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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Paracetamol disposition in Thai patients during and after treatment of falciparum malaria (1995)
    Springer
    European journal of clinical pharmacology 48 (1995), S. 65-69 
    Details
    ISSN: 1432-1041
    Keywords: Paracetamol ; Malaria ; pharmacokinetics ; phase II conjugation ; glucuronidation ; sulphation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Investigations in animals have suggested that conjugation of paracetamol may be reduced in malaria. We have measured plasma concentrations and the urinary excretion of paracetamol and its phase II metabolites in eight Thai patients during uncomplicated falciparum malaria and in convalescence, following a 1000 mg single oral dose. The apparent oral clearance (Malaria, 3.6; Convalescence, 3.9; ml·min−1·kg−1), the elimination half-life (Malaria, 3.8; Convalescence, 3.7 h) and apparent volume of distribution (Malaria, 1.2; Convalescence, 1.2; l·kg−1) of paracetamol were similar during malaria and convalescence. In addition, the urinary excretion of paracetamol and its major phase II metabolites and their formation clearances from paracetamol were not significantly different between the two study phases. These data show that clinical malaria infection has no effect on the conjugation of paracetamol in man.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00202175
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  • 3
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of quinine in patients with chronic renal failure (1996)
    Springer
    European journal of clinical pharmacology 49 (1996), S. 497-501 
    Details
    ISSN: 1432-1041
    Keywords: Quinine ; Malaria ; pharmacokinetics ; chronic renal failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Methods: We investigated the pharmacokinetics of quinine (Qn) following administration of a single oral dose of 600 mg Qn sulphate in six male Thai patients with a moderate degree of chronic renal failure (CRF), and six male Thai subjects with normal renal function. Results: The drug was well tolerated in both groups of subjects; no major adverse reactions were observed. A marked alteration in the pharmacokinetics of Qn was found in patients with CRF compared to healthy subjects; there were six signifiicant changes in the pharmacokinetic parameters. Absorption was delayed, but increased in CRF (tmax 4.5 vs 1.6 h, Cmax 6.17 vs 3.45 μg·ml−1). Total clearance was significantly reduced 0.94 vs 2.84 ml·min−1·kg−1, whereas Vz/f remained unchanged (1.82 vs 2.78 1·kg−1). This resulted in the increased values of AUC and prolongation of the t1/2z and MRT in the patients (AUC 181.5 vs 61.8 μg·min−1·ml−1, t1/2z 26 vs 9.7 h, MRT 36.4 vs 11.3 h). Median concentrations of plasma unbound fraction of Qn collected at 4 h after drug administration in patients and healthy subjects were 7.3 vs 9.8%, respectively.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00195937
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  • 4
    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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    Paper (German National Licenses)
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