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Hanna Krawczyk - One of the best experts on this subject based on the ideXlab platform.

  • Research Article Uraemic Toxins Generated in the Presence of Fullerene C60, Carbon-Encapsulated Magnetic Nanoparticles, and Multiwalled Carbon Nanotubes
    2016
    Co-Authors: Magdalena Popbawska, Hanna Krawczyk
    Abstract:

    Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Uraemic toxins—creatol and N-Methylguanidine—are generated in conversion of creatinine in water in the presence of various forms of carbon such as fullereneC 60, carbon-encapsulatedmagnetic nanoparticles, andmultiwalled carbon nanotubes and oxygen. The conversion degree for creatinine was different for fullerene

  • Uraemic Toxins Generated in the Presence of Fullerene C60, Carbon-Encapsulated Magnetic Nanoparticles, and Multiwalled Carbon Nanotubes
    Hindawi Limited, 2013
    Co-Authors: Magdalena Popławska, Hanna Krawczyk
    Abstract:

    Uraemic toxins—creatol and N-Methylguanidine—are generated in conversion of creatinine in water in the presence of various forms of carbon such as fullerene C60, carbon-encapsulated magnetic nanoparticles, and multiwalled carbon nanotubes and oxygen. The conversion degree for creatinine was different for fullerene C60, CEMNPs, and MWCNTs and was 9% (3.6% creatol, 5.4% N-Methylguanidine), 35% (12% creatol, 23% N-Methylguanidine), and 75% (16% creatol, 59% N-Methylguanidine), respectively

  • production of uremic toxin Methylguanidine from creatinine via creatol on activated carbon
    Journal of Pharmaceutical and Biomedical Analysis, 2009
    Co-Authors: Hanna Krawczyk
    Abstract:

    Abstract The mixture of creatinine, activated charcoal and water was stirred. As a result the conversion of creatinine into two products was observed. 1 H, 13 C NMR and HMBC spectra were recorded and the chemical shifts assigned. Two uremic toxins: creatol and N-Methylguanidine were identified. To interpret the NMR data obtained, the optimum structure of creatol, which can exist in the forms of seven tautomers, has been calculated using the DFT B3LYP/6-311G(2d,p) method. The influence of the solvent was described by the polarizable continuum model (PCM). The calculated energy of the most energetically stable tautomeric form A is lower by 12.2, 16.9, 33.8, 81.5, 106.3, 130.4 kJ/mol in water than that of the tautomers B – G , respectively, which suggests that the A form of creatol should prevail in solution. In DMSO, the calculated energy of the most energetically stable tautomeric form A is lower than that of both D and B and the remaining tautomeric forms ( C , E – G ) are less energetically stable. Subsequently, we sought the correlations between the experimental and the calculated chemical shifts of protons and carbons-13 for the forms – A , B (in water) and A , B , D (in DMSO) – of creatol. The population of the A tautomer is predominant in both H 2 O and DMSO. We have also recorded the spectra of creatol and N-Methylguanidine at different pH. Our data are complete enough to be used in the analysis of body fluids.

Takako Yokozawa - One of the best experts on this subject based on the ideXlab platform.

  • site of Methylguanidine production and factors that influence production levels
    Nephron, 2002
    Co-Authors: Takako Yokozawa, Yasuko Muto, Kunihiko Wakaki, Hiroshi Kashiwagi
    Abstract:

    The site of Methylguanidine (MG) production in the kidney was investigated using animal models of renal disease and cultured renal epithelial cells. In rats with proximal tubular injury induced by adenine, the blood and urinary levels of MG increased as the severity of injury increased. In contrast, in cases of glomerular injury, there were no such changes in MG levels. Thus, it was apparent that proximal tubular injury served to promote MG production. In addition, a marked increase was observed in the intensities of bands attributable to 5,5-dimethyl-1-pyrroline-N-oxide (DMPO)-OH in the electron spin resonance spectrum of the kidney in the rats given adenine. In these rats, the activity of the radical-scavenging enzymes superoxide dismutase, catalase, and glutathione peroxidase was decreased. This suggests that the formation of excessive radicals and deterioration of defense mechanisms that contribute to the development of oxidative stress underlie the enhanced MG production. The experiments using cultured cells revealed that an oxide of adenine, 2,8-dihydroxyadenine (DHOA), directly induced renal tubular injury. These findings indicate that the accumulation of creatinine due to DHOA, combined with oxidative stress, resulted in increased MG production.

  • proof that green tea tannin suppresses the increase in the blood Methylguanidine level associated with renal failure
    Experimental and Toxicologic Pathology, 1997
    Co-Authors: Takako Yokozawa, Erbo Dong, Hikokichi Oura
    Abstract:

    The effects of a green tea tannin mixture and its individual tannin components on Methylguanidine were examined in rats with renal failure. The green tea tannin mixture caused a dose-dependent decrease in Methylguanidine, a substance which accumulates in the blood with the progression of renal failure. Among individual tannin components, the effect was most conspicuous with (-)-epigallocatechin 3-O-gallate and (-)-epicatechin 3-O-gallate, while other components not linked to gallic acid showed only weak effects. Thus, the effect on Methylguanidine was found to vary among different types of tannin.

  • uraemic toxin reduction a newly found effect of hydrolysable type tannin containing crude drug and gallotannin
    Phytotherapy Research, 1995
    Co-Authors: Takako Yokozawa, Koji Fujioka, Hikokichi Oura, Takashi Tanaka, Gen-ichiro Nonaka, Itsuo Nishioka
    Abstract:

    The levels of urea nitrogen, creatinine, Methylguanidine and guanidinosuccinic acid, which accumulate in blood in parallel with the progress of renal failure after adenine administration, were decreased significantly in rats given Galla Rhois, Moutan Cortex or Paeoniae Radix extract. Administration of Galla Rhois extract was found to be more effective than the other two crude drugs in decreasing the uraemic toxin parameters. A uraemic toxin-decreasing effect similar to that of crude drug was also obtained using 1,3,6-tri-O-galloyl-β-D-glucopyranose and 1,2,3,4,6-penta-O-galloyl-β-D-glucopyranose.

  • l gulono gamma lactone oxidase is the enzyme responsible for the production of Methylguanidine in the rat liver
    Nephron, 1993
    Co-Authors: Naoki Fujitsuka, Takako Yokozawa, Hikokichi Oura, Teruaki Akao, Kyoichi Kobashi, Kazuharu Ienaga, Ko Nakamura
    Abstract:

    A Methylguanidine-synthesizing enzyme localized in rat liver microsomes produces Methylguanidine via the intermediates creatone A and creatone B from the substrate, creatol, a substance produced from

  • comparison of renal effects of creatinine creatol and Methylguanidine in rats with adenine induced chronic renal failure
    Nephron, 1993
    Co-Authors: Takako Yokozawa, Hikokichi Oura, Kazuharu Ienaga, Ko Nakamura
    Abstract:

    Creatinine (Cr), creatol and Methylguanidine (MG), which accumulate in the body with the progress of renal failure after adenine administration, were given separately to rats in order to compare their

Ko Nakamura - One of the best experts on this subject based on the ideXlab platform.

Hikokichi Oura - One of the best experts on this subject based on the ideXlab platform.

Aldo Pinto - One of the best experts on this subject based on the ideXlab platform.

  • effect of Methylguanidine in a model of septic shock induced by lps
    Free Radical Research, 2004
    Co-Authors: Stefania Marzocco, Raffaella Sorrentino, Aldo Pinto, Rosanna Di Paola, Giuseppina Autore, Maria Teresa Ribecco, Britti Domenico, Massimini Genesio, Salvatore Cuzzocrea
    Abstract:

    Septic shock, a severe form of sepsis, is characterized by cardiovascular collapse following microbial invasion of the body. The progressive hypotension, hyporeactivity to vasopressor agents and vascular leak leads to circulatory failure with multiple organ dysfunction and death. Many inflammatory mediators (e.g. TNF-α, IL-1 and IL-6) are involved in the pathogenesis of shock and, among them, nitric oxide (NO). The overproduction of NO during septic shock has been demonstrated to contribute to circulatory failure, myocardial dysfunction, organ injury and multiple organ failure. We have previously demonstrated with in vitro and in vivo studies that Methylguanidine (MG), a guanidine compound deriving from protein catabolism, significantly inhibits iNOS activity, TNF-α release and carrageenan-induced acute inflammation in rats. The aim of the present study was to evaluate the possible anti-inflammatory activity of MG in a model of septic shock induced by lipopolysaccharide (LPS) in mice. MG was administered ...

  • effect of Methylguanidine in carrageenan induced acute inflammation in the rats
    European Journal of Pharmacology, 2004
    Co-Authors: Stefania Marzocco, Raffaella Sorrentino, Aldo Pinto, Rosanna Di Paola, Ivana Serraino, Rosaria Meli, Giuseppina Mattaceraso, Salvatore Cuzzocrea, Giuseppina Autore
    Abstract:

    In vitro and in vivo studies have demonstrated that Methylguanidine, an inhibitor of nitric oxide synthase (NOS), is also able to reduce tumour necrosis factor-alpha (TNF-alpha) release. In the present study, we evaluated the anti-inflammatory potential of Methylguanidine treatment in two models of acute inflammation (carrageenan-induced paw edema and pleurisy) where oxyradical, nitric oxide (NO) and prostaglandins play a crucial role in the inflammatory processes. Our data show that Methylguanidine, given intraperitoneally at the dose of 30 mg/kg, inhibits the inflammatory response reducing significantly (P<0.05) paw swelling, pleural exudates formation, mononuclear cell infiltration and histological injury. Furthermore, our data suggests that there is a significant (P<0.05) reduction in the activity and expression both of the inducible NOS (iNOS) and of cyclooxygenase-2 in lung tissue of pleurisy model. Methylguanidine is also able to reduce the appearance of nitrotyrosine and of the nuclear enzyme poly(adenosine diphosphate [ADP]-ribose) synthase immunoreactivity in the inflamed lung tissues. Treatment with aminoguanidine, the reference drug, significantly reduced all the evaluated pro-inflammatory parameters in carrageenan-treated rats. Taken together, the present results demonstrate that Methylguanidine exerts potent anti-inflammatory effects that could be, in part, related to an inhibition of the expression/activity of the iNOS and cyclooxygenase-2 and, another part, may be related to a reduction of TNF-alpha release.

  • effect of Methylguanidine guanidine and structurally related compounds on constitutive and inducible nitric oxide synthase activity
    Life Sciences, 1997
    Co-Authors: Raffaella Sorrentino, Lidia Sautebin, Aldo Pinto
    Abstract:

    Abstract The inhibitory activity of Methylguanidine, guanidine and their precursors, creatine and creatinine, on both the neuronal constitutive and lung inducible isoforms of nitric oxide synthase were examined in this study. Methylguanidine and guanidine (0.01–3 mM) significantly (P 0.4 for both Methylguanidine and guanidine). In contrast, creatine and creatinine, although containing guanidine group, were totally ineffective on either enzyme even at concentration up to 3 mM. The results obtained for tested compounds also suggest a role for the lateral chain of guanidine group in the enzyme inhibition. The lack of selectivity of Methylguanidine and guanidine in inhibiting both the nitric oxide synthase enzymes could account for some pathological manifestations like neurological disorders, host defense impairment and probably hypertension, that often occur in patients with uremia or chronic renal failure.