Fish peroxiredoxins and their role in immunity

Peroxiredoxins (Prxs) are a family of antioxidant enzymes that protect cells from oxidative damage. In addition, Prxs may act as modulators of inflammation, protect against cell death and tumour progression, and facilitate tissue repair after damage. The most studied roles of Prx1 and Prx2 are immunological. Here we present a review on the effects of some immunostimulant treatments and bacterial, viral, or parasitic infections on the expression of fish Prxs at the gene and/or protein level, and point to their important role in immunity. The Prxs show antioxidant activity as well as a protective effect against infection. Some preliminary data are presented about the role of fish Prx1 and Prx2 in virus resistance although further studies are needed before the role of fish Prx in immunity can be definitively defined.AGL2010-20801-C02-02 and AGL2013-43588-P (MINECO and FEDER) and 04538/GERM/06 (Fundación Séneca de la Región de Murcia, Spain)Versión del edito

Hematologic complications in vascular malformations: A case study of 2 patients

Vascular malformations are congenital vascular anomalies resulting from a disruption in the vasculogenesis process. (1)  They are congenital changes that enlarge as the child develops and do not undergo spontaneous involution. They can be classified based on the type of vessels involved (capillary, arterial, venous, lymphatic, mixed) and the nature of the vascular flow (low-flow and high-flow). The clinical presentation of vascular malformations is highly diverse, and despite being congenital, they can remain asymptomatic for a long time, complicating the diagnostic process. (1,3)   The presence of malformations carries the risk of health-threatening complications. One such complication is Kasabach-Merritt syndrome, characterized by thrombocytopenia, microangiopathic hemolytic anemia, and consumptive coagulopathy in the presence of a rapidly enlarging vascular tumor. (4,5) Another threat is a coagulopathy limited to the vascular anomaly (LIC). It is characterized by elevated D-dimers and fibrin degradation products, low levels of fibrinogen, FV, FVIII, FXIII, and antithrombin, and sometimes mild to moderate thrombocytopenia. (6,7) Early implementation of anticoagulant therapy allows for the avoidance of health-threatening conditions and the development of disseminated intravascular coagulation syndrome (DIC). (8

Hematologic complications in vascular malformations: A case study of 2 patients

Vascular malformations are congenital vascular anomalies resulting from a disruption in the vasculogenesis process. (1)  They are congenital changes that enlarge as the child develops and do not undergo spontaneous involution. They can be classified based on the type of vessels involved (capillary, arterial, venous, lymphatic, mixed) and the nature of the vascular flow (low-flow and high-flow). The clinical presentation of vascular malformations is highly diverse, and despite being congenital, they can remain asymptomatic for a long time, complicating the diagnostic process. (1,3)   The presence of malformations carries the risk of health-threatening complications. One such complication is Kasabach-Merritt syndrome, characterized by thrombocytopenia, microangiopathic hemolytic anemia, and consumptive coagulopathy in the presence of a rapidly enlarging vascular tumor. (4,5) Another threat is a coagulopathy limited to the vascular anomaly (LIC). It is characterized by elevated D-dimers and fibrin degradation products, low levels of fibrinogen, FV, FVIII, FXIII, and antithrombin, and sometimes mild to moderate thrombocytopenia. (6,7) Early implementation of anticoagulant therapy allows for the avoidance of health-threatening conditions and the development of disseminated intravascular coagulation syndrome (DIC). (8

Tyrosine dephosphorylation of ASC modulates the activation of the NLRP3 and AIM2 inflammasomes

The inflammasome is an intracellular multi-protein complex that orchestrates the release of the pro-inflammatory cytokines IL-1β and IL-18, and a form of cell death known as pyroptosis. Tyrosine phosphorylation of the inflammasome sensors NLRP3, AIM2, NLRC4, and the adaptor protein, apoptosis-associated speck-like protein (ASC) has previously been demonstrated to be essential in the regulation of the inflammasome. By using the pharmacological protein tyrosine phosphatase (PTPase) inhibitor, phenylarsine oxide (PAO), we have demonstrated that tyrosine dephosphorylation is an essential step for the activation of the NLRP3 and AIM2 inflammasomes in human and murine macrophages. We have also shown that PTPase activity is required for ASC nucleation leading to caspase-1 activation, IL-1β, and IL-18 processing and release, and cell death. Furthermore, by site-directed mutagenesis of ASC tyrosine residues, we have identified the phosphorylation of tyrosine Y60 and Y137 of ASC as critical for inflammasome assembly and function. Therefore, we report that ASC tyrosine dephosphorylation and phosphorylation are crucial events for inflammasome activation

The yeast Mig1 transcriptional repressor is dephosphorylated by glucosedependent and independent mechanisms

A yeast Saccharomyces cerevisiae Snf1 kinase, an analog of mammalian AMPK, regulates glucose derepression of genes required for utilization of alternative carbon sources through the transcriptional repressor Mig1. It has been suggested that the Glc7-Reg1 phosphatase dephosphorylates Mig1. Here we report that Mig1 is dephosphorylated by Glc7-Reg1 in an apparently glucose-dependent mechanism but also by a mechanism independent of glucose and Glc7-Reg1. In addition to serine/threonine phosphatases another process including tyrosine phosphorylation seems crucial for Mig1 regulation. Taken together, Mig1 dephosphorylation appears to be controlled in a complex manner, in line with the importance for rapid and sensitive regulation upon altered glucose concentrations in the growth medium

Biosorpcja Cr(III) z roztworów wodnych przez osad czynny

The biosorption of Cr(III) from aqueous solution using activated sludge (AS) microorganisms was investigated under various experimental conditions regarding pH and temperature. Biosorption equilibrium parameters were determined based on the Langmuir and Freundlich isotherm model. The kinetic parameters were established using the equations of pseudo-first order and pseudo-second order. Moreover thermodynamic parameters have been calculated. Langmuir isotherm provided a better fit to the equilibrium data. The maximum experimentally determined sorption capacity 26.95 mg · g–1 obtained at 25oC and pH 5.0. The kinetics model of pseudo-second order row has been better describing experimental data. The negative value of free Gibbs energy (ΔG0) proves spontaneous Cr(III) biosorption by AS biomass and its decreasing along with temperature increase. The negative value of enthalpy (ΔH0) and entropy (ΔS0) indicates exothermic process and limitation of degree of freedom Cr(III) ions on the interphase surface solution/biosorbent. FT-IR spectroscopy analysis indicated the contribution of carboxylate groups towards the biosorption of Cr(III) by AS.W pracy badano proces biosorpcji jonów chromu(III) z roztworów wodnych przez mikroorganizmy osadu czynnego (OC), w różnych warunkach pH i temperatury. Parametry równowagowe biosorpcji wyznaczono w oparciu o modele izoterm Langmuira i Freundlicha. Parametry kinetyczne określono za pomocą równań pseudopierwszego i pseudodrugiego rzędu. Obliczono również parametry termodynamiczne procesu. Izoterma Langmuira lepiej opisywała dane równowagowe. Maksymalna pojemność sorpcyjna wyznaczona eksperymentalnie wynosiła 26,95 mg · g–1 przy 25oC i pH 5,0. Model kinetyki pseudodrugiego rzędu lepiej opisywał dane doświadczalne. Ujemna wartość energii swobodnej Gibbsa (ΔG0) świadczyła o spontaniczności biosorpcji Cr(III) przez biomasę OC i jej spadku wraz ze wzrostem temperatury. Ujemna wartość entalpii (ΔH0) i entropii (ΔS0) wskazywała na egzotermiczność procesu i ograniczenie stopni swobody jonów Cr(III) na powierzchni międzyfazowej roztwór/biosorbent. Analiza FT-IR wykazała udział grup karboksylanowych w biosorpcji Cr(III) przez OC

Biochemical and medical importance of vanadium compounds

Vanadium belongs to the group of transition metals and is present in the air and soil contaminants in large urban agglomerations due to combustion of fossil fuels. It forms numerous inorganic compounds (vanadyl sulfate, sodium metavanadate, sodium orthovanadate, vanadium pentoxide) as well as complexes with organic compounds (BMOV, BEOV, METVAN). Depending on the research model, vanadium compounds exhibit antitumor or carcinogenic properties. Vanadium compounds generate ROS as a result of Fenton's reaction or of the reaction with atmospheric oxygen. They inactivate the Cdc25B2 phosphatase and lead to degradation of Cdc25C, which induces G2/M phase arrest. In cells, vanadium compounds activate numerous signaling pathways and transcription factors, including PI3K-PKB/Akt-mTOR, NF-κB, MEK1/2-ERK, that cause cell survival or increased expression and release of VEGF. Vanadium compounds inhibit p53-dependent apoptosis and promote entry into the S phase of cells containing functional p53 protein. In addition, vanadium compounds, in particular organic derivatives, have insulin-mimetic and antidiabetic properties. Vanadium compounds lower blood glucose levels in animals and in clinical trials. They also inhibit the activity of protein tyrosine phosphatase 1B. By activating the PI3K-PKB/Akt pathway, vanadium compaunds increase the cellular uptake of glucose by the GLUT4 transporter. The PKB/Akt pathway is also used to inactivate glycogen synthase kinase-3. The impact of vanadium compounds on inflammatory reactions has not been fully studied. Vanadium pentoxide causes expression of COX-2 and the release of proinflammatory cytokines in a human lung fibroblast model. Other vanadium compounds activate NF-κB in macrophages by activating IKKβ

Vanadium Compounds as Pro-Inflammatory Agents: Effects on Cyclooxygenases

This paper discusses how the activity and expression of cyclooxygenases are influenced by vanadium compounds at anticancer concentrations and recorded in inorganic vanadium poisonings. We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling. We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2. For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds