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Biomedical subjects

B Wachowicz

Publications and source records attributed to B Wachowicz.

At least 55 records · Page 3Linked to original sources
PubMed1996

Cisplatin-induced changes in biological activity of blood platelets: thiol-related mechanisms.

The effects of cisplatin (cis-diamminedichloroplatinum (II), CDDP) and transplatin (trans-diamminedichloroplatinum(II), TDDP), and their complexes with glutathione (GS-Pt) in vitro on oxygen free radical generation O2-.), lipid peroxidation and ADP-induced aggregation in pig blood platelets were studied. Incubation of pig blood platelets with cisplatin or transplatin caused a loss of both protein -SH and the thiol groups of GSH. In pig blood platelets exposed to cisplatin or transplatin (20 microM) the GS-Pt complex was formed as a major metabolite. The formation of GS-Pt complexes in platelet cytosol was time dependent and the intracellular content of this complex reached a maximal level after 24 h. GS-Pt complexes were found to induce platelet lipid peroxidation, measured as thiobarbituric acid reactive substance level, and O2-. generation, and it was more active than cisplatin or transplatin alone. Cisplatin and its GS-Pt complex had an inhibitory effect on ADP-induced platelet aggregation. These results showed that GS-Pt complexes affect platelet metabolism and function. It seems that glutathione-associated metabolism of platinum compounds plays an important role in the cytotoxicity and biological activity of these drugs.

Animals↗
PubMed1995

Effects of cisplatin and selenite on the level of thiols in pig blood platelets.

The level of free sulfhydryl groups of glutathione and proteins in pig blood platelets after short lasting incubation (30 min.) of these cells with cisplatin (cis-diamminedichloroplatinum II) and sodium selenite was investigated in vitro. The concentration of the platelet thiols after sodium selenite or cisplatin treatment distinctly decreased (p < 0.001). Pretreatment of blood platelets with sodium selenite at the low concentration (0.1 microM) protected platelet glutathione against the reaction with cisplatin (p < 0.001). The present study shows that in blood platelets after the incubation with cisplatin the GS-platinum complex was formed. The results of our experiments demonstrated also that the extracellular GSH (1 mM) had the protective effect against cisplatin-induced peroxidation of platelet lipids.

Animals↗
PubMed1995

Effects of submaximal physical exercise and immobilization in bed on the adenine nucleotides concentration in human blood platelets.

The effects of submaximal physical exercise (75% VO2max) and one month immobilization in bed on the adenine nucleotides concentration in human blood platelets were studied and compared. We have shown that after submaximal exercise and after immobilization in bed the concentrations of adenine nucleotides in blood platelets mainly ATP and ADP were decreased and probably caused by the stimulation of platelet secretory process. Thrombin which stimulated the release of 58.2% +/- 1.5% of total adenine nucleotides from control platelets, liberated decreased amounts of nucleotides from platelets after physical exercise and after immobilization in bed (39.9 +/- 2.1% and 23.6 +/- 2.03% of total, respectively).

Adenine Nucleotides↗
PubMed1993

Changes in antioxidant enzymes activities, aggregability and malonyldialdehyde concentration in blood platelets from patients with coronary heart disease.

In 41 patients with coronary heart disease (CHD) the concentrations of total blood platelet malonyldialdehyde (MDA: 2.11 +/- 0.25 nmol/10(9) platelets) and MDA corresponding to thromboxane A2 (TXA2 0.84 +/- 0.13 nmol/10(9) platelets) were increased in comparison with values in blood platelets of healthy subjects (1.19 +/- 0.09 and 0.71 +/- 0.05 nmol/10(9) platelets), respectively. The increased aggregability with ADP and thrombin of patient platelets was also observed. In relation to the blood platelets of healthy subjects, the antioxidant enzymes activities of patient blood platelets were significantly (P < 0.001) decreased. Platelet glutathione peroxidase (GSH-Px) activity of the patients (11.3 +/- 0.85 U/g protein) was significantly lower than controls (18.3 +/- 1.12 U/g protein). In patients with CHD the activities of the other antioxidative platelet enzymes: catalase (Cat, 7.37 +/- 1.38 U/g protein) and superoxide dismutase (SOD, 1529.4 +/- 167 U/g protein) were also significantly decreased in comparison with values for healthy subjects (Cat: 9.06 +/- 1.30 U/g protein and SOD: 1987 +/- 230 U/g protein, respectively). It is suggested that antioxidative defense in blood platelets may affect the haemostatic processes and lipid peroxidation in patients with CHD.

Adenosine Diphosphate↗
PubMed1993

Inhibitory effect of cisplatin on the enzymatic peroxidation of platelet endogenous arachidonate.

The effect of cisplatin at concentrations of 0.1-33 microM on the enzymatic transformation of arachidonate in pig blood platelets was investigated. Estimation of the level of malonyl dialdehyde (MDA) after stimulation of pig platelets with thrombin (endogenous arachidonate pathway) and exogenous arachidonate served as an indicator of the transformation. MDA concentration was determined by means of a modified method with thiobarbituric acid. The effect of cisplatin on the thrombin-induced formation of MDA in blood platelets was dependent on the time of platelet preincubation with the drug. It was reduced significantly (p < 0.001) after 30 min action of cisplatin on the platelets. In contrast, cisplatin had no effect (p > 0.05) on the arachidonate pathway dependent on the activity of thromboxane synthase.

Animals↗
PubMed1992

Effect of cisplatin on lipid peroxidation in pig blood platelets.

The effect of cisplatin (cis-diamminedichloroplatinum II) on the activities of the blood platelet antioxidative enzymes (glutathione peroxidase, superoxide dismutase) as well as on the peroxidation of blood platelet lipids was investigated. Cisplatin was found to cause a significant inhibition of platelet free radical scavering enzyme activity and an increase of malonyldialdehyde levels in blood platelets incubated with cisplatin in vitro.

Animals↗
PubMed1991

Effect of submaximal physical exercise on antioxidative protection of human blood platelets.

The study was performed on healthy volunteers subjected to submaximal physical exercise (75% VO2max). Activities of catalase (CT) (EC 1.11.1.6), glutathione peroxidase (GPO) (EC 1.11.1.9), superoxide dismutase (ZnCu-SOD) (EC 1.15.1.1) and malonyldialdehyde (MDA) concentration in blood platelets before and after physical exercise were estimated. Physical exercise was found to induce a significant increase in the blood platelet enzymes activity accompanied by lowering platelet MDA concentration and platelet aggregability. The obtained results suggest that physical exercise has some effect on platelet reactivity and on platelet antioxidative enzymes.

Adult↗
PubMed1991

Effect of cisplatin on lipid peroxidation in blood platelets.

Cisplatin (cis-diamminedichloroplatinum II) at the concentrations of 2-20 micrograms induces non-enzymatic peroxidation of pig platelet lipids. At low concentration (0.1 microgram) it inhibits the enzymatic thrombin-stimulated transformation of platelet endogenous arachidonic acid. This drug also reduces the activities of platelet enzymes: superoxide dismutase and glutathione peroxidase.

Animals↗
PubMed1991

Effect of bed rest on the adenine nucleotides concentration in human blood platelets.

The effect of immobilization in bed on metabolism and function of human blood platelet was studied. Blood platelets taken from patients with bone fractures after long term bed rest (14 days and 28 days) demonstrated significantly reduced concentration of total adenine nucleotides (after 28 days reduction about 30%). This decrease of total platelet adenine nucleotides after immobilization in bed is probably caused by stimulation of platelet secretory process. Thrombin which released from control platelets 58.2% +/- 1.5% of total adenine nucleotides liberated decreased amounts (only 23.1% +/- 3.3% of total) of nucleotides from patient platelets isolated after 28 days of immobilization in bed. Loss of nucleotides from platelets was accompanied by slightly increased extent of platelet aggregation. It is concluded that during bed rest the reactivity of blood platelets (aggregation and release reaction) is stimulated.

Adenine Nucleotides↗
PubMed1990

Protective effect of ceruloplasmin against lipid peroxidation in blood platelets.

The effect of ceruloplasmin on the peroxidation of blood platelet lipids was tested. Using thiobarbituric acid reactivity for measuring lipid peroxidation it was shown that ceruloplasmin inhibited peroxidation of pig platelet lipids induced by UV-irradiation, and much less when enzymatic peroxidation was stimulated by thrombin.

Animals↗
PubMed1988

Avian thrombocyte thrombospondin.

A high molecular weight glycoprotein (450,000) was obtained from thrombin-treated duck thrombocytes by barium citrate adsorption technique followed by heparin-agarose affinity chromatography. Amino acid composition (high number of acidic amino acids and cystine) as well as carbohydrate contents (1.3 per cent hexosamine, 0.9 per cent sialic acid and 1.5 per cent hexose) showed similarity to mammalian platelet thrombospondin.

Amino Acids↗
PubMed1985

UV light-induced changes in washed pig platelets.

The effect of ultraviolet radiation (UV-A, 360 nm) on the thrombin-induced aggregation of washed pig platelets as well as on the release of adenine nucleotides and proteins was studied. The level in platelets of adenine nucleotides, mainly ADP and ATP, decreased rapidly following the exposure of platelets to a high dose of UV-A (0.5 W/cm2, 30 min). Through thrombin-induced aggregation of irradiated platelets was inhibited, the release reaction occurred. The amount of the released adenine nucleotides and proteins was, however, dependent on the dose of UV light. These findings suggest that UV-A light can stimulate the platelet release reaction.

Adenine Nucleotides↗
PubMed1984

Adenine nucleotides in thrombocytes of birds.

Analysis of free nucleotide composition of both avian thrombocytes and pig platelets showed quantitative differences in the level of adenine nucleotides. 3H-adenine taken up by turkey thrombocytes was metabolized mainly to adenine nucleotides was not released after thrombin action. Thrombin liberated non-radioactive adenine nucleotides (18.2 +/- 1.5%, 20.6 +/- 1.9%) of the total, probably localized in a storage pool. Malonyldialdehyhyde (MDA) production due to thrombin was observed in both platelets and thrombocytes.

Adenine Nucleotides↗
PubMed1984

Effects of gamma radiation on pig platelet function.

The effects of gamma radiation (60Co source) on pig platelet aggregation, protein secretion, and malonyldialdehyde (MDA) formation were studied. It was observed that gamma radiation (0.1-1 kGy ) modified platelet function, i.e., inhibited platelet aggregation and secretion with concomitant lipid peroxidation expressed by increased amounts of malonyldialdehyde. MDA production in irradiated platelets was dependent on the dose of gamma radiation.

Animals↗
PubMed1983

Effects of mercurial compounds on adenine nucleotides of washed pig platelets.

The effects of methylmercuric chloride, mercuric chloride, and phenylmercuric acetate (10(-6) - 10(-3) mole/liter) on thrombin-induced release of adenine nucleotides from washed pig platelets were investigated. The inhibitory effects of mercurials were always reached when the higher thrombin concentration (0.74 units NIH/ml) was used. Incubation of washed pig platelets with methylmercuric chloride caused a decrease of intracellular level of platelet ATP and statistically significant changes in ATP/ADP ratio.

Adenine Nucleotides↗
PubMed1982

Binding of adenosine diphosphate to turkey thrombocytes.

Adenosine diphosphate (ADP) caused rapid and reversible aggregation of turkey thrombocytes, as determined by optical and microscopical examination. To investigate the binding of ADP to these cells, turkey thrombocyte-rich plasma was incubated with ADP-8-14C or ADP-3-3H and with human serum albumin labeled with 125I. The thrombocytes were rapidly separated by centrifugation through silicone oil. From radioactivity determination of plasma and thrombocyte pellets the uptake of ADP radioactivity by thrombocytes was calculated. Scatchard analysis of concentration-dependent binding yielded a hyperbolic plot which indicates that turkey thrombocytes similarly to human platelets have more than one type of binding site for ADP.

Adenosine Diphosphate↗