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  • 1
    Electronic Resource
    Electronic Resource
    The role of glutathione in the acute nephrotoxicity of sodium dichromate (1992)
    Springer
    Archives of toxicology 66 (1992), S. 646-651 
    Details
    ISSN: 1432-0738
    Keywords: Sodium dichromate ; Nephrotoxicity ; Glutathione ; Ascorbate ; Carbohydrate metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ascorbate treatment 30 min prior to sodium dichromate (20 or 30 mg/kg, s.c.) shows higher potency than that of glutathione (GSH) in protecting against both the metabolic disturbance and nephrotoxicity induced by dichromate. However, ascorbate treatment after 2 h of dichromate intoxication had no effect on dichromate-induced blood urea nitrogen (BUN) elevation 3 days after intoxication. In contrast, dichromate-induced glucosuria, which reached maximum levels at 3 days after treatment, was significantly decreased by GSH or N-acetyl cysteine (NAC) treatment, even if its administration was after 24 h of dichromate intoxication. Pretreatment with GSH depletors such as diethyl maleate (DEM) and buthionine sulfoximine (BSO) had no effect on dichromate-induced nephrotoxicity. GSH levels in the liver and kidney were not affected at 3 h after dichromate treatment. However, dichromate significantly increased tissue GSH levels with a marked increase in liver per kidney GSH ratio at 24 h after treatment, if food was withheld subsequent to dichromate treatment, indicating that GSH biosynthesis resulted from the accelerated protein breakdown. These results suggest that GSH-mediated dichromate reduction is not a kinetically favorable pathway in vivo; however, GSH plays an important role in protection against dichromate-induced nephrotoxicity. In addition, the cellular metabolism of dichromate in the early period after treatment is important in the pathogenesis of its nephrotoxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01981504
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  • 2
    Electronic Resource
    Electronic Resource
    Nephrotoxicity of sodium dichromate depending on the route of administration (1991)
    Springer
    Archives of toxicology 65 (1991), S. 537-541 
    Details
    ISSN: 1432-0738
    Keywords: Sodium dichromate ; Nephrotoxicity ; Hepatotoxicity ; Lipid peroxidation ; Phenobarbital
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A comparison of the effects of intraperitoneal and subcutaneous routes of administration of sodium dichromate on nephrotoxicity in rats was studied. Dichromate when injected subcutaneously (SC group) produced a higher degree of nephrotoxicity than when administered intraperitoneally (IP group). It caused severe progressive proteinuria followed by polyuria and glucosuria, reaching maximum levels at 3 days after treatment in the SC group, whereas it produced mild proteinuria without glucosuria in the IP group. The dose-dependent increases in blood urea nitrogen (BUN) and creatinine concentrations, shown in the SC group, were not observed in the IP group. However, between the two groups, there were no great differences in either the urinary excretion rate of chromium or the electrophoretic patterns of urinary protein in the day 1 urine specimens. Pretreatment of phenobarbital (PB) had no remarkable effect on the dichromate-induced nephrotoxicity. In contrast, it potentiated dichromate-induced hepatotoxicity, the indices of which were the elevation in serum alanine aminotransferase (ALT) activity and hepatic lipid peroxide formation. These results suggest that the dependence of dichromate-induced nephrotoxicity on the route of administration is related to the chemical forms of chromium reaching the kidney, and the necrotizing property of dichromate results from its metabolic fate in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01973713
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  • 3
    Electronic Resource
    Electronic Resource
    Conjugation of Arg-Gly-Asp sequence into thermo-reversible gel as an extracellular matrix for 3T3-L1 fibroblast cell culture (2000)
    Springer
    Biotechnology letters 22 (2000), S. 1553-1556 
    Details
    ISSN: 1573-6776
    Keywords: fibroblast cell ; gel ; GRGDS ; integrin family ; N-isopropylacrylamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract High molecular weight N-isopropylacrylamide copolymers with small amounts of acrylic acid (typically 2–5 mol% in feed) were synthesized by free radical polymerization in benzene and then conjugated with adhesion molecules of Gly-Arg-Gly-Asp-Ser (GRGDS) peptides. Aqueous polymer solutions (5, 6, 8 and 10% w/v) in culture medium (pH 7.4, ionic strength; 0.15 M) with 3T3-L1 fibroblast cells were mixed and poured in Millicells, which supported the gel formation without a significant gel induction time at 36 °C (gelation temperature). The initially formed gel was translucent and became more opaque as the temperature increased. The interaction between fibroblast cells and an artificial matrix of GRGDS containing p(NiPAAm-co-AAc) copolymer gel resulted in effective cell attachment, proliferation and growth. This study supported that specific attachment is the result of the interaction between the integrin families on the fibroblast and the RGD sequence on the p(NiPAAm-co-AAc) copolymer gel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005680800420
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  • 4
    Electronic Resource
    Electronic Resource
    Inactivation of p16INK4a in Primary Tumors and Cell Lines of Head and Neck Squamous Cell Carcinoma (2000)
    Springer
    Molecules and cells 10 (2000), S. 557-565 
    Details
    ISSN: 0219-1032
    Keywords: DNA Methylation ; Head and Neck Squamous Cell Carcinoma ; p16INK4a
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Inactivation of the p16INK4a gene by mutation and deletion is common in head and neck squamous cell carcinoma (HNSCC). The present study demonstrates that hypermethylation of the 5′ CpG islands can serve as an alternative mechanism for the inactivation of the p16INK4a gene in this tumor. We studied 11 HNSCC cell lines and 17 oral squamous cell carcinoma (OSCC) primary tumors for p16INK4a gene status by protein/mRNA and DNA genetic/epigenetic analyses to determine the incidence of its inactivation. Our study indicates that: (1) inactivation of p16 protein is frequent in HNSCC cell lines (6/11, 54.5%) and OSCC primary tumors (15/17, 88.2%), (2) inactivation of p16INK4a protein is commonly associated with the presence of gene alteration such as mutation, homozygous deletion and especially aberrant methylation, and (3) genomic sequencing of bisulfite-modified DNA shows that the carcinoma develops a heterogeneous pattern of hypermethylation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s10059-000-0557-8
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    Paper (German National Licenses)
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