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Susan J. Van Rensburg - One of the best experts on this subject based on the ideXlab platform.

  • A Mechanism for Zinc Toxicity in Neuroblastoma Cells.
    Metabolic Brain Disease, 2004
    Co-Authors: Willie M. U. Daniels, Jacobus Hendricks, Ruduwaan Salie, Susan J. Van Rensburg
    Abstract:

    Zinc is an important component of proteins essential for normal functioning of the brain. However, it has been shown in vitro that this metal, at elevated levels, can be toxic to cells leading to their death. We investigated possible mechanisms of cell death caused by zinc: firstly, generation of reactive oxygen species, and secondly, the activation of the MAP-kinase pathway. Cell viability was assessed by means of the methyl-thiazolyl tetrazolium salt (MTT) assay and confirmed by tetramethylrhodamine methyl ester (TMRM) staining. We measured the phosphorylation status of Erk and p38 as indicators of MAP-kinase activity, using Western Blot techniques. A time curve was established when neuroblastoma (N2α) cells were exposed to 100 μM of zinc for 4, 12, and 24 h. Zinc caused a significant reduction in cell viability as early as 4 h, and indirectly stimulated the accumulation of reactive oxygen species as determined by 2.7 Dichlorodihydrofluorescein Diacetate (DCDHF) staining and confocal microscopy. Investigation of the MAP-kinase pathway indicated that Erk was downregulated, while p38 was stimulated. Our results therefore led us to conclude that in vitro, zinc toxicity involved the generation of reactive oxygen species and the activation of the MAP-kinase pathway.

  • A Mechanism for Zinc Toxicity in Neuroblastoma Cells
    Metabolic Brain Disease, 2004
    Co-Authors: Willie M. U. Daniels, Jacobus Hendricks, Ruduwaan Salie, Susan J. Van Rensburg
    Abstract:

    Zinc is an important component of proteins essential for normal functioning of the brain. However, it has been shown in vitro that this metal, at elevated levels, can be toxic to cells leading to their death. We investigated possible mechanisms of cell death caused by zinc: firstly, generation of reactive oxygen species, and secondly, the activation of the MAP-kinase pathway. Cell viability was assessed by means of the methyl-thiazolyl tetrazolium salt (MTT) assay and confirmed by tetramethylrhodamine methyl ester (TMRM) staining. We measured the phosphorylation status of Erk and p38 as indicators of MAP-kinase activity, using Western Blot techniques. A time curve was established when neuroblastoma (N2α) cells were exposed to 100 μM of zinc for 4, 12, and 24 h. Zinc caused a significant reduction in cell viability as early as 4 h, and indirectly stimulated the accumulation of reactive oxygen species as determined by 2.7 Dichlorodihydrofluorescein Diacetate (DCDHF) staining and confocal microscopy. Investigation of the MAP-kinase pathway indicated that Erk was downregulated, while p38 was stimulated. Our results therefore led us to conclude that in vitro, zinc toxicity involved the generation of reactive oxygen species and the activation of the MAP-kinase pathway.Conference Pape

Youjin Jeon - One of the best experts on this subject based on the ideXlab platform.

  • Protective effect of a freshwater alga, Spirogyra sp., against lipid peroxidation in vivo zebrafish and purification of antioxidative compounds using preparative centrifugal partition chromatography
    Journal of Applied Phycology, 2016
    Co-Authors: Ju-young Ko, Youjin Jeon
    Abstract:

    A freshwater alga, Spirogyra sp., collected in shallow ponds in South Korea, was evaluated for its antilipid peroxidative effect against 2,2′-azobis (2-amidinopropane) dihydrochloride (AAPH)-induced in vivo zebrafish, and antioxidative compounds from the alga were efficiently identified using 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS^+) online high-performance liquid chromatography (HPLC) and preparative centrifugal partition chromatography. The ethyl acetate fraction of Spirogyra sp. (SPE) in each fraction showed the strongest 2,2-diphenyl-1-picrylhydrazyl scavenging activity and significantly scavenged 2′,7′-Dichlorodihydrofluorescein Diacetate and diphenyl-1-pyrenylphosphine fluorescence, respectively, in AAPH-induced zebrafish embryo without any cytotoxicity in the concentrations between 25 and 50 μg mL^−1. The two main antioxidative compounds in SPE were confirmed by ABTS^+ online HPLC and were identified as gallic acid and methyl gallate, respectively, by HPLC–diode array detection (DAD)–electrospray ionization (ESI)/mass spectrometry (MS), ^1H- and ^13C-NMR. We conclude therefore that Spirogyra sp. is rich in gallic acid and methyl gallate, and it might be useful as a strong antilipid peroxidation material.

  • protective effect of fucoxanthin isolated from sargassum siliquastrum on uv b induced cell damage
    Journal of Photochemistry and Photobiology B-biology, 2009
    Co-Authors: Soojin Heo, Youjin Jeon
    Abstract:

    Abstract Fucoxanthin is a carotenoid isolated from Sargassum siliquastrum and is considered to be one of major active compound of marine algae. In this study, we investigated and confirmed the protective effect of fucoxanthin on UV-B induced cell injury in human fibroblast via 2′,7′-Dichlorodihydrofluorescein Diacetate (DCFH-DA), 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT), and comet assays. Intracellular ROS generated by exposure to UV-B radiation, which was significantly decreased by addition with various concentrations of fucoxanthin. Cell survival rate was increased with fucoxanthin pre-treated cells, which was reached around 81.47% at 100 μM, and the inhibitory effect of cell damage exhibited dose-dependent manner. Moreover, fucoxanthin having protective properties was demonstrated via Hoechst 33342/PI staining. Hence, on the basis of the above-mentioned studies, fucoxanthin has the ability to protect against oxidative stress induced by UV-B radiation and which might be applied to antioxidant and cosmeceutical industries.

Willie M. U. Daniels - One of the best experts on this subject based on the ideXlab platform.

  • A Mechanism for Zinc Toxicity in Neuroblastoma Cells.
    Metabolic Brain Disease, 2004
    Co-Authors: Willie M. U. Daniels, Jacobus Hendricks, Ruduwaan Salie, Susan J. Van Rensburg
    Abstract:

    Zinc is an important component of proteins essential for normal functioning of the brain. However, it has been shown in vitro that this metal, at elevated levels, can be toxic to cells leading to their death. We investigated possible mechanisms of cell death caused by zinc: firstly, generation of reactive oxygen species, and secondly, the activation of the MAP-kinase pathway. Cell viability was assessed by means of the methyl-thiazolyl tetrazolium salt (MTT) assay and confirmed by tetramethylrhodamine methyl ester (TMRM) staining. We measured the phosphorylation status of Erk and p38 as indicators of MAP-kinase activity, using Western Blot techniques. A time curve was established when neuroblastoma (N2α) cells were exposed to 100 μM of zinc for 4, 12, and 24 h. Zinc caused a significant reduction in cell viability as early as 4 h, and indirectly stimulated the accumulation of reactive oxygen species as determined by 2.7 Dichlorodihydrofluorescein Diacetate (DCDHF) staining and confocal microscopy. Investigation of the MAP-kinase pathway indicated that Erk was downregulated, while p38 was stimulated. Our results therefore led us to conclude that in vitro, zinc toxicity involved the generation of reactive oxygen species and the activation of the MAP-kinase pathway.

  • A Mechanism for Zinc Toxicity in Neuroblastoma Cells
    Metabolic Brain Disease, 2004
    Co-Authors: Willie M. U. Daniels, Jacobus Hendricks, Ruduwaan Salie, Susan J. Van Rensburg
    Abstract:

    Zinc is an important component of proteins essential for normal functioning of the brain. However, it has been shown in vitro that this metal, at elevated levels, can be toxic to cells leading to their death. We investigated possible mechanisms of cell death caused by zinc: firstly, generation of reactive oxygen species, and secondly, the activation of the MAP-kinase pathway. Cell viability was assessed by means of the methyl-thiazolyl tetrazolium salt (MTT) assay and confirmed by tetramethylrhodamine methyl ester (TMRM) staining. We measured the phosphorylation status of Erk and p38 as indicators of MAP-kinase activity, using Western Blot techniques. A time curve was established when neuroblastoma (N2α) cells were exposed to 100 μM of zinc for 4, 12, and 24 h. Zinc caused a significant reduction in cell viability as early as 4 h, and indirectly stimulated the accumulation of reactive oxygen species as determined by 2.7 Dichlorodihydrofluorescein Diacetate (DCDHF) staining and confocal microscopy. Investigation of the MAP-kinase pathway indicated that Erk was downregulated, while p38 was stimulated. Our results therefore led us to conclude that in vitro, zinc toxicity involved the generation of reactive oxygen species and the activation of the MAP-kinase pathway.Conference Pape

Jan Gminski - One of the best experts on this subject based on the ideXlab platform.

  • tetrabromobisphenol a tbbpa stimulated reactive oxygen species ros production in cell free model using the 2 7 Dichlorodihydrofluorescein Diacetate h2dcfda assay limitations of method
    Environmental Science and Pollution Research, 2016
    Co-Authors: Konrad A Szychowski, Kamila Rybczynskatkaczyk, Marcin L Leja, Anna Wojtowicz, Jan Gminski
    Abstract:

    Tetrabromobisphenol A (TBBPA) is a widely used brominated flame retardant, applied in a variety of commercial and household products, mainly electronic ones. Since the production of reactive oxygen species (ROS) is considered one of the principal cytotoxicity mechanisms, numerous studies undertake that aspect of TBBPA's mechanism of action. The present study verifies if the fluorogenic substrate 2',7'-Dichlorodihydrofluorescein Diacetate (H2DCFDA) should be used to detect ROS production induced by TBBPA. To determine the ability of TBBPA alone to stimulate the conversion of H2DCFDA to its fluorescent product 2',7'-dichlorofluorescein (DCF), we used a cell-free model. In the experiments we check different cultured media also in combination with free radical scavenger N-acetyl-l-cysteine (NAC). Additionally, experiments with stable free radical 2,2-diphenyl-1-picrylhydrazyl (DPPH·) have been made. The presented data showed that TBBPA in all tested concentrations interacts with H2DCFDA in phosphate-buffered saline (PBS) buffer while in micromolar concentrations in the DMEM/F12 medium with and without serum. The addition of NAC inhibited the interaction of TBBPA with H2DCFDA. Experiments with DPPH· showed that, in the presence of NAC, TBBPA acts like a free radical. TBBPA has similar properties to free radical and is susceptible to free radical scavenging properties of NAC. Our results indicated that H2DCFDA assay cannot be used to evaluate cellular ROS production in TBBPA studies. The study connected with TBBPA-stimulated ROS production in cell culture models using the H2DCFDA assay should be revised using a different method. However, due to the free radical-like nature of TBBPA, it can be very difficult. Therefore, further investigation of the nature of TBBPA as a compound with similar properties to free radical is required.

Ruduwaan Salie - One of the best experts on this subject based on the ideXlab platform.

  • A Mechanism for Zinc Toxicity in Neuroblastoma Cells.
    Metabolic Brain Disease, 2004
    Co-Authors: Willie M. U. Daniels, Jacobus Hendricks, Ruduwaan Salie, Susan J. Van Rensburg
    Abstract:

    Zinc is an important component of proteins essential for normal functioning of the brain. However, it has been shown in vitro that this metal, at elevated levels, can be toxic to cells leading to their death. We investigated possible mechanisms of cell death caused by zinc: firstly, generation of reactive oxygen species, and secondly, the activation of the MAP-kinase pathway. Cell viability was assessed by means of the methyl-thiazolyl tetrazolium salt (MTT) assay and confirmed by tetramethylrhodamine methyl ester (TMRM) staining. We measured the phosphorylation status of Erk and p38 as indicators of MAP-kinase activity, using Western Blot techniques. A time curve was established when neuroblastoma (N2α) cells were exposed to 100 μM of zinc for 4, 12, and 24 h. Zinc caused a significant reduction in cell viability as early as 4 h, and indirectly stimulated the accumulation of reactive oxygen species as determined by 2.7 Dichlorodihydrofluorescein Diacetate (DCDHF) staining and confocal microscopy. Investigation of the MAP-kinase pathway indicated that Erk was downregulated, while p38 was stimulated. Our results therefore led us to conclude that in vitro, zinc toxicity involved the generation of reactive oxygen species and the activation of the MAP-kinase pathway.

  • A Mechanism for Zinc Toxicity in Neuroblastoma Cells
    Metabolic Brain Disease, 2004
    Co-Authors: Willie M. U. Daniels, Jacobus Hendricks, Ruduwaan Salie, Susan J. Van Rensburg
    Abstract:

    Zinc is an important component of proteins essential for normal functioning of the brain. However, it has been shown in vitro that this metal, at elevated levels, can be toxic to cells leading to their death. We investigated possible mechanisms of cell death caused by zinc: firstly, generation of reactive oxygen species, and secondly, the activation of the MAP-kinase pathway. Cell viability was assessed by means of the methyl-thiazolyl tetrazolium salt (MTT) assay and confirmed by tetramethylrhodamine methyl ester (TMRM) staining. We measured the phosphorylation status of Erk and p38 as indicators of MAP-kinase activity, using Western Blot techniques. A time curve was established when neuroblastoma (N2α) cells were exposed to 100 μM of zinc for 4, 12, and 24 h. Zinc caused a significant reduction in cell viability as early as 4 h, and indirectly stimulated the accumulation of reactive oxygen species as determined by 2.7 Dichlorodihydrofluorescein Diacetate (DCDHF) staining and confocal microscopy. Investigation of the MAP-kinase pathway indicated that Erk was downregulated, while p38 was stimulated. Our results therefore led us to conclude that in vitro, zinc toxicity involved the generation of reactive oxygen species and the activation of the MAP-kinase pathway.Conference Pape