sis or apoptosis. Necrosis is characterized by cell swelling Toxic bile salts cause hepatocyte necrosis at high conand autolysis with breakdown of the plasma membrane percentrations and apoptosis at lower concentrations. Almeability barrier. 4 In contrast, apoptosis is characterized by though fructose prevents bile salt-induced necrosis, the cell shrinkage, chromatin condensation, nuclear and DNA effect of fructose on bile salt-induced apoptosis is unfragmentation, and ultimately fragmentation of the cell into clear. Our aim was to determine if fructose also protects membrane-defined cell bodies referred to as apoptotic bodies. salt-induced necrosis and apoptosis would be of scientific by 0.2 U. However, extracellular acidification (pH 6.8),and clinical importance. Not only would an understanding of which decreased hepatocyte pH i 0.35 U and is known to the common mechanisms responsible for bile salt-induced inhibit necrosis, actually potentiated apoptosis 1.6-fold.necrosis and apoptosis provide basic information on the Fructose cytoprotection also could not be explained by mechanisms of cell death, but the information may also geninduction of bcl-2 transcription or metal chelation. Beerate strategies for the treatment of cholestatic liver diseases. cause we could not attribute fructose cytoprotection to Cytoprotective agents provide a unique paradigm with metabolic effects, alterations in the expression of bclwhich to help identify the common mechanisms responsible 2, or metal chelation, we next determined if the poorly for cell death. Cytoprotection by an agent against multiple metabolized ketohexoses, tagatose and sorbose, also inmodels or modes of cell death suggests common mechanisms hibited apoptosis; unexpectedly, both ketohexoses inare involved in the death process. Conversely, cytoprotection hibited apoptosis. Because bile salt-induced apoptosis in one model and a lack of protection in another model would and necrosis are inhibited by fructose, these data sugsuggest dissimilar mechanisms of cell death. We have demongest that similar processes initiate bile salt-induced hestrated that fructose, a cytoprotective agent in many models patocyte necrosis and apoptosis. In contrast, acidosis, of cell necrosis, prevents bile salt-induced necrosis of hepatowhich inhibits necrosis, potentiates apoptosis. Thus, ketohexose-sensitive pathways appear to initiate both bile cytes. 6 Fructose cytoprotection is thought to be mediated by salt-induced cell apoptosis and necrosis, whereas dis-glycolytic generation of adenosine triphosphate (ATP) or insimilar, pH-sensitive, effector mechanisms execute these tracellular acidification.9,10 However, the effect of fructose two different cell death processes. (HEPATOLOGY and its metabolic effects on cellular ATP and pH during bile 1997;25:81-86.) salt-induced apoptosis is unknown. Thus, the overall objective of this study was to determine if fructose also protects against bile salt-induced apoptosis. Our specific aims were The impairment of bile flow in chronic cholestatic liver ...
sis or apoptosis. Necrosis is characterized by cell swelling Toxic bile salts cause hepatocyte necrosis at high conand autolysis with breakdown of the plasma membrane percentrations and apoptosis at lower concentrations. Almeability barrier. 4 In contrast, apoptosis is characterized by though fructose prevents bile salt-induced necrosis, the cell shrinkage, chromatin condensation, nuclear and DNA effect of fructose on bile salt-induced apoptosis is unfragmentation, and ultimately fragmentation of the cell into clear. Our aim was to determine if fructose also protects membrane-defined cell bodies referred to as apoptotic bodies. salt-induced necrosis and apoptosis would be of scientific by 0.2 U. However, extracellular acidification (pH 6.8),and clinical importance. Not only would an understanding of which decreased hepatocyte pH i 0.35 U and is known to the common mechanisms responsible for bile salt-induced inhibit necrosis, actually potentiated apoptosis 1.6-fold.necrosis and apoptosis provide basic information on the Fructose cytoprotection also could not be explained by mechanisms of cell death, but the information may also geninduction of bcl-2 transcription or metal chelation. Beerate strategies for the treatment of cholestatic liver diseases. cause we could not attribute fructose cytoprotection to Cytoprotective agents provide a unique paradigm with metabolic effects, alterations in the expression of bclwhich to help identify the common mechanisms responsible 2, or metal chelation, we next determined if the poorly for cell death. Cytoprotection by an agent against multiple metabolized ketohexoses, tagatose and sorbose, also inmodels or modes of cell death suggests common mechanisms hibited apoptosis; unexpectedly, both ketohexoses inare involved in the death process. Conversely, cytoprotection hibited apoptosis. Because bile salt-induced apoptosis in one model and a lack of protection in another model would and necrosis are inhibited by fructose, these data sugsuggest dissimilar mechanisms of cell death. We have demongest that similar processes initiate bile salt-induced hestrated that fructose, a cytoprotective agent in many models patocyte necrosis and apoptosis. In contrast, acidosis, of cell necrosis, prevents bile salt-induced necrosis of hepatowhich inhibits necrosis, potentiates apoptosis. Thus, ketohexose-sensitive pathways appear to initiate both bile cytes. 6 Fructose cytoprotection is thought to be mediated by salt-induced cell apoptosis and necrosis, whereas dis-glycolytic generation of adenosine triphosphate (ATP) or insimilar, pH-sensitive, effector mechanisms execute these tracellular acidification.9,10 However, the effect of fructose two different cell death processes. (HEPATOLOGY and its metabolic effects on cellular ATP and pH during bile 1997;25:81-86.) salt-induced apoptosis is unknown. Thus, the overall objective of this study was to determine if fructose also protects against bile salt-induced apoptosis. Our specific aims were The impairment of bile flow in chronic cholestatic liver ...
Gum arabic (GA) from Acacia senegal var. senegal was orally administered to patients suffering from gout. Out of fifty randomly selected patients, twenty-five patients were given a GA dose of 50 g/day for 120 days, and the remaining twenty-five patients represented the control group. Blood samples were collected from all patients on the first day of administering GA, and once every two weeks. Uric acid, urea, creatinine, haemoglobin (Hb), packed cell volume (PCV) and erythrocyte sedimentation rate (ESR), were determined using standard methods. After a 60 day depletion period, the same parameters were determined using doses of 75 and 25 g/day of GA. The results indicate that GA consumption reduces average serum uric acid levels in both male and female gout patients in a dose dependent manner, higher doses (50 and 75 g/day) causing uric acid levels to fall below normal levels. Urea and creatinine levels, which were initially within the normal range, also decreased significantly in a GA dose dependent manner. Hb and PCV levels, which were initially decreased (compared to the control group), increased significantly in a GA dose dependent manner back towards normal (control group) levels, and at the highest GA dose (75 g/day) increased beyond normal levels. ESR levels, which were initially elevated (compared to the control group), decreased significantly in a GA dose dependent manner back towards normal (control group) levels, and at the higher GA doses (50 and 75 g/day) decreased below normal levels.
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