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1
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Biochemical and medical importance of vanadium compounds

100%
Korbecki J., Baranowska-Bosiacka I., Gutowska I., Chlubek D.
Acta Biochimica Polonica
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2012
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vol. 59
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issue 2
195-200
EN
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.
2
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Pro-inflammatory properties of cadmium

100%
Olszowski T., Baranowska-Bosiacka I., Gutowska I., Chlubek D.
Acta Biochimica Polonica
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2012
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vol. 59
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issue 4
475-482
EN
Cadmium is a toxic and carcinogenic heavy metal that nowadays constitutes a serious environmental health problem. The aim of this study is to review the effects of cadmium on selected inflammatory mediators and markers, such as NF-κB and AP-1 transcription factors, IL-6, TNF-α, IL-1β cytokines, IL-8 or MIP-2 chemokine, MPO, iNOS, MMPs and COX-2 enzymes, PGE2 (product of COX-2 enzyme), ICAM-1, VCAM-1 and PECAM-1 adhesion molecules, and CRP. The research strategy identified articles available in Medline, published between 1998 and 2012; we included both in vivo and in vitro studies carried out on humans and rodents. Most of the reviewed research findings suggest that cadmium in micromolar concentrations (especially in the 1-10 μM range) causes up-regulation of the mediators and markers of inflammation, and appears to have pro-inflammatory properties. However, it is worth mentioning that a contradictory or even opposite hypothesis exists, which suggests cadmium to be an anti-inflammatory factor. Further research including detailed histological analyses should solve this discrepancy. Nevertheless, it appears that the main reason for these contradictory findings is the experimental setup: different biological systems analyzed and different doses of cadmium applied.
3
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Cyclooxygenase pathways

100%
Korbecki J., Baranowska-Bosiacka I., Gutowska I., Chlubek D.
Acta Biochimica Polonica
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2014
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vol. 61
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issue 4
639-649
EN
This review compiles the current knowledge on the effects of prostanoids - arachidonic acid metabolites - on their own synthesis, activity and degradation. Interaction mechanisms between the receptors for the relevant compounds are presented, in particular with regard to the cooperation between a thromboxane A2 and prostaglandin I2 receptors. The questions of desensitization and internalization of receptors are discussed. The stages of the inflammatory response and tumor progression are analyzed against the background of the disruption of the synthesis of prostanoids. Special attention is given to the significance of 15-deoxy-Δ12,14-prostaglandin J2 in the regulation of the synthesis of prostanoids and its role as an anti-inflammatory agent. Ultimately, therapeutic approaches as used in various treatments are discussed in the light of the available knowledge.
4
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Zespół Kelleya-Seegmillera jako przyczyna nawracającego ostrego uszkodzenia nerek u 9-letniego chłopca

76%
Marciniak H., Jarmoliński T., Safranow K., Jakubowska K., Olszewska M., Chlubek D.
Annales Academiae Medicae Silesiensis
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2017
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vol. 71
116-121
EN
Defekt fosforybozylotransferazy hipoksantynoguaninowej (HPRT) jest drugą co do częstości występowania po ksantynurii wrodzoną wadą metabolizmu puryn. Opisany w 1967 r. u pacjentów z dną moczanową i kamicą nerkową zespół Kelleya-Seegmillera wynika z częściowego niedoboru tego enzymu. Jego całkowity brak wywołuje ponadto ciężkie objawy neurobehawioralne i znany jest od 1964 r. jako zespół Lescha-Nyhana. Badania enzymatyczne i molekularne, pozwalające na dokładną diagnostykę tych wad, są w Polsce trudno dostępne, co wpływa na bardzo rzadkie ich rozpoznawanie. Przedstawiono przypadek 9-letniego chłopca z nawracającym ostrym uszkodzeniem nerek (4 epizody), u którego analiza obrazu klinicznego i proste testy laboratoryjne pozwoliły na wstępne rozpoznanie zespołu Kelleya-Seegmillera, potwierdzone badaniem aktywności HPRT.
PL
Hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency is the second most common, after xanthinuria, inherited defect of purine metabolism. Described in 1967 in patients with gout and nephrolithiasis, the Kelley-Seegmiller syndrome is caused by HPRT partial deficiency. A complete lack of enzyme activity leads to additional severe neurobehavioral symptoms with self-mutilation creating clinical a picture known since 1964 as the Lesh-Nyhan syndrome. Enzymatic and molecular analyses useful for precise diagnosis are not routinely available in Poland, so the prevalence of HPRT defects is very low. Here we presented a case of a 9-year-old boy suffering from recurrent acute kidney injury (4 episodes) with diagnosis of the Kelley-Seegmiller syndrome based on the clinical picture and simple laboratory tests confirmed by evaluation of HPRT enzyme activity.
5
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Conjugated linoleic acids regulate triacylglycerol and cholesterol concentrations in macrophages/foam cells by the modulation of CD36 expression

64%
Stachowska E., Baskiewicz M., Marchlewicz M., Czupryńska K., Kaczmarczyk M., Wiszniewska B., Machaliński B., Chlubek D.
Acta Biochimica Polonica
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2010
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vol. 57
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issue 3
379-384
EN
Atherosclerosis is an inflammatory disease characterised by the accumulation of lipids and their metabolites in the artery wall. During inflammation circulating LDL are taken up by macrophages through two major scavenger receptors: CD36 and scavenger receptor A (SRA). Fatty acids that are common in food, e.g. linoleic acid and n-3 unsaturated fatty acids can modulate expression of CD36 on the macrophage surface. Conjugated linoleic acid isomers (CLA) that originate from the human diet, have demonstrated antiatherogenic properties in several experiments. Animal study evidenced that CLA could induce resolution of plaque by activation of peroxisome proliferator activated receptors and down-regulation of pro-inflammatory genes. Less unequivocal results were obtained in human studies (on the CLA effects on the inflammatory process). Therefore in this study we investigated the influence of CLA on CD36 expression and lipid accumulation in human macrophages. Macrophages were incubated with 30 µM cis-9,trans-11 CLA, trans-10,cis-12 CLA or linoleic acid for 48 h. After that, expression of CD36 as well as accumulation of lipids were measured by flow cytometry, microscopy and a spectroscopic method. We demonstrate that both cis-9,trans-11 C 18:2 CLA and linoleic acid slightly elevated expression of CD36, whereas second isomer - trans-10,cis-12 CLA - did not. Nevertheless, only trans-10,cis-12 CLA triggered delipidation of macrophages, that is decreased triacylglycerols concentration. Also in human adipocytes, trans-10,cis-12 CLA causes cell delipidation by reduction of PPAR receptor expression. We propose a similar mechanism for human macrophages/foam cells.
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