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  • 1
    Electronic Resource
    Electronic Resource
    Studies of the biochemical toxicology of uranyl nitrate in the rat (1994)
    Springer
    Archives of toxicology 68 (1994), S. 29-39 
    Details
    ISSN: 1432-0738
    Keywords: Key words: 3-d-Hydroxybutyrate – 2-D COSY – Glucose – Lactate – Nephrotoxicity –1H NMR urinalysis – Uranyl nitrate – Urinary enzymes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. High resolution 1H NMR spectroscopy of urine and plasma, conventional clinical chemical methods and histopathology have been applied to investigate the effects of uranyl nitrate (UN) on renal function and biochemistry in the Fischer 344 (F344) rat. Administration of UN (5 – 20 mg/kg) to male F344 rats resulted in a dose-related proximal nephropathy assessed conventionally by histopathology and urinary excretion of N-acetyl-β-d-glucosaminidase (NAG), and related to changes in the patterns of low MW metabolites observed in 400 MHz 1H NMR spectra of urine. The changes in urinary metabolite profiles included elevations in glucose accompanied by minor elevations in certain amino acids (alanine, valine and glutamate). 1H NMR urinalysis also revealed altered excretion of low MW metabolites which are not routinely measured, such as l-lactate, acetate, citrate, succinate and 2-oxoglutarate (2-OG). In addition, the striking appearance of high concentrations of 3-d-hydroxybutyrate (HB) in the urine was noted, in the absence of acetoacetate or acetone, and it is suggested that this may provide a new marker of proximal tubular damage for certain types of nephrotoxic mechanism. Broadening of the 1H NMR signals of citrate following 10 mg/kg UN was shown to be due to a dynamic exchange process involving chelation with urinary Ca2+ and Mg2+ ions. Conventional biochemical analysis of plasma from UN-treated rats revealed dose-related increases in creatinine, urea and HB concentrations. 1H NMR-detected evidence of raised alanine aminotransferase (ALT) levels in rats administered the highest dose of UN was indicated by the partial deuteration of alanine in lyophilised plasma reconstituted in 2H2O. The degree of 1H NMR-detected abnormalities agreed well with histopathological observations and conventional biochemical indices of nephrotoxicity and more fully characterised the renal changes produced by UN. The significance of HB-uria in UN-induced proximal nephropathy is discussed in relation to biochemical observations on other proximal nephrotoxins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050028
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  • 2
    Electronic Resource
    Electronic Resource
    Cephaloridine-induced nephrotoxicity in the Fischer 344 rat: proton NMR spectroscopic studies of urine and plasma in relation to conventional clinical chemical and histopathological assessments of nephronal damage (1992)
    Springer
    Archives of toxicology 66 (1992), S. 525-537 
    Details
    ISSN: 1432-0738
    Keywords: Cephaloridine ; 3-d-Hydroxybutyric acid ; Glucose ; Lactic acid ; Nephrotoxicity ; Proton NMR urinalysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The acute toxicological effects of the nephrotoxic antibiotic cephaloridine (CPH, 0–1500 mg/kg) in male Fischer 344 (F344) rats, have been investigated over 48 h using clinical chemistry, histopathology and proton nuclear magnetic resonance (1H NMR) spectroscopy of urine and plasma. High field (400 and 600 MHz)1H NMR urinalysis revealed increased excretion of lactic acid, acetoacetate, alanine, valine, lysine, glutamine and glutamate and a severe, time-dependent glycosuria. A major change observed in urine of CPH-treated animals was the dose-dependent increase in HB which may relate to altered energy metabolism. CPH also caused dose-dependent decreases in the urinary excretion of hippurate, allantoin and protein (conventional assay). This abnormal metabolic profile is consistent with a functional defect in the S1/S2 regions of the proximal tubule, and was confirmed by histologypost mortem. Functional changes observed included elevations in blood urea nitrogen (BUN) and urine flow rate (UFR) and dose-related decreases in urine osmolality. Spin-echo1H NMR spectroscopic analysis of lyophilised plasma, reconstituted with2H2O revealed an abnormal phase modulation of the methyl signal from free alanine and it is postulated that this is due to the release of transaminases from damaged tissue which via a reversible conversion to pyruvate, cause variable deuteration of alanine at the α-CH position. This observation suggests that1H NMR spectral patterns are also dependent on the level of plasma transaminases and this may provide a novel indicator of tissue damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01973382
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  • 3
    Electronic Resource
    Electronic Resource
    Studies on the effects ofl(αS,5S)-α-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid (AT-125) on 4-aminophenol-induced nephrotoxicity in the Fischer 344 rat (1993)
    Springer
    Archives of toxicology 67 (1993), S. 696-705 
    Details
    ISSN: 1432-0738
    Keywords: Amino aciduria ; AT-125 ; 4-Aminophenol ; Glutathione ; Glycosuria ; Lactic aciduria ; Nephrotoxicity ; 1H NMR urinalysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 4-Aminophenol (para-aminophenol; PAP) causes selective necrosis to the S3 segment of the proximal tubule in experimental animals. The mechanism of PAP nephrotoxicity has not been fully elucidated, although it has been suggested to involve glutathione (GSH)-dependentS-conjugation followed by processing by the enzyme γ-glutamyl transpeptidase (γGT) to the corresponding cysteineS-conjugate. This proposed toxicity mechanism was probed further by administering L-(αS,5S)-α-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid (AT-125), a potent γGT inhibitor, to Fischer 344 (F344) rats before treatment with PAP (100 mg/kg). AT-125 pretreatment did not appear to protect against PAP-induced nephrotoxicity as assessed by renal histopathology, clinical chemistry and proton nuclear magnetic resonance (1H NMR) spectroscopy of urine. These data suggest that renal γGT activity is not a prerequisite for PAP nephrotoxicity and that the generation of a cysteineS-conjugate is not a unique requirement for the induction of PAP nephrotoxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01973694
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  • 4
    Electronic Resource
    Electronic Resource
    Determination of the relative NH proton lifetimes of the peptide analogue viomycin in aqueous solution by NMR-based diffusion measurement (1999)
    Springer
    Journal of biomolecular NMR 13 (1999), S. 25-30 
    Details
    ISSN: 1573-5001
    Keywords: amide ; diffusion ; exchange ; viomycin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract In aqueous solution, exchanging peptide NH protons experience two environments, that of the peptide itself with a relatively slow diffusion coefficient and that of the water solvent with a faster diffusion coefficient. Although in slow exchange on the NMR chemical shift timescale, the magnetic field gradient dependence of the NH peak intensities in an experiment used to measure diffusion coefficients reflects the relative time periods spent in the two environments and this allows the determination of the relative solvent accessibility of exchangeable protons in peptides or proteins. To test this approach, the magnetic field gradient dependent intensities of the chemically shifted amide and amine NH protons of the peptide antibiotic viomycin have been measured using the high resolution longitudinal-eddy-current-delay (LED) NMR method incorporating solvent water peak elimination by non-excitation. The NH resonances of viomycin have been assigned previously and their relative exchange rates determined. Here, the gradient dependence of each NH proton intensity is reported, and these, after a bi- exponential least squares fitting, yield the fractional lifetimes of the protons spent in the peptide and water environments during the diffusion period of the experiment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008393202076
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