tellurium and Hemolysis

In-depth understanding the toxicity of nanomaterials in red blood cells (RBCs) is of great interest, because of the importance of RBCs in transporting oxygen in blood circulation. Although the toxic effects of nanoparticles in RBCs have been revealed, the conclusions from the literature are conflicting, and in particular, the toxic mechanism is still at the infant stage. Herein, we investigated the size-dependent toxicity of well-known CdTe semiconductor quantum dots (QDs) and revealed the exact toxic mechanism at the molecular level by confocal microscopy and Fourier transform infrared (FT-IR) spectroscopy techniques. We found that smaller mercaptosuccinic acid-capped CdTe QDs (MSA-QDs) with the green-emitting color could cause hemagglutination whereas the middle-size yellow-emitting MSA-QDs induced the formation of stomatocytes and echinocytes and the bigger size red-emitting MSA-QDs induced heavy hemolysis and the formation of lots of ghost cells. The FT-IR data proved that all the MSA-QDs were likely to bond to the RBCs membranes and caused the structural changes of lipid and protein in RBCs. But only the red-emitting MSA-QDs caused the breakage of the phosphodiester bond, which might cause the heavy hemolysis. To some extent, this is the first example that reveals the hemolysis mechanism at the molecular level.

Topics: Cadmium Compounds; Cell Membrane; Cell Survival; Erythrocytes; Hemolysis; Humans; Lipids; Proteins; Quantum Dots; Tellurium

Local and rapid heating by microwave (MW) irradiation is important in the clinical treatment of tumors using hyperthermia. We report here a new thermo-seed technique for the highly efficient MW irradiation ablation of tumors in vivo based on gelatin microcapsules. We achieved 100% tumor elimination in a mouse model at an ultralow power of 1.8 W without any side-effects. The results of MTT assays, a hemolysis test and the histological staining of organs indicated that the gelatin microcapsules showed excellent compatibility with the physiological environment. A possible mechanism is proposed for MW hyperthermia using gelatin microcapsules. We also used gelatin microcapsules capped with CdTe quantum dots for in vivo optical imaging. Our study suggests that these microcapsules may have potential applications in imaging-guided cancer treatment.

Topics: Animals; Biocompatible Materials; Cadmium Compounds; Cell Survival; Colloids; Erythrocyte Membrane; Erythrocytes; Female; Fluorescent Dyes; Gelatin; Hemolysis; Hep G2 Cells; Humans; Hyperthermia, Induced; L-Lactate Dehydrogenase; Mice; Mice, Inbred ICR; Microscopy, Electron, Scanning; Microwaves; Neoplasm Transplantation; Neoplasms; Optics and Photonics; Quantum Dots; Rabbits; Spectroscopy, Fourier Transform Infrared; Tellurium; Tissue Distribution

Although it has been reported that fluorescent quantum dots (QDs) have obvious acute toxic effects in vitro, their toxic effects at low doses or threshold doses are still unknown. Therefore, we evaluated the biological histocompatibility and in vitro toxicity of three types of QDs at threshold doses. Also, we compared the toxic effects of QDs with different raw chemical compositions and sizes. The results showed that low concentrations of QDs (≤7 μg/mL) had no obvious effect on cell viability and cell membrane damage, oxidative damage, cell apoptosis or DNA damage. However, QD exposure led to a significant cytotoxicity at higher doses (≥14 μg/mL) and induced abnormal cellular morphology. In addition, when comparing the three types of QDs, 2.2 nm CdTe QDs exposure showed a significantly increased proportion of apoptotic cells and significant DNA damage, suggesting that size and composition contribute to the toxic effects of QDs. Based on these discussions, it was concluded that the concentration (7 μg/mL) may serve as a threshold level for these three types of QDs only in L929 fibroblasts, whereas high concentrations (above 14 μg/mL) may be toxic, resulting in inhibition of proliferation, induction of apoptosis and DNA damage in L929 fibroblasts.

Topics: Animals; Apoptosis; Cadmium Compounds; Cell Line; Cell Survival; DNA Damage; Fibroblasts; Hemolysis; Mice; Oxidative Stress; Particle Size; Quantum Dots; Selenium Compounds; Tellurium; Toxicity Tests

Oxidative stress can induce complex alterations of membrane proteins in red blood cells (RBCs) eventually leading to hemolysis. RBCs represent a good model to investigate the damage induced by oxidizing agents. Literature data have reported that chalcogen compounds can present pro-oxidant properties with potent inhibitory effects on cell growth, causing tissue damage and inhibit a variety of enzymes. In this study, human erythrocytes were incubated in vitro with various chalcogen compounds at 37 degrees C: diphenyl ditelluride (1), dinaphthalen diteluride (2), diphenyl diselenide (3), (S)-tert-butyl 1-diselenide-3-methylbutan-2-ylcarbamate (4), (S)-tert-butyl 1-diselenide-3-phenylpropan-2-ylcarbamate (5), selenium dioxide (6) and sodium selenite (7) in order to investigate their potential in vitro toxicity. After 6h of incubation, all the tested compounds increased the hemolysis rate, when compared to control and compound (2) had the most potent hemolytic effect. The addition of reduced glutathione (GSH) or glucose to the incubation medium enhanced hemolysis caused by chalcogen compounds. The thiol oxidase activity of these compounds was evaluated by measuring the rate of cysteine (CYS) and dithiotreitol (DTT) oxidation. DTT and cysteine oxidation was increased by all the compounds tested. The results suggest a relationship between the oxidation of intracellular GSH and subsequent generation of free radicals with the hemolysis by chalcogen compounds.

Topics: Adult; Chalcogens; Cysteine; Dithiothreitol; Erythrocytes; Glucose; Glutathione; Hemolysis; Humans; Oxidation-Reduction; Reactive Oxygen Species; Selenium Compounds; Superoxides; Tellurium; Time Factors

This study investigated the hemolytic and genotoxic effect of different organoselenium and organotellurium compounds in human blood cells, as simple tests for screening the toxicity of organochalcogenides. For osmotic fragility (OF) test, samples of total blood were incubated with the organochalcogens at 4, 8, 50, 75 and 100 microM or vehicle (DMSO) for 90 min at 37 degrees C. The EC(50) values for hemolysis were significantly increased in erythrocytes exposed to diphenyl selenide (II), diphenyl diselenide (III), diphenyl telluride (IV), diphenyl ditelluride (V), (S)-2-amino-1-diselenide-3-methylpropanyl (IX), butyl(styryl)telluride (XIII) and 2-(butyltellurium)furan (XIV) at higher concentrations tested. The exposure of erythrocytes to organochalcogens diphenyl diselenide (II) and butyl(styryl)telluride (XIII), which had greater hemolytic effect, did not modify catalase activity, reactive oxygen species (ROS) production and -SH content. On the other hand, Na(+)/K(+) ATPase activity of erythrocyte ghosts was significantly inhibited by the compounds diphenyl diselenide (II) and butyl(styryl)telluride (XIII) (P<0.05) in a concentration-dependent manner. The inhibition of Na(+)/K(+) ATPase activity was completely reversed by dithiothreitol (DTT); indicating reaction of these organochalcogens with thiol groups of the enzyme. The thiol oxidase activity of the compounds II and XIII was supported by the fact that the rate of DTT oxidation was increased significantly by both chalcogens. In the higher concentrations, the compounds (II) and (XIII) were strongly genotoxic and cytotoxic to human leukocytes cells, as verified by the DNA damage and cell viability evaluation. Our results suggest that at relatively high concentration organochalcogenides exhibit hemolytic and genotoxic action in human blood cells, which are probably linked to their thiol oxidase activity and preferential interaction with sulfhydryl groups critical to enzymes.

Topics: Cell Survival; DNA Damage; Dose-Response Relationship, Drug; Erythrocytes; Hemolysis; Humans; Leukocytes; Mutagenicity Tests; Organoselenium Compounds; Osmotic Fragility; Sulfhydryl Compounds; Tellurium

Previous literature reports have demonstrated that nucleated trout erythrocytes in conditions of oxidative stress are subjected to DNA and membrane damage, and inactivation of glutathione peroxidase. The present study was undertaken to evaluate the ability of three diaryl tellurides and the organoselenium compound ebselen to protect trout (Salmo irideus) erythrocytes against oxidative stress, induced thermally and by a variation of pH. The antioxidant ability of these molecules was evaluated through chemiluminescence. Impairment of DNA was assessed using the comet assay, a rapid and sensitive single cell gel electrophoresis technique, used to detect primary DNA damage in individual cells. At low concentrations (<10 microM), all the compounds used presented a protective effect on DNA damage without altering the hemolysis rate. In higher concentrations, they accelerated the hemolysis rate and two of the diaryl tellurides were strongly genotoxic.

Topics: Animals; Antioxidants; Azoles; Comet Assay; DNA Damage; Dose-Response Relationship, Drug; Erythrocytes; Hemolysis; Hot Temperature; Hydrogen-Ion Concentration; Isoindoles; Luminescent Measurements; Mutagenicity Tests; Oncorhynchus mykiss; Organometallic Compounds; Organoselenium Compounds; Oxidative Stress; Tellurium

Topics: Drug Resistance, Microbial; Drug Tolerance; Enterococcus; Hemolysis; Microbial Sensitivity Tests; Pigmentation; Pyrrolidinones; Pyruvic Acid; Streptococcus; Tellurium; Vancomycin

The influence of potassium tellurite (PT) and brain heart infusion agar (Difco), two components of modified Listeria selective agar medium (LSAMm), on the hemolytic phenotype of Listeria spp. was studied. L. monocytogenes and L. ivanovii displayed bigger zones of hemolysis on brain heart intusion agar compared with on Columbia agar base. The addition of PT increased the sizes of zones of hemolysis displayed by L. monocytogenes. This effect seemed to be produced by the enhancement of the cytolytic effect of listeriolysin O. PT decreased the hemolysis produced by L. ivanovii, and this effect seemed to be due to an inhibition of the sphingomyelinase C produced by this species.

Topics: Culture Media; Hemolysis; Listeria; Phenotype; Tellurium

Topics: Animals; Erythrocytes; Glucose; Glutathione; Hemolysis; In Vitro Techniques; Selenious Acid; Selenium; Sheep; Tellurium; Time Factors

Topics: Animals; Erythrocytes; Glutathione; Hemolysis; Kinetics; Oxidation-Reduction; Selenium; Sheep; Tellurium

Topics: Cell Membrane; Drug Synergism; Erythrocytes; Glutathione; Hemolysis; Humans; Oxidation-Reduction; Tellurium

Topics: Amides; Cadmium; Cell Membrane; Cysteine; Erythrocyte Aging; Erythrocytes; Glucose; Glutathione; Hemolysis; Humans; In Vitro Techniques; Oxidation-Reduction; Phosphatidylcholines; Sulfhydryl Compounds; Tellurium

Topics: Erythrocytes; Glutathione; Hemolysis; Humans; Tellurium