Cytotoxic effect of aluminium ions on unicellular eukaryotic organism

Article Details: Received: 2019-10-08 | Accepted: 2019-11-26 | Available online: 2019-12-31https://doi.org/10.15414/afz.2019.22.04.130-137Aluminium is abundant in nature, food, or water and thus its exposition is part of everyday life. However, overexposure can result in cellular malfunctions. Therefore, the aim of this study was to investigate the effects of aluminium on eukaryotes, with the use of Schizosaccharomyces pombe as model organism. Spectrophotometry at OD600, inductively-coupled plasma optical emission spectroscopy (ICP-OES) and microscopy techniques were used to analyse aluminium responses on the living system. Our results revealed that exposition of increasing aluminium concentrations lead to cell growth inhibition in a concentration dependent manner. Furthermore, aluminium incorporation by the cell from media markedly increased with rising Al concentration. Our results indicate that the yeast self-protection system in the presence of lower Al(OH)3 concentration in the environment avoids to large extent dramatic uptake of aluminium by the cell while cells surrounded by higher aluminium concentrations lose this ability. Supplementation of the growth media with 100 μM Al(OH)3 doubled the amount of Al in the cell compared to untreated control (232 mg/kg vs. 459 mg/kg), whereas addition of 1 mM Al(OH)3 caused more than hundred fold increase of intracellular Al content (27,781 mg/kg). Here we also show that high concentrations of aluminium have an impact on cell morphology leading to cell integrity disruption. Findings presented in this study have the ambition to bring more light in an issue of how aluminium mediates impairments of the living organism.ReferencesANOOP, V.M. et al. (2003) Modulation of citrate metabolism alters aluminum tolerance in yeast and transgenic canola overexpressing a mitochondrial citrate synthase. 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Aspirin Induces Platelet Receptor Shedding via ADAM17 (TACE)

Aspirin is effective in the therapy of cardiovascular diseases, because it causes acetylation of cyclooxygenase 1 (COX-1) leading to irreversible inhibition of platelets. Additional mechanisms can be suspected, because patients treated with other platelet COX inhibitors such as indomethacin do not display an increased bleeding tendency as observed for aspirin-treated patients. Recently, aspirin and other anti-inflammatory drugs were shown to induce shedding of L-selectin in neutrophils in a metalloproteinase-dependent manner. Therefore, we investigated the effects of aspirin on the von Willebrand Factor receptor complex glycoprotein (GP) Ib-V-IX, whose lack or dysfunction causes bleeding in patients. As quantified by fluorescence-activated cell sorting analysis in whole blood, aspirin, but not its metabolite salicylic acid, induced dose-dependent shedding of human and murine GPIbalpha and GPV from the platelet surface, whereas other glycoproteins remained unaffected by this treatment. Biotinylated fragments of GPV were detected by immunoprecipitation in the supernatant of washed mouse platelets, and the expression level of GPIbalpha was decreased in these platelets as measured by Western blot analysis. Although shedding occurred normally in COX-1-deficient murine platelets, shedding was completely blocked by a broad-range metalloproteinase inhibitor and, more importantly, in mouse platelets expressing an inactive form of ADAM17. Shed fragments of GPIbalpha and GPV were elevated in the plasma of aspirin-injected mice compared with animals injected with control buffer. These data demonstrate that aspirin at high concentrations induces shedding of GPIbalpha and GPV by an ADAM17-dependent mechanism and that this process can occur in vivo

Studien von formation und stabilizierung den pathologischen Thrombus in vivo

Platelet activation and adhesion resulting in thrombus growth is essential for normal hemostasis, but can lead to irreversible, life-threatening vessel occlusion. In the current study, the contribution of platelet integrins, activation receptors and the contact system of blood coagulation in such pathological conditions was investigated in mice.Plättchenaktivierung, -adhäsion und nachfolgende Thrombusbildung ist ein für die Hämostase essentieller Prozess, der jedoch zu irreversiblem lebensbedrohlichen Gefäßverschluss führen kann. In der vorliegenden Arbeit wurde die Rolle von Thrombozyten-Integrinen, aktivierenden Rezeptoren, sowie dem Kontaktsystem der Koagulation unter pathologischen Bedingungen im Maussystem untersucht

Prp4 kinase is required for proper segregation of chromosomes during meiosis in Schizosaccharomyces pombe

Chromosome segregation during meiosis is a complex process, which leads to production of four haploid gametes from two precursor cells. Reversible phosphorylation of proteins plays a crucial role in this process. The Schizosaccharomyces pombe Prp4 is an essential serine/threonine protein kinase, which belongs to the Clk/Sty family. To study the role of Prp4 in meiosis, we analysed chromosome segregation in a strain carrying conditional analog-sensitive allele of Prp4 protein kinase (prp4-as2). Our data show, that Prp4 protein kinase plays important role in chromosome segregation during meiosis, as revealed by enhanced missegregation of chromosomes in prp4-as2 mutant cells

Diminished thrombus formation and alleviation of myocardial infarction and reperfusion injury through antibody- or small-molecule-mediated inhibition of selectin-dependent platelet functions

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Casein kinase 1 is required for efficient removal of Rec8 during meiosis I

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