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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Archives of toxicology 64 (1990), S. 644-649 
    ISSN: 1432-0738
    Keywords: Sodium dichromate ; Glycolysis ; Hyperglycemia ; Glycogenolysis ; Cyanosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of sodium dichromate on cellular metabolism was investigated. Intraperitoneal injection of sodium dichromate into the rat (20 or 40 mg/kg) caused significant increases in serum lactate, pyruvate, and creatinine concentrations within 15 min after intoxication. Severe hyperglycemia occurred thereafter, as a result of increased hepatic glycogenolysis, which was seen in the first 2 h after dichromate. However, liver glycogen was resynthesized in 24 h-fasted rats after glucose refeeding. Dichromate decreased serum total amino acids, with a consequent increase in blood urea nitrogen (BUN) concentration. Unlike HgCl2 (2 mg/kg, i.p.), As2O3 (5 mg/kg, i.p.), and KCN (5 mg/kg, i. p.), dichromate showed the largest metabolic disturbance only in the early period after treatment. In addition, dichromate produced cyanosis, which appeared during the period of the accelerated glycolysis and breakdown of creatine phosphate. Regardless of chemical species, only the hexavalent chromium compounds had an effect on the cellular metabolism. Trivalent chromium compounds had no effect at all. These results suggest that dichromate possesses a characteristic dual action on cellular metabolism, which might be related to its metabolic fate.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Archives of toxicology 65 (1991), S. 537-541 
    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
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 49 (1996), S. 497-501 
    ISSN: 1432-1041
    Keywords: Key words 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 l ⋅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
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 49 (1996), S. 497-501 
    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
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Archives of toxicology 66 (1992), S. 646-651 
    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
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