipid profile, uric acid, and high sensitivity C-reactive protein (hsCRP) were estimated among routine parameters. We determined plasma concentrations of E-selectin and total antioxidant status. RESULTS: We found progressively decreasing concentrations of TAS (P=0.03) and increased concentrations of E-selectin (P=0.0001) from OSA-0 to OSA-3 subjects. No correlation between E-selectin and metabolic parameters was noted. - CONCLUSION: In the studied OSA groups, E-selectin appeared an independent proatherogenic factor.

Onconeuronal and antineuronal antibodies in patients with neoplastic and non-neoplastic pulmonary pathologies and suspected for paraneoplastic neurological syndrome.

OBJECTIVE: Onconeuronal antibodies are important diagnostic tool in patients with suspicion of paraneoplastic neurological syndromes (PNS). However, their role in PNS pathophysiology and specificity for particular neurological manifestation remains unclear. The aim of this study was to evaluate onconeuronal and antineuronal antibodies in patients with pulmonary pathologies and suspected for PNS. MATERIAL AND METHODS: Twenty one patients with pulmonary pathologies were selected from the database of 525 consecutive patients with suspicion of PNS. Patients' sera were screened for the presence of onconeuronal and antineuronal antibodies by means of indirect immunofluorescence; the presence was confirmed by Western blotting. Clinical data were obtained from medical records, hospital data base, and questionnaire-based direct telephone contact with patients. RESULTS: Among 21 patients, aged 54 +/-11, with pulmonary pathologies, the most frequent neurological manifestations were neuropathies. Typical PNS included paraneoplastic cerebellar degeneration (PCD) and limbic encephalitis (LE). We found cases with multiple onconeuronal antibodies (anti-Ri and anti-Yo) and coexisting PNS (PCD/LE). Well-defined onconeuronal antibodies were identified in 23.8% of patients. Among antineuronal antibodies, the most frequent were anti-MAG (23.8%). ROC curves analysis revealed high sensitivity of onconeuronal and antineuronal antibodies for typical PNS and lower for pulmonary malignancies. CONCLUSIONS: Tests for antibodies are highly sensitive for the diagnosis of typical paraneoplastic neurological syndromes. Anti-myelin and anti-MAG antibodies are associated with non-neoplastic pulmonary diseases. Patients with well-defined onconeuronal antibodies require careful screening and follow-up, because the PNS diagnosis indicates a high probability of an underlying malignancy.

Adipocytokines in sleep apnea syndrome.

OBJECTIVE: Biomarkers of adipose tissue may affect glucose and lipid metabolism and present pro-inflammatory properties, thus could be involved in the pathobiochemistry of cardiovascular disease (CVD). The coexistence of sleep apnea syndrome (OSA) and metabolic risk factors of CVD is worth explaining. The aim of the study was to compare the serum adipocytokines in subjects with and without OSA, who had all elevated body mass index (BMI). METHODS: Overweight (BMI: 25.0-29.9 kg/m2) and obese (BMI: 30.0-39.9 kg/m2) OSA-suspected Caucasian males, aged 30-63, with no acute disease or chronic disorder underwent polysomnographic evaluation to select OSA-positive (AHI > or = 5) and OSA-negative (AHI <5) subjects. Four subgroups were created of 18 persons each: Over(weight)-OSA-Neg, Over-OSA-Pos, Obese-OSA-Neg, Obese-OSA-Pos. In all subjects, plasma carbohydrate and lipid metabolism parameters, and serum uric acid, resistin and leptin concentrations were determined. RESULTS: A decreased resistin level was observed in Over-OSA-Pos vs. Over-OSA-Neg subjects (P=0.037) as well as in Obese-OSA-Pos vs. Obese-OSA-Neg (P=0.045). No differences in leptin concentrations were observed. A positive correlation between leptin and BMI was in both overweight subgroups and a negative one between resistin and fasting glucose was in both obese subgroups. CONCLUSIONS: OSA may decrease the serum resistin level in subjects with excess body mass and also may contribute to glucose metabolism, but has no influence on the leptin level.

Oxidative stress markers in the blood of persons with different stages of obstructive sleep apnea syndrome.

The aim of the study was to determine some biochemical factors reflecting oxidant-antioxidant balance in the blood of patients being in different stages of the obstructive sleep apnea syndrome (OSAS). The patients, suspected of OSAS, were submitted to biochemical and somnographic examinations. APolyMesam device was used to establish the severity of apnea episodes. The control group was composed of subjects without OSAS. The following parameters were determined: concentration of plasma total antioxidant status, TAS; activity of erythrocyte Cu, Zn-superoxide dysmutase, SOD; plasma lipid peroxidation products, TBARS. The OSAS patients had lower levels of SOD and TAS, and increased level of TBARS. We conclude that oxidative stress markers increase in the blood of OSAS patients to a variable degree, depending on the severity of the syndrome and, therefore, may be suitable for a clinical follow-up of such patients.

The impact of the sleep apnea syndrome on oxidant-antioxidant balance in the blood of overweight and obese patients.

The aim of the study was to assess the markers of oxidant-antioxidant status in excess body mass index (BMI) persons with and without the obstructive sleep apnea syndrome (OSAS). In overweight (BMI-1: 25.0-29.9 kg/m(2)) control and OSAS and obese (BMI-2: 30.0-34.9 kg/m(2)) control and OSAS subjects with no acute or chronic disorder the following markers were determined: concentration of plasma total antioxidant status, TAS, (Randox); activity of erythrocyte Cu, Zn-superoxide dysmutase, SOD, (Randox); plasma concentration of thiobarbituric acid reacting substances, TBARS, (Yagi method). BMI-1-OSA presented decreased SOD, compared with the BMI-1-C group (P=0.006). BMI-2-OSA showed both SOD (P=0.002) and TAS (P=0.047) decreased, and elevated TBARS (P=0.03) compared with the BMI-2-C group. There was a positive correlation between TAS & SOD and a negative one between TAS & TBARS in the BMI-1-C group. In BMI-2-C, a negative correlation between TAS & TBARS was observed. We conclude that OSAS decreases the blood antioxidant status in high BMI persons and may change the relationship between oxidative stress markers.

Overexpression of the apple MpNPR1 gene confers increased disease resistance in Malus x domestica.

The NPR1 gene plays a pivotal role in systemic acquired resistance in plants. Its overexpression in Arabidopsis and rice results in increased disease resistance and elevated expression of pathogenesis-related (PR) genes. An NPR1 homolog, MpNPR1-1, was cloned from apple (Malus x domestica) and overexpressed in two important apple cultivars, Galaxy and M26. Apple leaf pieces were transformed with the MpNPR1 cDNA under the control of the inducible Pin2 or constitutive Cauliflower mosaic virus (CaMV)35S promoter using Agrobacterium tumefaciens. Overexpression of MpNPR1 mRNA was shown by reverse transcriptase-polymerase chain reaction. Activation of some PR genes (PR2, PR5, and PR8) was observed. Resistance to fire blight was evaluated in a growth chamber by inoculation of the shoot tips of our own rooted 30-cm-tall plants with virulent strain Ea273 of Erwinia amylovora. Transformed Galaxy lines overexpressing MpNPR1 had 32 to 40% of shoot length infected, compared with 80% in control Galaxy plants. Transformed M26 lines overexpressing MpNPR1 under the control of the CaMV35S promoter also showed a significant reduction of disease compared with control M26 plants. Some MpNPR-overexpressing Galaxy lines also exhibited increased resistance to two important fungal pathogens of apple, Venturia inaequalis and Gymnosporangium juniperi-virginianae. Selected transformed lines have been propagated for field trials for disease resistance and fruit quality.

Activation of the pathogen-inducible Gst1 promoter of potato after elicitation by Venturia inaequalis and Erwinia amylovora in transgenic apple (Malus x domestica).

Rather than using a constitutive promoter to drive transgenes for resistance against fungal and bacterial diseases in genetic engineering of apple (Malus x domestica) cultivars, a promoter induced only after infection was preferred. The ability of the Pgst1 promoter from potato (Solanum tuberosum L.) to drive expression of the gusA reporter gene was determined in two genotypes of apple: the fruit cultivar Royal Gala and the M.26 rootstock. beta-Glucuronidase activity in the transgenic lines grown in a growth chamber was determined quantitatively using fluorometric assays and compared to the activity in Cauliflower Mosaic Virus (CaMV) 35S promoter-driven transgenic lines. In both apple genotypes, the Pgst1 promoter exhibited a low level of expression after bacterial and fungal inoculation compared to the level obtained with the PCaMV35S promoter (15% and 8% respectively). The Pgst1 promoter was systematically activated in apple at the site of infection with a fungal pathogen. It was also activated after treatment with salicylic acid, but not after wounding. Taken together, these data show that, although the Pgst1 promoter is less active than the PCaMV35S promoter in apple, its pathogen responsiveness could be useful in driving the expression of transgenes to promote bacterial and fungal disease resistance.

Identification of the partitioning site within the repABC-type replicon of the composite Paracoccus versutus plasmid pTAV1.

The replicator region of composite plasmid pTAV1 of Paracoccus versutus (included in mini-replicon pTAV320) belongs to the family of repABC replicons commonly found in plasmids harbored by Agrobacterium and Rhizobium spp. The repABC replicons encode three genes clustered in an operon, which are involved in partitioning (repA and repB) and replication (repC). In order to localize the partitioning site of pTAV320, the two identified incompatibility determinants of this mini-replicon (inc1, located in the intergenic sequence between repB and repC; and inc2, situated downstream of the repC gene) were PCR amplified and used together with purified RepB fusion protein (homologous to the type B partitioning proteins binding to the partitioning sites) in an electrophoretic mobility shift assay. The protein bound only inc2, forming two complexes in a protein concentration-dependent manner. The inc2 region contains two long (14-bp) repeated sequences (R1 and R2). Disruption of these sequences completely eliminates RepB binding ability. R1 and R2 have sequence similarities with analogous repeats of another repABC replicon of plasmid pPAN1 of Paracoccus pantotrophus DSM 82.5 and with centromeric sequences of the Bacillus subtilis chromosome. Excess RepB protein resulted in destabilization of the inc2-containing plasmid in Escherichia coli. On the other hand, the inc2 region could stabilize another unstable replicon in P. versutus when RepA and RepB were delivered in trans, proving that this region has centromere-like activity. Thus, it was demonstrated that repA, repB, and inc2 constitute a functional system for active partitioning of pTAV320.

Oxidase activity of ceruloplasmin and concentrations of copper and zinc in serum of cancer patients.

A balance between oxidant carcinogens and endogenous antioxidant defence is of particular relevance to the carcinogenesis. Ceruloplasmin (Cp) carries up to 90% of Cu in plasma and performs ferroxidase, antioxidant and amine oxidase activity. Cu and Zn, as trace elements, have been recognized to play an important role as cofactors of SOD. The study presents the relationship of the Cp oxidase activity and concentrations of Cu and Zn in serum of 62 patients with breast (BCA), lung (LCA), gastrointestinal (GICA) and gynecological (GYNCA) cancer. The Cp oxidase activity was determined in serum with o-dianisidine as a substrate. Cu and Zn concentrations in serum were measured by using atomic absorption spectrometry. The results of the study have shown significant increase in the mean serum Cp oxidase activity and total Cu concentrations in all patient groups compared with the control one. The total mean serum Zn concentration was found to be decreased only in LCA group as compared with the control. The effect of the cancer progress on the Cp oxidase activity and concentrations of Cu and Zn was observed within the group of all cancer patients (ALLCA) and within the GICA group. The only significant difference in Cu concentrations among various stages of the disease was observed in GICA between local and distant one. Significant positive correlation coefficients were caLculated for the Cp activity and Cu concentrations in the control group and all patients groups, also according to the cancer progress. Future research is needed to evaLuate the consequences of the elevation of the serum Cp oxidase activity and concentration of Cp, Cu and Zn for the host antioxidant-oxidant balance.