Novel Knowledge about Molecular Mechanisms of Heparin-Induced Thrombocytopenia Type II and Treatment Targets.

Heparin-induced thrombocytopenia type II (HIT II), as stated in the literature, occurs in about 3% of all patients and in 0.1-5% of surgical patients. Thrombosis develops in 20-64% of patients with HIT. The mortality rate in HIT II has not decreased using non-heparin treatment with anticoagulants such as argatroban and lepirudin. An improved understanding of the pathophysiology of HIT may help identify targeted therapies to prevent thrombosis without subjecting patients to the risk of intense anticoagulation. The review will summarize the current knowledge about the pathogenesis of HIT II, potential new therapeutic targets related to it, and new treatments being developed. HIT II pathogenesis involves multi-step immune-mediated pathways dependent on the ratio of PF4/heparin and platelet, monocyte, neutrophil, and endothelium activation. For years, only platelets were known to take part in HIT II development. A few years ago, specific receptors and signal-induced pathways in monocytes, neutrophils and endothelium were revealed. It had been shown that the cells that had become active realised different newly formed compounds (platelet-released TF, TNFα, NAP2, CXCL-7, ENA-78, platelet-derived microparticles; monocytes-TF-MPs; neutrophils-NETs), leading to additional cell activation and consequently thrombin generation, resulting in thrombosis. Knowledge about FcγIIa receptors on platelets, monocytes, neutrophils and FcγIIIa on endothelium, chemokine (CXCR-2), and PSGL-1 receptors on neutrophils could allow for the development of a new non-anticoagulant treatment for HIT II. IgG degradation, Syk kinase and NETosis inhibition are in the field of developing new treatment possibilities too. Accordingly, IdeS and DNases-related pathways should be investigated for better understanding of HIT pathogenesis and the possibilities of being the HIT II treatment targets.

Analysis of Morphological and Morphometric Changes in a Parenchymal Tissue after the Radiofrequency Ablation Procedure.

Background and Objectives: Prostate cancer is on the rise in the European Union, and radiofrequency ablation (RFA) is one of the minimally invasive treatment options used for its treatment. Therefore, the aim of this study was to investigate and analyze the effects of RFA on prostate tissues. Materials and Methods: A standard prostate RFA procedure was performed on 13 non-purebred dogs in three sessions: no cooling (NC), cooling with a 0.1% NaCl solution (C.01), and cooling using a 0.9% NaCl solution (C.09). Microtome-cut 2-3 µm sections of prostate samples were stained with hematoxylin and eosin and further examined. Results: A histopathologic evaluation identified four zones of exposure: direct, application, necrosis, and transitional, as the damage on tissues decreased going further from the ablation site. The areas and perimeters of these zones were calculated, and geometric shapes of ablative lesions were evaluated using the quotient formula. Areas and perimeters of prostate tissue lesions in the NC and C.09 sessions were of similar size, whereas those found in C.01 were statistically significantly smaller. Lesions observed in session C.01 were of the most regular geometric shape, while the most irregular ones were found in session C.09. The shapes of lesions closest to the ablation electrode were the most irregular, becoming more regular the further away from the electrode they were. Conclusions: Prostate RFA leads to tissue damage with distinct morphological zones. Notably, the prostate lesions were the smallest and the most regular in shape after RFA procedures using the 0.1% NaCl cooling solution. It can be argued that smaller ablation sites may result in smaller scars, thus allowing for faster tissue healing if the blood flow and innervation at the ablation site are not compromised.

Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress.

Aluminum accumulation, glutathione (GSH) and malondialdehyde (MDA) concentrations as well as catalase (CAT) and superoxide dismutase (SOD) activities were determined in erythrocytes and brain and liver homogenates of BALB/c mice treated with Al3+ (7.5 mg/kg/day (0.15 LD50) as AlCl3 (37.08 mg/kg/day), whereas HCl (30.41 mg/kg/day) was used as Cl- control, the treatments were performed for 21 days, i.p., in the presence and absence of rosmarinic acid (0.2805 mg/kg/day (0.05 LD50), 21 days, i.g.) or carvacrol (0.0405 mg/kg/day (0.05 LD50), 21 days, i.g.). The treatment with AlCl3 increased GSH concentration in erythrocytes only slightly and had no effect on brain and liver homogenates. Rosmarinic acid and carvacrol strongly increased GSH concentration in erythrocytes but decreased it in brain and liver homogenates. However, AlCl3 treatment led to Al accumulation in mice blood, brain, and liver and induced oxidative stress, assessed based on MDA concentration in the brain and liver. Both rosmarinic acid and carvacrol were able to counteract the negative Al effect by decreasing its accumulation and protecting tissues from lipid peroxidation. AlCl3 treatment increased CAT activity in mice brain and liver homogenates, whereas the administration of either rosmarinic acid or carvacrol alone or in combination with AlCl3 had no significant effect on CAT activity. SOD activity remained unchanged after all the treatments in our study. We propose that natural herbal phenolic compounds rosmarinic acid and carvacrol could be used to protect brain and liver against aluminum induced oxidative stress leading to lipid peroxidation.

The Effect of Oxidant Hypochlorous Acid on Platelet Aggregation and Dityrosine Concentration in Chronic Heart Failure Patients and Healthy Controls.

Background and objective: One of the reasons for thrombosis in chronic heart failure (CHF) might be reactive forms of oxygen activating platelets. The aim of this study was to evaluate the effect of oxidant hypochlorous acid (HOCl) on platelet aggregation and dityrosine concentration in CHF patients and healthy controls. Materials and Methods: CHF patients (n 67) and healthy (n 31) were investigated. Heart echoscopy, 6-min walking test, complete blood count, platelet aggregation, and dityrosine concentration were performed. Platelet aggregation and dityrosine concentration were measured in plasma samples after incubation with different HOCl concentrations (0.15, 0.0778, and 0.0389 mmol/L). Results: Platelet aggregation without oxidant was lower (p = 0.049) in CHF patients than in controls. The spontaneous platelet aggregation with oxidant added was higher in CHF patients (p = 0.004). Dityrosine concentration was also higher (p = 0.032) in CHF patients. Platelet aggregation was the highest in samples with the highest oxidant concentration in both healthy controls (p = 0.0006) and in CHF patients (p = 0.036). Platelet aggregation was higher in NYHA III group in comparison to NYHA II group (p = 0.0014). Concentration of dityrosine was significantly higher in CHF samples (p = 0.032). The highest concentration of dityrosine was obtained in NYHA IV group samples (p 0.05). Intensity of platelet aggregation, analyzed with ADP, was correlated with LV EF (r 0.42, p = 0.007). Dityrosine concentration was correlated with NYHA functional class (r 0.27, p 0.05). Conclusions: The increase in platelet aggregation in CHF and healthy controls shows the oxidant effect on platelets. The increase in dityrosine concentration in higher NYHA functional classes shows a higher oxidative stress in patients with worse condition.

Effect of Acanthopanax senticosus on the accumulation of cadmium and on the immune response of spleen cells.

Exposure to cadmium (Cd) is known to alter immune responses. Acanthopanax senticosus (Rupr. et Maxim.) Harms (AS) extract, an antioxidant-containing complex of phenolic compounds, tetracyclic triterpenoids/steroids, and polysaccharides, is known to produce Cd mobilization and excretion in vivo. Building upon earlier findings, the aim of the study was to evaluate the effects of an AS extract on Cd accumulation and changes in the presence of splenic immune cells in hosts during a chronic metal exposure. Chronic Cd exposure of BALB/c mice was induced by providing them solutions containing different levels of CdCl2 (25 or 250 mg/L) in double-distilled water, with/without a concurrent presence of AS root extract (approximately 151 g material/L), for 8 wk. At the study end, Cd levels in spleen were measured. Levels of key splenic immune cells, including macrophages, T-lymphocytes, and B-lymphocytes, were determined by immunohistochemistry using, respectively, CD68, CD3, and CD20 antibodies. The results indicated that chronic consumption of AS extract in the presence of the high dose of CdCl2 led to a significant decrease in Cd levels in mouse spleen. The effects of AS on the lower CdCl2 dose were less apparent. In addition, the presence of AS and Cd increased the amount of macrophages and both B and T lymphocytes in mouse spleen relative to concentrations that were lowered as a result of chronic metal only intake.

The effect of Polyscias filicifolia bailey biomass tincture on the protein synthesis process in the heterogeneous system from the isolated pig heart.

BACKGROUND AND OBJECTIVE: An insufficient supply of oxygen to the heart influences the process of protein synthesis. The aim of this study was to determine the effect of the Polyscias filicifolia Bailey biomass tincture on the protein synthesis process in a heterogeneous translation system from the isolated pig heart. MATERIALS AND METHODS: The effect of anoxia was evaluated after 20- and 90-minute anoxia. With the aim to determine the effect of Polyscias, the pig hearts were perfused with a buffer containing the Polyscias filicifolia Bailey biomass tincture. To determine the rate and the level of translation, the incorporation of [(14)C]-leucine into translational products in a cell-free system was measured. RESULTS: The protein synthesis level decreased by 23%-42% when the translation system containing cytosol from the anoxic heart was used. When the translation system containing a ribosomal fraction after 20-minutes anoxia was used, the protein synthesis level was the same as in the control. In the case of 90-minute anoxia, it decreased by 16%. The protein synthesis rate and the level in the translation system containing cytosol from the heart after 20-minute anoxic perfusion with the buffer containing Polyscias was the same as in the control. CONCLUSIONS: A decrease in the protein synthesis rate and the level after 20-minute anoxia was determined by changes in cytosol. On the other hand, 90-minute anoxia caused changes in cytosol and the ribosomal fraction. The Polyscias filicifolia Bailey biomass tincture restored the protein synthesis process acting on the components of the translation system in cytosol and the ribosomal fraction.

The effect of Ginkgo biloba extract on mitochondrial oxidative phosphorylation in the normal and ischemic rat heart.

Free radical-induced myocardial damage and impairment of vascular endothelium-dependent relaxation are amongst the most important mechanisms responsible for ischemic heart injury. Ginkgo biloba leaf extract (GE) has been reported to improve blood circulation in the brain and have a beneficial impact on the cardiovascular system but its cardioprotective effects have not been elucidated yet. Therefore, this study investigated the influence of GE in 70% ethanol (1:5) administered orally to rats on the functions of isolated heart mitochondria under normal and ischemic conditions. Wistar rats were given GE or ethanol (solvent control) at a dosage of 0.32 mL/kg in drinking water for 10 and 18 days, while the control animals received untreated drinking water. Mitochondrial respiration rates were determined oxygraphically. Pyruvate and malate, succinate or palmitoyl-L-carnitine and malate were used as substrates. The GE treatment partially uncoupled mitochondrial oxidation from phosphorylation, reduced the generation of free radicals in the mitochondria, diminished the ischemia-induced V3 decrease and the degree of respiration stimulation by exogenous cytochrome c. Thus, these results indicate that GE exerts cardioprotective effects reducing ischemia-caused impairment of the functions of heart mitochondria.

The coagulation system changes in patients with chronic heart failure.

Though heart failure can mainly be caused by systolic or diastolic dysfunction, the impairments of the neurohormonal, immune, and hemostatic systems are observed too. Therefore, it is not easy to determine etiology of the syndrome. Parameters that can be helpful to predict chronic heart failure, to evaluate its course and the risk of complications are still being searched. The aim of this article is to review the recent studies in order to find the links between the coagulation system and the development of chronic heart failure. Stress is a key factor for the development of most diseases including chronic heart failure too. Signals of emotional and physical stress via particular structures trigger an increase in concentrations of the following hormones: noradrenaline, renin, angiotensin II, aldosterone, vasopressin. It is proved that it causes the disorders of the coagulation system: an increase in the following factors of plasma coagulation (fibrinogen, VII, VIII, fibrinopeptide A, thrombin-antithrombin complex), fibrinolysis (D-dimer), endothelium (interleukin 1, endothelin 1, vascular cell adhesion molecules, endothelial growth factor), platelet activity (von Willebrand factor, intercellular adhesion molecules, platelet factor 4, P-selectin, thromboxane A(2), thromboglobulin, CD63P) and cytokines (tumor necrosis factor, interleukin 6) and decrease in E-selectin. The role of particular coagulation factors for the development of chronic heart failure has not been understood yet. Thus, it is necessary to carry out further studies.

Effect of anoxia and Polyscias filicifolia Bailey biomass tincture on the activity of tRNA and aminoacyl-tRNA synthetases in isolated pig heart.

OBJECTIVE: The aim of this study was to investigate effect of anoxia and Polyscias filicifolia Bailey biomass tincture on the activities of different tRNA and aminoacyl-tRNA synthetases in isolated pig heart. MATERIAL AND METHODS: The isolated pig heart was perfused according to the modified method of Langendorf, using an artificial blood circulation apparatus. Anoxia 20 min in duration was performed by perfusion of isolated heart with Krebs-Henseleit bicarbonate buffer saturated with gas mixture (95% N(2) and 5% CO(2)). Control heart was perfused with the same buffer saturated with gas mixture (95% O(2) and 5% CO(2)). Effect of Polyscias filicifolia Bailey biomass tincture was evaluated by perfusion of isolated heart with a buffer containing tincture. Total tRNA and aminoacyl-tRNA synthetases were isolated from pig heart. Activities of tRNA and aminoacyl-tRNA synthetases were measured by the aminoacylation reaction using C(14)-amino acids. RESULTS: Anoxia 20 min in duration has caused a decrease in the acceptor activity of tRNA and increase in the activities of aminacyl-tRNA synthetases. Polyscias filicifolia Bailey tincture did not affect the acceptor activity of tRNA and activities aminacyl-tRNA synthetases. After 20-min anoxic perfusion with the buffer containing Polyscias filicifolia Bailey biomass tincture, the acceptor activities of tRNA increased to the control value and activities of aminacyl-tRNA synthetases reached the control value. CONCLUSIONS: The acceptor activity of tRNA from isolated pig heart decreased and activities of aminacyl-tRNA synthetases increased under anoxia. Perfusion with buffer containing tincture of Polyscias filicifolia Bailey biomass restored acceptor activities of tRNA and activities of aminacyl-tRNA synthetases.

Effect of Zinc on the Oxidative Stress Biomarkers in the Brain of Nickel-Treated Mice.

The overexposure to nickel due to the extensive use of it in modern technology remains a major public health concern. The mechanisms of pathological effects of this metal remain elusive. The present study was devoted to evaluate the effect of nickel on the oxidative state of the brain cells of mice and to assess whether zinc as redox state modulator could efficiently protect cells against nickel's neurotoxicity. As oxidative stress biomarkers in the present study, we have measured the concentrations of reduced glutathione, metallothioneins, and malondialdehyde and the activity of the enzyme δ-aminolevulinate dehydratase. For the single metal exposure, mice were i.p. injected once with solutions of NiCl2 and/or ZnSO4; repeated exposure was performed i.p. injecting metal salt solutions for 14 days (once a day). The control mice received i.p. injections of saline. Results of our study demonstrate that single and 14 days of Ni2+ exposure decreased reduced glutathione and increased malondialdehyde contents in the brain of mice. Repeated Ni2+ administration significantly inhibited δ-aminolevulinate dehydratase while increasing brain metallothionein concentration at both exposure periods. Zinc exhibited a protective effect against nickel-induced glutathione and lipid peroxidation in brain cells of mice at both intervals of time, while repeated exposure to this metal significantly raised the brain metallothionein content. Repeated Zn2+ pretreatment protected δ-aminolevulinate dehydratase from Ni2+-induced inhibition and significantly increased metallothionein concentration at both investigated time intervals.

Subacute effects of cadmium and zinc ions on protein synthesis and cell death in mouse liver.

OBJECTIVE: The aim of this study was to evaluate in vivo the effects of cadmium and zinc ions on translational machinery and death of mouse liver cells. MATERIAL AND METHODS: Outbred mice received intraperitoneal injections of cadmium chloride solution (1.4 micromoles cadmium per 1 kg of body weight) and/or zinc sulfate solution (4.8 micromoles zinc per kg of body weight) three times per week for six weeks. Analogical volume of saline solution was injected to the control mice. Protein synthesis was evaluated by incorporation of [(14)C]-labeled leucine into peptides and proteins. Total tRNAs were isolated using deproteinized extract of liver tissue. Postmitochondrial supernatant was as a source of leucyl-tRNA synthetase. Activities of tRNA(Leu) and leucyl-tRNA synthetase were measured by an aminoacylation reaction using [(14)C]-labeled leucine. Liver cell apoptosis was detected by TUNEL assay using in situ cell death detection kit. RESULTS: A decrease in incorporation of [(14)C]-labeled leucine into proteins was detected in liver, kidney, and heart as well as diminution of tRNA(Leu) acceptor activity in cadmium-exposed liver. Cadmium caused activation of the leucyl-tRNA synthetase and induced liver cell apoptosis. Pretreatment of mice with zinc sulfate solution favored to protection of protein synthesis and acceptor activity of tRNA(Leu) against cadmium-induced inhibition. Under co-exposure of mouse liver to cadmium and zinc, activity of the leucyl-tRNA synthetase was at the level of control. Zinc did not influence TUNEL-positive cell number in cadmium-exposed mouse liver. CONCLUSIONS: Under subacute intoxication of mice by cadmium, zinc ions protect the translation machinery against inhibition, but do not decrease the number of apoptotic cells in the liver.

The Effects of Buckwheat Leaf and Flower Extracts on Antioxidant Status in Mouse Organs.

This study was undertaken to investigate the effects of the extracts of buckwheat leaf and flower on the antioxidant status of the brain and liver tissue. The administration of buckwheat extracts (both concentrations were 10%) to mice (at the dose 10 mL/kg of body weight) for 21 days significantly decreased superoxide dismutase (SOD) activity and reduced the amount of glutathione (GSH) and malondialdehyde (MDA) in the mouse brain, while catalase (CAT) activity significantly increased. In the mouse liver, the amount of GSH and activity of SOD increased, while the CAT activity after administering buckwheat leaf and flower extracts was lower in experimental mice than in the control group. However, the administration of 10% ethanol (for 21 days) to control animals also had a significant effect on the antioxidant system in brain and liver cells. Experimental animals demonstrated rather marked changes in the activities of the antioxidant enzymes SOD and CAT in their liver and brain cells, and changes in the levels of GSH and MDA were observed when compared with the control group.

Direct effects of (-)-epicatechin and procyanidin B2 on the respiration of rat heart mitochondria.

Flavonol (-)-epicatechin and its derived dimer procyanidin B2, present in high amounts in cocoa products, have been shown to exert beneficial effects on the heart and cardiovascular system; however, their mechanism of action has not been fully elucidated. We studied effects of (-)-epicatechin and procyanidin B2 on the oxidative phosphorylation of isolated rat heart mitochondria. (-)-Epicatechin and procyanidin B2 had stimulating effect (up to 30% compared to control) on substrate-driven (State 2) mitochondrial respiration. Their effect was dependent on the respiratory substrates used. (-)-Epicatechin at higher concentrations (from 0.27 µg/mL) significantly decreased (up to 15%) substrate- and ADP-driven (State 3) mitochondrial respiration in case of pyruvate and malate oxidation only. Procyanidin B2 (0.7-17.9 ng/mL) inhibited State 3 respiration rate up to 19%, the most profound effect being expressed with succinate as the substrate. (-)-Epicatechin at concentrations of 0.23 µg/mL and 0.46 µg/mL prevented loss of the cytochrome c from mitochondria when substrate was succinate, supporting the evidence of membrane stabilizing properties of this flavonol. Thus, both (-)-epicatechin and procyanidin B2 directly influenced mitochondrial functions and the observed effects could help to explain cardiometabolic risk reduction ascribed to the consumption of modest amounts of cocoa products.

Effect of Polyscias filicifolia Bailey biomass on protein synthesis process in isolated pig heart.

OBJECTIVE: The aim of this study was to investigate effect of Polyscias filicifolia Bailey biomass on protein synthesis process in normoxic and anoxic pig heart. MATERIAL AND METHODS: Experiments were done on isolated pig hearts weighing 100-150 g. Effects of anoxia were evaluated after 20 and 90 min of anoxic perfusion. Control hearts were perfused under aerobic conditions. Investigating action of Polyscias filicifolia Bailey, pig heart was perfused under normoxic and anoxic condition with buffer, which contains tincture Polyscias filicifolia Bailey. For the determination of protein synthesis rate (time of incubation was 15 min) and level (time of incubation was 60 min), incorporation of [14C]-leucine into translational products in a cell-free system was measured. RESULTS: Protein synthesis rate and level in cell-free system decreased by 30% and 20% respectively after 20 min anoxic perfusion and by 48% and 45% respectively after 90 min anoxic perfusion in comparison to the control. Polyscias filicifolia Bailey tincture did not affect the protein synthesis rate and level in cell-free translation system from control pig heart. Polyscias filicifolia Bailey tincture has protective effect on protein synthesis system from pig hearts after 20 min and 90 min anoxic perfusion. Protein synthesis rate and level after 20 min anoxic perfusion with Polyscias filicifolia Bailey tincture was the same as at a control level. However, after 90 min anoxic perfusion with Polyscias filicifolia Bailey tincture protein synthesis rate and level did not reach control level and represented 81% and 76% respectively of control values. Spectrum of newly synthesized polypeptides in cell-free protein synthesis system under anoxic conditions and after treatment with Polyscias filicifolia Bailey tincture did not differ. CONCLUSIONS: Protein synthesis rate and level decreased under long and short-term anoxia. Polyscias filicifolia Bailey biomass restore protein synthesis system under anoxia. Neither anoxia, nor Polyscias filicifolia Bailey tincture did not influence spectrum of newly synthesized proteins.

Protective effect of selenium on aluminium-induced oxidative stress in mouse liver in vivo.

The aim of the study was to evaluate possible protective effects of selenium (Se) against systemic aluminium (Al) toxicity and the redox status of mouse liver after short-term (16 h) exposure to Al in vivo. BALB/c mice were injected i.p. with AlCl(3) (25mg Al(3+) per kg of body mass) or/and Na(2)SeO(3) (1.25mg Se per kg of body mass). The 4-fold increased activity of ALT in serum showed systemic hepatotoxicity that Se could not prevent by competitive mechanisms. The protective effects of Se could only be observed on intracellular oxidative stress events as determined by glutathione status. Exposure to Al leads to the decrease in the total glutathione (GSH(tot)) and GSH/GSSG redox ratio to about 50% of the control. Upon co-exposure to Se+Al, the concentration of GSH(tot) and the redox ratio was restored to the control values. Our results indicate that Se did not have a protective effect on Al-linked liver toxicity, but did ameliorate intracellular oxidative stress processes mediated by glutathione.

[Effects of lead ions on activities of tRNALeu and leucyl-tRNA synthetase of mouse liver]. / Svino jonu poveikis peliu kepenu tRNRLeu ir leucil-tRNR-sintetazes aktyvumui.

UNLABELLED: The objective of this study was to examine effect of lead ions on activities of mice liver tRNA(Leu) and leucyl-tRNA synthetase. MATERIAL AND METHODS: For researching white non-breed laboratory mice (20-25 g) were used. Intoxication with ions of lead was performed by injection of sublethal dose of lead acetate solution (50 mg ions of lead per 1 kg of body weight) into abdominal cavity of laboratory animals. Eight hours after intoxication from intoxicated and normal (control) mice liver preparations of tRNA and aminoacyl-tRNA synthetases were isolated. Acceptor activity of tRNA(Leu) and activity of leucyl-tRNA synthetase were determined in tRNA aminoacylation reaction using [(14)C]-labeled leucine. Actions of lead ions on acceptor activity of tRNA(Leu) and on activity of leucyl-tRNA synthetase from liver of control animals in vitro were determined after addition into reaction mixture different concentrations of lead acetate solution. RESULTS: It was determined that acceptor activity of mice liver tRNA(Leu) 8 h after intoxication with lead ions was reduced by 37 percent and activity of leucyl-tRNA synthetase was increased by 22 percent as compared to control. Experiments in vitro have shown that 10 micro M concentration of lead ions in reaction mixture stimulate acceptor activity of mice liver tRNA(Leu) by 17 percent, higher concentrations of lead ions (30-60 microM)--suppress it by 9-80 percent. The study of leucyl-tRNA synthetase activity in vitro has shown that 30 microM concentration of lead ions in reaction mixture increases activity of this enzyme by 16 percent, higher concentrations of lead ions (40-60 microM)--decrease by 17-23 percent. CONCLUSIONS: After 8 h intoxication with lead ions acceptor activity of tRNA(Leu) was decreased and activity of leucyl-tRNA synthetase was increased. It may be part of the compensatory mechanism of the cell to keep synthesis of proteins at the normal level under extreme conditions. Low concentrations of lead ions in reaction mixture increase tRNA(Leu) and leucyl-tRNA synthetase activities, higher concentrations of these ions decrease activity of those components of protein synthesis system. The results show that ions of lead directly suppress activity of both components of translation machinery.