Activation of the Nrf2 pathway, but decreased gamma-glutamylcysteine synthetase heavy subunit chain levels and caspase-3-dependent apoptosis during exposure of primary mouse hepatocytes to diphenylarsinic acid.
暂无分享,去创建一个
D. Sumi | Y. Kumagai | T. Toyama | Y. Shinkai | Aiko Manji
[1] D. Sumi,et al. Arsenic: signal transduction, transcription factor, and biotransformation involved in cellular response and toxicity. , 2007, Annual review of pharmacology and toxicology.
[2] Kayoko Kita,et al. Glutathione plays a role in regulating the formation of toxic reactive intermediates from diphenylarsinic acid. , 2006, Toxicology.
[3] T. Ishii,et al. Sulforaphane, an activator of Nrf2, suppresses cellular accumulation of arsenic and its cytotoxicity in primary mouse hepatocytes , 2006, FEBS letters.
[4] H. Aposhian,et al. Arsenic toxicology: five questions. , 2006, Chemical research in toxicology.
[5] Makoto Kobayashi,et al. Molecular mechanisms activating the Nrf2-Keap1 pathway of antioxidant gene regulation. , 2005, Antioxidants & redox signaling.
[6] F. Otsuka,et al. Diphenylarsinic acid poisoning from chemical weapons in Kamisu, Japan , 2004, Annals of neurology.
[7] T. Kaise,et al. In vitro cytotoxic and genotoxic effects of diphenylarsinic acid, a degradation product of chemical warfare agents. , 2004, Toxicology and applied pharmacology.
[8] S. Hirano,et al. The accumulation and toxicity of methylated arsenicals in endothelial cells: important roles of thiol compounds. , 2004, Toxicology and applied pharmacology.
[9] S. Hirano,et al. Accumulation and toxicity of monophenyl arsenicals in rat endothelial cells , 2004, Archives of Toxicology.
[10] Wei Qu,et al. Transcription factor Nrf2 activation by inorganic arsenic in cultured keratinocytes: involvement of hydrogen peroxide. , 2003, Experimental cell research.
[11] T. Kavanagh,et al. TGFβ1‐induced suppression of glutathione antioxidant defenses in hepatocytes: caspase‐dependent posttranslational and caspase‐independent transcriptional regulatory mechanisms , 2003, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[12] K. Itoh,et al. Activation of Nrf2 and accumulation of ubiquitinated A170 by arsenic in osteoblasts. , 2003, Biochemical and biophysical research communications.
[13] S. Hirano,et al. Difference in uptake and toxicity of trivalent and pentavalent inorganic arsenic in rat heart microvessel endothelial cells , 2003, Archives of Toxicology.
[14] T. Inaoka,et al. Skin manifestations of arsenicosis in two villages in Bangladesh , 2002, International Journal of Dermatology.
[15] D. Nordstrom. Worldwide Occurrences of Arsenic in Ground Water , 2002, Science.
[16] K. Itoh,et al. A Sulforaphane Analogue That Potently Activates the Nrf2-dependent Detoxification Pathway* , 2002, The Journal of Biological Chemistry.
[17] R. S. Magee,et al. Critical evaluation of proven chemical weapon destruction technologies (IUPAC Technical Report) , 2002 .
[18] Jie Liu,et al. Overexpression of glutathione S-transferase II and multidrug resistance transport proteins is associated with acquired tolerance to inorganic arsenic. , 2001, Molecular pharmacology.
[19] M. Freeman,et al. Multi‐faceted regulation of γ‐glutamylcysteine synthetase , 2000 .
[20] Wild Ac,et al. Regulation of gamma-glutamylcysteine synthetase subunit gene expression by the transcription factor Nrf2. , 1999 .
[21] O. Griffith,et al. Biologic and pharmacologic regulation of mammalian glutathione synthesis. , 1999, Free radical biology & medicine.
[22] Y. Akao,et al. Arsenic trioxide induces apoptosis in neuroblastoma cell lines through the activation of caspase 3 in vitro , 1999, FEBS letters.
[23] Shelly C. Lu. Regulation of hepatic glutathione synthesis: current concepts and controversies , 1999, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[24] M. W. Anders,et al. Identification of an important cysteine residue in human glutamate-cysteine ligase catalytic subunit by site-directed mutagenesis. , 1998, The Biochemical journal.
[25] Jen-kun Lin,et al. Involvement of reactive oxygen species and caspase 3 activation in arsenite‐induced apoptosis , 1998, Journal of cellular physiology.
[26] R. Flavell,et al. Evidence that the multidrug resistance protein (MRP) functions as a co-transporter of glutathione and natural product toxins. , 1997, Cancer research.
[27] K. Itoh,et al. An Nrf2/small Maf heterodimer mediates the induction of phase II detoxifying enzyme genes through antioxidant response elements. , 1997, Biochemical and biophysical research communications.
[28] E. Alnemri,et al. Resistance of actin to cleavage during apoptosis. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[29] T. Rossman,et al. Efflux-mediated resistance to arsenicals in arsenic-resistant and -hypersensitive Chinese hamster cells. , 1996, Toxicology and applied pharmacology.
[30] M. Lai,et al. Increased prevalence of hypertension and long-term arsenic exposure. , 1995, Hypertension.
[31] A. Smith,et al. Vascular effects of chronic arsenic exposure: a review. , 1994, Epidemiologic reviews.
[32] Te-Chang Lee,et al. Glutathione S-Transferase π Facilitates the Excretion of Arsenic from Arsenic-Resistant Chinese Hamster Ovary Cells , 1993 .
[33] T. Lee,et al. Glutathione S-transferase pi in an arsenic-resistant Chinese hamster ovary cell line. , 1992, The Biochemical journal.
[34] W. Tseng,et al. Prevalence of skin cancer in an endemic area of chronic arsenicism in Taiwan. , 1968, Journal of the National Cancer Institute.