Biomedical subjects

D Beyersmann

Publications and source records attributed to D Beyersmann.

59 records · Page 4Linked to original sources

PubMedDate not supplied

Chromate effects on red cells membranes.

The modification of human erythrocyte membrane proteins by chromate previously had been investigated by kinetic (4) and electrophoretic techniques (5). In the Coulter Counter we now observed that chromate (10 mM) caused an increase in the intracellular resistivity but also an augmentation of the critical voltage where the membrane resistance breaks down owing to electroporation. Furthermore, a slight chromate-induced augmentation of echinocyte shape was observed. Also, chromate causes the intracellular pH to shift to higher values.

Chromates↗

PubMedDate not supplied

Comutagenicity and inhibition of DNA repair by metal ions in mammalian cells.

Mutagenic and/or carcinogenic metal compounds may act directly by interaction with DNA and/or indirectly by interference with genetic control and repair mechanisms. In a previous report, we investigated the mutagenicity and comutagenicity of nickel(II) in the V79 Chinese hamster HGPRT-assay. Our present findings demonstrate that like nickel(II), chromium(VI) and cadmium(II) are also comutagenic with UV. Furthermore, there is only a weak concordance with comutagenic effects observed in bacterial test systems. In the case of nickel(II), there is a good correlation between comutagenicity and inhibition of DNA repair, as determined by using the nucleoid sedimentation technique with HeLa cells. This inhibition may occur via replacement of other divalent ions essential in repair enzymes.

Animals↗

PubMedDate not supplied

Functions of zinc in signaling, proliferation and differentiation of mammalian cells.

Zinc is essential for cell proliferation and differentiation, especially for the regulation of DNA synthesis and mitosis. On the molecular level, it is a structural constituent of a great number of proteins, including enzymes of cellular signaling pathways and transcription factors. Zinc homeostasis in eukaryotic cells is controlled on the levels of uptake, intracellular sequestration in zinc storing vesicles ('zincosomes'), nucleocytoplasmic distribution and elimination. These processes involve the major zinc binding protein metallothionein as a tool for the regulation of the cellular zinc level and the nuclear translocation of zinc in the course of the cell cycle and differentiation. In addition, there is also increasing evidence for a direct signaling function for zinc on all levels of signal transduction. Zinc can modulate cellular signal recognition, second messenger metabolism, protein kinase and protein phosphatase activities, and it may stimulate or inhibit activities of transcription factors, depending on the experimental systems studied. Zinc has been shown to modify specifically the metabolism of cGMP, the activities of protein kinase C and mitogen activated protein kinases, and the activity of transcription factor MTF-1 which controls the transcription of the genes for metallothionein and the zinc transporter ZnT-1. As a conclusion of these observations new hypotheses regarding regulatory functions of zinc ions in cellular signaling pathways are proposed.

Animals↗

PubMedDate not supplied

Modification of the erythrocyte anion carrier by chromate.

It was confirmed that chromate is taken up by human erythrocytes via the general anion carrier. The chromate flux is unidirectional and chromium is accumulated within red cells presumably due to intracellular reduction of Cr(VI) to Cr(III). The analysis of the initial rates of uptake of chromate revealed two distinct uptake mechanisms at low (0.001-0.01 mM) and at high (0.05-1.0 mM) chromate concentrations. After prolonged incubation with 1 mM chromate, the subsequent rate of uptake of chromate was decreased. It is suggested that the decreased uptake is due to a modification of the anion-transport protein by chromate.

Anion Transport Proteins↗

PubMedDate not supplied

Effects of cadmium on cellular calcium and proto-oncogene expression.

Effects of the carcinogenic metal cadmium on cellular calcium signalling and proto-oncogene expression were studied in mammalian cells. Cadmium ions interfered with bradykinin- and adenosinetriphosphate (ATP)-stimulated calcium transients in rat pheocromocytoma PC12 cells, but Cd2+ as such did not evoke intracellular Ca2+ spikes. At variance, cadmium ions caused a sustained elevation of intracellular free Ca2+ by inhibition of active calcium transport systems in various cell types. Problems of mutual interference of Ca2+ and Cd2+ analysis with the fluorescent probe Fura-2 could be overcome by the use of the fluorine 19 nuclear magnetic resonance (19F-NMR) probe acetoxymethyl ester of 1,2-bis(2-amino-5-fluorophenoxy)ethane-N,N,N'N'-tetraacetic acid (5F-BAPTA), which allows the measurement of free intracellular Ca2+, Cd2+ and other metal ions concurrently. Furthermore, the induction of the cellular protooncogenes c-fos and c-jun by Cd2+ was studied in PC12 cells. A dose of 0.5 microM Ca2+ sufficed to induce the c-Fos and c-Jun proteins within 30 min. These results support a model which suggests that cadmium stimulates cell proliferation by interference with intracellular calcium and induction of immediate early genes.

Adenosine Triphosphate↗