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  • 1.
    Andersson, Maria
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Stenqvist, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Hellman, Björn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Interindividual differences in initial DNA repair capacity when evaluating H2O2-induced DNA damage in extended-term cultures of human lymphocytes using the comet assay2007In: Cell Biology and Toxicology, ISSN 0742-2091, E-ISSN 1573-6822, Vol. 23, no 6, p. 401-411Article in journal (Refereed)
    Abstract [en]

    It has been suggested that extended-term cultures of human lymphocytes could be used as a complement to cell lines based on transformed cells when testing the genotoxicity of chemicals. To investigate whether the pattern of induced DNA damage and its subsequent repair differs significantly between cultures based on different blood donors, hydrogen peroxide (H2O2)-induced DNA damage was measured in cultures from four different subjects using the comet assay. The DNA damage was significantly increased in all cultures after 10 min exposure to 0.25 mmol/L H2O2, and there was a significant decrease in the H2O2-induced DNA damage in all cultures after 30 min of DNA repair. The level of damage varied between the different donors, especially after the repair. Using PCR and DNA sequencing, exon 5 of the p53 gene was sequenced in the lymphocytes from the donors with the lowest and highest residual damage. No such mutation was found. Mouse lymphoma L5178Y cells carrying the p53 mutation in exon 5 were included as a reference. These cells were found to be less sensitive toward the H2O2-induced DNA damage, and they were also found to have a rather low DNA repair capacity. The demonstrated variation in H2O2-induced DNA damage and DNA repair capacity between the cultures from the different subjects may be important from a risk assessment perspective, but is obviously not of decisive importance when it comes to the development of a routine assay for genotoxicity.

  • 2.
    Axelsson, V
    et al.
    Stockholm University, Faculty of Science, Department of Neurochemistry.
    Pikkarainen, K
    Stockholm University, Faculty of Science, Department of Neurochemistry.
    Forsby, A
    Stockholm University, Faculty of Science, Department of Neurochemistry.
    Glutathione intensifies gliotoxin-induced cytotoxicity in human neuroblastoma SH-SY5Y cells.2006In: Cell Biology and Toxicology, ISSN 0742-2091, E-ISSN 1573-6822, Vol. 22, no 2, p. 127-36Article in journal (Refereed)
    Abstract [en]

    Gliotoxin is a fungal second metabolite produced by diverse species that can be found in compost, stored crops, moist animal feed and sawdust. The role of glutathione in gliotoxin-induced toxicity was studied in order to elucidate the toxic mechanisms leading to neurite degeneration and cell death in differentiated human neuroblastoma (SH-SY5Y) cells. After 72 h of exposure to gliotoxin, moderate cytotoxicity was induced at 0.1 micromol/L, which was more severe at higher concentrations. A reduction in the number of neurites per cell was also observed. By decreasing the level of intracellular glutathione with L: -buthionine-sulfoxamine (BSO) a specific inhibitor of glutathione synthesis, the cytotoxic effect of gliotoxin was significantly attenuated. The gliotoxin-induced cytotoxicity was also slightly reduced by the antioxidant vitamin C. However, the neurite degenerative effect was not altered by BSO, or by vitamin C. A concentration-dependent increase in the ratio between oxidized and reduced forms of glutathione, as well as the total intracellular glutathione levels, was noted after exposure to gliotoxin. The increase of glutathione was also reflected in western blot analyses showing a tendency for the regulatory subunit of gamma-glutamylcysteine synthetase to be upregulated. In addition, the activity of glutathione reductase was slightly increased in gliotoxin-exposed cells. These results indicate that glutathione promotes gliotoxin-induced cytotoxicity, probably by reducing the ETP (epipolythiodioxopiperazine) disulfide bridge to the dithiol form.

  • 3. Jin, T.
    et al.
    Chen, L
    Lei, L.J
    Nordberg, M
    Nordberg, G.F
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Factors influencing dose-response relationships of cadmium in humans – diabetes, metalllothionein and metallothionein antibodies.2008In: Cell Biology and Toxicology, ISSN 0742-2091, E-ISSN 1573-6822, Vol. 24, no 5, p. 451-55Article in journal (Refereed)
  • 4.
    Jin, Taiyi
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Environmental Medicine. Fudan University, School of Public Health, Department of Occupational Health, Shanghai 200032, Peoples Republic of China.
    Chen, Liang
    Lei, Lijian
    Nordberg, Monica
    Nordberg, Gunnar F
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Environmental Medicine.
    An invited paper presented in the symposium "Health effects of low dose exposure to toxic metals"2008In: Cell Biology and Toxicology, ISSN 0742-2091, E-ISSN 1573-6822, Vol. 24, no 5, p. 451-455Article in journal (Refereed)
  • 5.
    Liang, Y
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Li, H
    Lei, L
    Yin, T
    Nordberg, M
    Nordberg, G
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Immunolocalization of metallothionein in liver and kidney of Wistar rats exposed to cadmium.2008In: Cell Biology and Toxicology, ISSN 0742-2091, E-ISSN 1573-6822, Vol. 24, no 1, p. 95-6Article in journal (Refereed)
  • 6.
    Nordberg, G
    et al.
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Skerfving, S
    Health effects of low dose exposure to toxic metals:: introduction and research recommendations2008In: Cell Biology and Toxicology, ISSN 0742-2091, E-ISSN 1573-6822, Vol. 24, p. 438-40Article in journal (Refereed)
  • 7.
    Nordin-Andersson, M
    et al.
    Stockholm University, Faculty of Science, Department of Neurochemistry.
    Walum, E
    Kjellstrand, P
    Forsby, A
    Stockholm University, Faculty of Science, Department of Neurochemistry.
    Acrylamide-induced effects on general and neurospecific cellular functions during exposure and recovery.2003In: Cell Biology and Toxicology, ISSN 0742-2091, E-ISSN 1573-6822, Vol. 19, no 1, p. 43-51Article in journal (Refereed)
    Abstract [en]

    Basal cytotoxicity, morphological changes and alterations in cell physiological and neurochemical functions were studied in differentiated human neuroblastoma (SH-SY5Y) cells during exposure to acrylamide and during a subsequent recovery period after cessation of exposure. Acrylamide induced a 20% reduction in the number of neurites per cell at 0.21 mmol/L and 20% decrease in the protein synthesis rate at 0.17 mmol/L after 72 h of exposure. Furthermore, the basal level of intracellular calcium concentration ([Ca2+]i) and receptor-activated (carbachol, 0.1 mmol/L) Ca2+ fluxes increased by 49% and 21%, respectively, at 0.25 mmol/L. These observations were made at noncytotoxic acrylamide concentrations, signifying specific neurotoxic alterations. Forty-eight hours after cessation of acrylamide exposure, the SH-SY5Y cells had recovered, i.e., the number of neurites per cell as well as the basal level of [Ca2+]i and rate of protein synthesis were comparable to those of control cells. The general calpain inhibitor calpeptin decreased the acrylamide-induced (0.5 mmol/L) neurite degeneration, determined as reduction in number of neurites per cell, from 52% to 17% as compared to control cells, which further supports the hypothesis that an increased [Ca2+]i plays a significant role for acrylamide-induced axonopathy.

  • 8.
    Pournara, Angeliki
    et al.
    Institute of Environmental Medicine, Karolinska Institutet, S-171 77 Stockholm, Sweden.
    Kippler, Maria
    Holmlund, Teresa
    Ceder, Rebecca
    Grafström, Roland
    Vahter, Marie
    Broberg, Karin
    Wallberg, Annika E.
    Arsenic alters global histone modifications in lymphocytes in vitro and in vivo2016In: Cell Biology and Toxicology, ISSN 0742-2091, E-ISSN 1573-6822, Vol. 32, no 4, p. 275-84Article, review/survey (Refereed)
    Abstract [en]

    Arsenic, an established carcinogen and toxicant, occurs in drinking water and food and affects millions of people worldwide. Arsenic appears to interfere with gene expression through epigenetic processes, such as DNA methylation and post-translational histone modifications. We investigated the effects of arsenic on histone residues in vivo as well as in vitro. Analysis of H3K9Ac and H3K9me3 in CD4+ and CD8+ sorted blood cells from individuals exposed to arsenic through drinking water in the Argentinean Andes showed a significant decrease in global H3K9me3 in CD4+ cells, but not CD8+ cells, with increasing arsenic exposure. In vitro studies of inorganic arsenic-treated T lymphocytes (Jurkat and CCRF-CEM, 0.1, 1, and 100 μg/L) showed arsenic-related modifications of H3K9Ac and changes in the levels of the histone deacetylating enzyme HDAC2 at very low arsenic concentrations. Further, in vitro exposure of kidney HEK293 cells to arsenic (1 and 5 μM) altered the protein levels of PCNA and DNMT1, parts of a gene expression repressor complex, as well as MAML1. MAML1 co-localized and interacted with components of this complex in HEK293 cells, and in silico studies indicated that MAML1 expression correlate with HDAC2 and DNMT1 expression in kidney cells. In conclusion, our data suggest that arsenic exposure may lead to changes in the global levels of H3K9me3 and H3K9Ac in lymphocytes. Also, we show that arsenic exposure affects the expression of PCNA and DNMT1—proteins that are part of a gene expression silencing complex.

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