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The uptake of iron by the liver and cerebellum was measured in rats using [59Fe]transferrin. An acute ethanol load (50 mmol/kg body wt., i.p.) elicited a significant increase in the hepatic and cerebellar non-heme iron concentration. The uptake of 59Fe by the liver and the cerebellum was significantly greater in the ethanol-treated rats than in control animals. The administration of allopurinol prior to the ethanol load prevented the changes in liver and cerebellar non-heme iron content. Moreover pretreatment with allopurinol reduced the ethanol-induced enhancement of 59Fe uptake by the liver and completely prevented the changes in 59Fe uptake by the cerebellum. These effects of allopurinol lead us to suggest that oxygen-derived free radicals are involved in the ethanol-induced disturbances of iron uptake both at the hepatic and cerebellar level.
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A patient with acute oliguric uric acid nephropathy was treated with hemodialysis. Recovery in this disorder is based on treatment of both the uremic state and the intrarenal crystal obstruction. Hemodialysis with high uric acid clearance is much more efficient than other forms of therapy in this disorder.
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A method of measuring the inhibition of sulfation in mucopolysaccharides employed the coupled enzyme system of Wortman. This procedure utilized the phenol and mucopolysaccharide sulfotransferases of beef cornea extract. Compounds tested against this system included amino acids, salicylates, 2-mercaptoethylamine and a derivative, heterocyclic ethanethiosulfuric acids, arylsulfonamidoethanethiosulfates, and several other compounds. In general, the salicylates and thiosulfates were inhibitory, with sodiumm 2-(4-acetamidobenzenesulfonamido)-ethanethiosulfate being the most inhibitory and 2-mercaptoethylguanidine trithiocarbonic acid the second most inhibitory. Salicylamide and allopurinol, which have been employed in kidney stone therapy, were inhibitors. Kidney stones have a mucopolysaccharide sulfate matrix, which is involved in their growth.
: Six RCTs totaling 1554 patients undergoing ERCP were included. When the RCTs were analyzed, odds ratios of allopurinol were 0.74 (95% confidence interval [CI], 0.37-1.48; P = 0.40) for PEP, 0.87 (95% CI, 0.33-2.28; P = 0.78) for severe PEP, 0.88 (95% CI, 0.37-2.11; P = 0.78) for post-ERCP hyperamylasemia, and 0.19 (95% CI, 0.01-3.91; P = 0.28) for case-fatality ratio of PEP, thus indicating no beneficial effects of allopurinol on acute pancreatitis, PEP death rate, and hyperamylasemia. No evidence of publication bias was found.
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Three hundred and sixty ADRs in 294 adults and 66 children were analysed. The prescription was considered inappropriate for 213 of the 659 (32%) drugs implicated in ADRs, corresponding to 161 patients (45%). The ADR was adjudged entirely avoidable for 32 (9%) patients, partly avoidable for 28 (8%) patients and unavoidable for 300 (83%) patients. Not taking into account a history of allergy or altered renal function and not respecting the recommended dose were the most frequent causes of entirely avoidable ADRs. Allopurinol and lamotrigine were the drugs most frequently involved in serious avoidable ADRs.
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Oxidative stress may contribute to heart failure (HF) progression. Inhibiting xanthine oxidase in hyperuricemic HF patients may improve outcomes.
To present the diagnosis and management of gouty arthropathy of the lumbar spine in one individual.
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The potential fast screening method is an ideal tool to rule out the high-risk allopurinol-induced SCARs patients.
Of the 88 patients, 41 were SJS/TEN and 47 were DRESS. Mortality rates of TEN and DRESS were 9.8 and 2.1%, respectively. Allopurinol and carbamazepine were the most common causes of both SJS/TEN and DRESS (34.7 and 62.9%, respectively). Some of the systemic presentations, such as fever and laboratory abnormalities were common in both phenotypes. Thrombocytopenia tended to be related to prolonged hospitalization (longer than 3 weeks) in SJS/TEN (odds ratio, OR = 5.1, 95% confidence interval, CI 0.8-31.8, p = 0.076). In DRESS patients, leukocytosis at presentation (OR 4.8, 95% CI 1.1-20.3, p = 0.03) was related to prolonged hospitalization.
Bile flow and bile acid output were increased by pretreatment of the livers with prostaglandin I2 and prostaglandin E1, as compared to the control group. More specifically, the maximum transport rate was tripled by prostaglandin I2 and by prostaglandin E1 preconditioning of liver grafts, in comparison to the control group (P < .01 vs prostaglanin I2 and E1).
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Gout is the most common inflammatory arthritis in men and is increasingly prevalent. Allopurinol is very effective at reducing plasma urate concentrations to a level sufficient to dissolve monosodium urate crystals. However, many patients fail to achieve a sufficient therapeutic response to allopurinol. Areas covered: This review covers the metabolism and pharmacokinetics of allopurinol and its active metabolite, oxypurinol and how these factors affect the plasma concentrations of urate at initiation and during long-term therapy with allopurinol. Significant aspects discussed are the importance of adherence to allopurinol therapy, allopurinol hypersensitivity reactions and insights into hyperuricemia. Expert opinion: The initial dosage of allopurinol should be low, particularly in patients with renal impairment. The dose should then be increased slowly until plasma concentrations of urate are sufficient to dissolve monosodium urate crystals (≤ 0.36 mmol/L). For this target, the maintenance dose of allopurinol can be estimated from the equation: Dose = 1413*(Up-0.36) where Up is the pre-treatment concentration of urate. Poor adherence is a major factor limiting successful therapy with allopurinol; however, its use can be improved considerably by education of patients and clinicians. Allopurinol is generally well tolerated and screening for genetic factors predictive of allopurinol hypersensitivity reactions can now be undertaken.
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Ninety cases of AGA were randomly divided into an EA group, an allopurinol group and a probenecid group, 30 cases in each group. The EA group were treated by EA at Sanyinjiao (SP 6), Fenglong (ST 40), Yinlingquan (SP 9), once a day; the allopurinol group by oral administration of Allopurinol, twice a day, 100 mg each time and the probenecid group by oral administration of Probenecid, twice daily, 0.25 g each time. Contents of blood uric acid (BUA) and urinary uric acid (UUA) in each group were detected.
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Hyperpolarized arrest with the potassium channel opener pinacidil has been shown to provide effective myocardial protection during short-term global ischemia. This study tested the hypothesis that pinacidil may provide effective long-term protection for heart transplant preservation.
Very little is known about iron metabolism and the mediators of iron metabolism in liver subjected to cold storage before transplantation. Therefore, in this study, we investigated the effect of cold storage on iron homeostasis in the rat liver. When livers were stored at 4 degrees C in University of Wisconsin solution for up to 6 and 24 hours, significant increases occurred in the labile iron pool, ferritin protein, and heme oxygenase activity. Significant decreases in heme content and iron regulatory protein 1 and 2 binding activities occurred by 24 hours. Liver injury indicated by significant increases in University of Wisconsin solution transaminase activity and liver lipid hydroperoxide levels occurred by 6 and 24 hours. Taken together, these results suggest that during pretransplantation cold storage of the liver, an aberrant iron homeostasis develops that contributes to preservation injury, and predisposes the liver to reperfusion injury by iron-dependent reactive oxygen species/Fenton reaction.
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Two tertiary care, referral hospitals in Johannesburg, South Africa.
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Patients clinically diagnosed with gout and baseline SUAs were identified in two South Auckland practices. A mail and phone intervention was introduced aimed at improving the control of gout. Intervention #1 took place in one practice over three months. Intervention #2 occurred in the other practice four to 16 months following baseline.
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After extended ischemia LPD provided superior graft function in respect to DLC (repeated measures ANOVA; LPD versus rEC P < 0.05; versus EC P < 0.03; versus UW P < 0.05) and AaDO2 (LPD versus rEC P < 0.04; versus EC P < 0.006). The PVR was significantly lower in LPD versus UW (P < 0.05). At the end of reperfusion the weight increase amounted to 229 +/- 49% in rEC, 207 +/- 22% in EC, 115 +/- 22% in UW and 87 + 17% in LPD (LPD versus rEC P < 0.01, LPD versus EC P < 0.001). The type of preservation solution used had little impact on graft function after 2 h ischemia.
Allopurinol reduced the concentrations of serum TNF-alpha when used at different times of ischemia followed by reperfusion, which might indicate reduction of the inflammation provoked by the reperfusion injury.
Blood chemerin concentration shows positive correlation not only with body mass index and serum triglyceride level but also with systolic blood pressure. While it seems likely that chemerin influences vascular smooth muscle cell (SMC) proliferation and migration, which are crucial to the development of hypertension, this remains to be clarified. In the present study, we investigated whether chemerin controls SMC proliferation and migration in vitro and also affects blood pressure in vivo. In vitro, chemerin significantly stimulated rat mesenteric arterial SMC proliferation and migration, as determined by a cell counting assay and Boyden chamber assay, respectively. The migratory effect of chemerin was confirmed in human aortic SMCs. Chemerin significantly increased ROS production in SMCs and phosphorylation of Akt (Ser(473)) and ERK, as measured by fluorescent staining and Western blot analysis, respectively. Various inhibitors (ROS inhibitor: N-acetyl-l-cysteine, phosphatidylinositol 3-kinase inhibitor: LY-294002, MAPKK inhibitor: PD-98059, NADPH oxidase inhibitor: gp91 ds-tat, and xanthine oxidase inhibitor: allopurinol) as well as chemokine-like receptor 1 small interfering RNA significantly inhibited chemerin-induced SMC proliferation and migration. Furthermore, chemerin-neutralizing antibody prevented carotid neointimal hyperplasia in the mouse ligation model. In vivo, chronic chemerin treatment (6 μg/kg, 6 wk) increased systolic blood pressure as well as phosphorylation of Akt and ERK in the mouse isolated aorta. In summary, we, for the first time, demonstrate that chemerin/chemokine-like receptor 1 stimulates SMC proliferation and migration via ROS-dependent phosphorylation of Akt/ERK, which may lead to vascular structural remodeling and an increase in systolic blood pressure.
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1. The anthelmintics disophenol (2,6-diiodo-4-nitrophenol), nitroxynil (3-iodo-4-hydroxy-5-nitrobenzonitrile) and nitrodan (3-methyl-5-(4-nitrophenylazo)rhodanine) were reduced in vitro to the corresponding amines by intact Ascaris suum, Moniezia expansa, by enzymes prepared from these helminths, and by mouse- and sheep-liver homogenates. Helminth reductases required NADH2 and glutathione as cofactors and were inhibited about 50% by 2.0 x 10(-7) M allopurinol. Azo bonds of nitrodan and its analogues were not reduced by the helminths but were reduced by mouse- and sheep-liver enzymes. 2. Mouse- and sheep-liver enzymes, in addition to effecting nitro reduction, metabolized nitroxynil by hydrolysis to 3-iodo-4-hydroxy-5-nitrobenzamide and 3-iodo-4-hydroxy-5-nitrobenzoic acid. No hydroxylation products were found. Nitrodan was oxidized by the mammalian microsomal oxidation enzyme system to the thiazolidinedione derivative, but not by helminth enzymes.
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Reactive oxygen species play an important role in pathogenesis of a variety of pathological processes, e.g., ischemia-reperfusion, acute viral infections, thermal injury, hepatic diseases, and acute lung injury. Xanthine oxidase (XO) may be a significant source of these cytotoxic oxygen species. We tested the hypothesis that hepatic ischemia-reperfusion releases xanthine dehydrogenase + XO (XDH + XO) into the circulation and that circulating XO damages isolated perfused lung. Isolated liver + lung preparation was perfused with Krebs-Henseleit buffer to minimize confounding effects of circulating neutrophils. In one group, livers were rendered globally ischemic for 2 h and then reperfused (I/R). In another group, livers were pretreated with allopurinol and perfused with buffer containing additional allopurinol (I/R + Allo). After 2 h of ischemia, an isolated lung was connected to liver, and liver + lung preparation was reperfused in series for 15 min. Liver reperfusion was terminated, and lung was recirculated with liver effluent for 45 min. Capillary filtration coefficient (ml.min-1.cmH2O-1.100 g lung dry wt-1) was 2.0 +/- 0.3 and 1.9 +/- 0.4 in control and I/R + Allo lungs, respectively, and 9.0 +/- 1.2 in I/R lungs (P < 0.001). Lung wet-to-dry weight ratio in control and I/R + Allo lungs was 8.6 +/- 0.3 and 9.1 +/- 0.5, respectively, and 14.9 +/- 1.1 in I/R lungs (P < 0.01). Control and I/R + Allo bronchoalveolar lavage protein content was < 1.0 mg/ml compared with 32.6 +/- 8.4 mg/ml in I/R group.(ABSTRACT TRUNCATED AT 250 WORDS)
Previous in vitro studies in our laboratory have shown that mancozeb (MZ) and maneb (MB), both widely used EBDC fungicides, are equipotent neurotoxicants that produce cell loss in mesencephalic dopaminergic and GABAergic cells after an acute 24h exposure. Mitochondrial uncoupling and inhibition were associated with fungicide exposure. Inhibition of mitochondrial respiration is known to increase free radical production. Here the mechanism(s) of neuronal damage associated with MZ exposure was further explored by determining the role that reactive oxygen species (ROS) played in toxicity. Damage to mesencephalic dopamine and GABA cell populations were significantly attenuated when carried out in the presence of ascorbate or SOD, indicative of a free radical-mediated contribution to toxicity. ROS generation monitored by hydrogen peroxide (H(2)O(2)) production using Amplex Red increased in a dose-dependent manner in response to MZ. Inhibition of intracellular catalase with aminotriazole had little effect on H(2)O(2) generation, whereas exogenously added catalase significantly reduced H(2)O(2) production, demonstrating a large extracellular contribution to ROS generation. Conversely, cells preloaded with the ROS indicator dye DCF showed significant MZ-induced ROS production, demonstrating an increase in intracellular ROS. Both the organic backbone of MZ as well as its associated Mn ion, but not Zn ion, were responsible and required for H(2)O(2) generation. The functionally diverse NADPH oxidase inhibitors, diphenylene iodonium chloride, apocynin, and 4-(2-aminoethyl)benzene-sulfonyl fluoride hydrochloride significantly attenuated H(2)O(2) production by MZ. In growth medium lacking cells, MZ produced little H(2)O(2), but enhanced H(2)O(2) generation when added with xanthine plus xanthine oxidase whereas, in cultured cells, allopurinol partially attenuated H(2)O(2) production by MZ. Minocycline, an inhibitor of microglial activation, modestly reduced H(2)O(2) formation in mesencephalic cells. In contrast, neuronal-enriched cultures or cultures treated with MAC-1-SAP to kill microglia, did not show an attenuation of ROS production. These findings demonstrate that Mn-containing EBDC fungicides such as MZ and MB can produce robust ROS generation that likely occurs via redox cycling with extracellular and intracellular oxidases. The findings further show that microglia may contribute to but are not required for ROS production by MZ.
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Antioxidants may reduce pancreatic cellular injury after coronary artery bypass grafting (CABG) Twenty patients (Group A) received vitamin E (600 mg/ day) for 28 days and vitamin C (2 g/day) and allopurinol (600 mg/day) 2 days before and 1 day after CABG. Seventeen patients (Group C) received all drugs for 3 days, and 25 (Group B) and 19 (Group D) patients served as corresponding controls. The pre- and postoperative pancreatic isoamylase (P-amylase), creatinine, and antioxidant concentrations were measured. Serum hyperamylasemia was highest on the first postoperative day and occurred in 73% of the patients. After surgery serum P-amylase increased in all study groups and urine P-amylase decreased. Postoperative serum hyperamylasemia, whether primarily renal or pancreatic, cannot be decreased by pretreatment with allopurinol, vitamin C, and vitamin E.
We sought evidence that azathioprine causes cell death through reduced glutathione (GSH) depletion and mitochondrial injury.