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1.
PharmacokineticsofintravenouslyadministeredsodiumdichloroacetateinrabbitsGuBin(顾斌);SongLing(宋岭);JiangYongpei(蒋永培);WenAidong(文...  相似文献   
2.
A convenient synthesis of chloramphenicol labelled with carbon‐14 in the dichloroacetyl group at the 1 position is described. It was prepared as part of a 4‐step sequence from [1 ‐ 14C] glycine and the product was purified by preparative HPLC. A radiochemical yield of 47% was obtained based on [1 ‐ 14C] glycine and the product had a specific activity of 0.47 mCi/mmol. The procedure can be employed for the synthesis of high specific activity [14C] chloramphenicol, labelled at 1, 2 or both the positions of dichloroacetyl group. Copyright © 2005 John Wiley & Sons, Ltd.  相似文献   
3.
Summary Subcutaneous injection of sodium dichloroacetate (1 mg/g body wt every 3 h) in suckling newborn rats caused in 6 h a fall of 2.5 mmol/l in blood glucose concentrations, and a rise of 2.4 mmol/ l in total blood ketone body levels, but no change in the high levels of plasma non esterified fatty acids. Glucose utilization, measured after intraperitoneal injection of D-glucose (2 mg/g body wt), was not increased in newborns injected with dichloroacetate. The hypoglycaemia resulted from a decrease in gluconeogenic rate, secondarily to a lowering effect of dichloroacetate on blood levels of lactate, pyruvate and alanine. The hypoglycaemia induced by dichloroacetate was completely reversed by injecting newborn rats with a mixture of gluconeogenic precursors (lactate, pyruvate and alanine). It is concluded that the high rate of gluconeogenesis observed in suckling newborn rats in sustained by an increased release of lactate and, to a much smaller extent of pyruvate and alanine, by peripheral tissues. This probably resulted from the low pyruvate dehydrogenase activity found in peripheral tissues of the newborn rat. The hyperketonaemia induced by dichloroacetate could result from an increased ketogenesis and/or a decreased ketone body utilization.  相似文献   
4.
目的研究二氯乙酸钠(Sodium dichloroacetate,DCA-Na)、顺铂(DDP)联合对人肺腺癌A549细胞株增殖和凋亡的影响及其作用机制。方法用MTT法检测DCA-Na、DDP应用对A549细胞增殖抑制作用的影响;流式细胞仪(Annexin V-FITC/PI法)检测DCA-Na、DDP单药及两药联合作用于A549细胞凋亡率的变化;用分光光度法检测DCA-Na作用于A549细胞后半胱氨酸天门冬氨酸蛋白酶(Caspase)-3、-8、-9蛋白的活性。结果DCA-Na、DDP单药组均对A549细胞增殖有抑制作用,且呈明显的剂量-时间依赖性。0.4、2μg/mL的DDP与37.5、75、150μg/mL的DCA-Na联合作用A549细胞24、48、72 h后的抑制率显著高于同浓度DDP单药组(P<0.05),且2μg/mL的DDP与75μg/mL的DCA联合在48 h表现为协同作用。流式细胞仪检测显示,A549细胞联合组凋亡率显著高于各单药组(P<0.05)。DCA-Na作用于A549细胞后,分别在12、24、48、72 h测得Caspase-3、-8、-9蛋白活性显著高于对照组(P<0.05)。结论 DCA-Na对人肺腺癌A549细胞的增殖有抑制作用,并且随着药物浓度增加、作用时间延长,其抑制作用也增加(呈剂量和时间依赖性)。一定浓度范围的DCA-Na和DDP联合作用于人肺腺癌A549细胞能够产生协同作用。DCA-Na可诱导人肺腺癌A549细胞凋亡,且与DDP联合后其诱导凋亡作用更为显著。  相似文献   
5.
李民  杨静  邱俊林 《西部医学》2008,20(5):1013-1014
目的观察二氯醋酸二异丙胺联合甘草酸二胺治疗慢性乙型肝炎合并脂肪肝的临床疗效。方法将87例慢性乙型肝炎合并脂肪肝患者随机分为两组:联合组42例,用二氯醋酸二异丙胺联合甘草酸二胺治疗;对照组38例,给予甘草酸二胺治疗,疗程均为8周。结果肝功能:治疗前两组比较差异无显著性(P〉0.05);两组治疗后与治疗前比较差异均有显著性(P〈0.05);治疗后两组比较差异亦有显著性(P〈0.05)。TC(总胆固醇)、TG(甘油三脂):治疗前两组比较差异无显著性(P〉0.05),对照组治疗后与治疗前比较差异无显著性(P〉0.05),治疗后联合组与对照组比较差异有显著性(P〈0.05)。结论二氯醋酸二异丙胺联合甘草酸二胺是治疗慢性乙型肝炎合并脂肪肝的有效药物,可改善肝功能,同时有明显降脂作用。  相似文献   
6.
7.
Reprogramming of metabolism is a well-established property of cancer cells that is receiving growing attention as potential therapeutic target. Oral squamous cell carcinomas (OSCC) are aggressive and drugs-resistant human tumours displaying wide metabolic heterogeneity depending on their malignant genotype and stage of development. Dichloroacetate (DCA) is a specific inhibitor of the PDH-regulator PDK proved to foster mitochondrial oxidation of pyruvate. In this study we tested comparatively the effects of DCA on three different OSCC-derived cell lines, HSC-2, HSC-3, PE15. Characterization of the three cell lines unveiled for HSC-2 and HSC-3 a glycolysis-reliant metabolism whereas PE15 accomplished an efficient mitochondrial oxidative phosphorylation. DCA treatment of the three OSCC cell lines, at pharmacological concentrations, resulted in stimulation of the respiratory activity and caused a remarkably distinctive pro-apoptotic/cytostatic effect on HSC-2 and HSC-3. This was accompanied with a large remodeling of the mitochondrial network, never documented before, leading to organelle fragmentation and with enhanced production of reactive oxygen species. The data here presented indicate that the therapeutic efficacy of DCA may depend on the specific metabolic profile adopted by the cancer cells with those exhibiting a deficient mitochondrial oxidative phosphorylation resulting more sensitive to the drug treatment.  相似文献   
8.
Background: Conventional approaches to management of congestive heart failure (CHF) rely on drugs that increase myocardial contractility or reduce ventricular afterload. These approaches often improve cardiac symptoms and survival, but may be associated with significant deleterious effects. An alternative approach is to enhance myocardial energy production. Dichloroacetate (DCA) stimulates pyruvate dehydrogenase activity and accelerates aerobic glucose, pyruvate, and lactate metabolism in myocardial cells. These alterations would be expected to improve myocardial function. Hypothesis: The purpose of the investigation was to assess the efficacy of DCA in patients with left ventricular systolic dysfunction and to examine the mechanism by which improvement occurs. Methods: A total of 25 patients (16 men, 9 women; age range 31-72 years, mean 59) with CHF and ejection fraction ≤40% received an intravenous infusion of 50 mg/kg DCA over 15 min. Indices of systolic and diastolic function were obtained by two-dimensional and Doppler echocardiography performed at baseline, 30 min, and 60 min following completion of DCA infusion. Results: Baseline ventricular ejection fraction was 27.3 ± 9.1%; 17 patients (68%) had nonischemic cardiomyopathy. Heart rate increased after DCA infusion from 73.9 ± 14.5 to 79.2 ± 14.9 beats/min at 60 min; p = 0.02. Left ventricular diastolic and systolic volumes increased at 30 min compared with baseline (248.7 ± 98.1 vs. 259.6 ± 99.6; p = 0.04, and 180.1 ± 80.4 vs. 192.2 ± 84.9; p = 0.002, respectively), but stroke volume (49.2 ± 19.1 vs. 48.9 ± 18.1; p = 0.9) and ejection fraction (27.3 ± 9.1 vs. 25.7 ± 9.8; p = 0.2) were un changed. Indices of diastolic function were also unchanged. Conclusion: Dichloroacetate infusion in patients with CHF is not associated with improvement in noninvasively assesse left ventricular function.  相似文献   
9.
We administered sodium dichloroacetate (DCA), which reduces the circulating lactate and pyruvate concentrations by stimulating the activity of the pyruvate dehydrogenase complex (PDHC), to three children with mitochondrial encephalomyelopathy. Significant clinical, biochemical and radiologic improvements were obtained following DCA therapy (approximately 30 mg/kg per day, divided into three doses). All three patients had non-pyruvate dehydrogenase complex (PDHC) deficiencies: two exhibited Leigh syndrome (complex I deficiency and unknown etiology), and one abnormal myelination (multienzyme deficiency), demonstrated on magnetic resonance imaging (MRI). The lactic and pyruvic acid concentrations in serum and cerebrospinal fluid (CSF) were decreased significantly by the oral DCA treatment. The lactic acid peak on MR spectroscopy also markedly decreased in parallel with the CSF level. In addition, the brain lesions observed on MRI were improved in all patients. No exacerbation was observed in any of the patients, who have been followed-up more than 21 months following the DCA therapy. These results suggest that DCA therapy should be considered in all patients with a mitochondria-related enzyme deficiency.  相似文献   
10.
Lactic acidaemia is sometimes associated with a defect of the pyruvate dehydrogenase complex (PDHC), catalysing the thiamine-dependent decarboxylation of pyruvate. The activity of PDHC for different thiamine pyrophosphate (TPP) concentrations was determined in 13 patients with lactic acidaemia, clinically responsive to thiamine treatment in order to assess the role of PDHC in the aetiology of thiamine-responsive lactic acidaemia. Culture of lymphoblastoid cells and skin fibroblasts and muscle biopsies were performed in these 13 patients. The activity of PDHC to sodium dichloroacetate (DCA), known as the activator of PDHC, was also examined. Three groups were identified according to PDHC activity. Group 1 (two patients) displayed very low PDHC activity, which was not increased by DCA. This PDHC activity increased at high TPP concentrations. Group 2 (five patients) displayed below normal PDHC activity at low TPP concentrations, increased by DCA. This PDHC activity became normal at high TPP concentrations. PDHC deficiency in these patients of groups 1 and 2 was due to a decreased affinity of PDHC for TPP. Group 3 included six patients with normal PDHC activity at low as well as high TPP concentrations. This PDHC activity was increased by DCA. Conclusion High concentrations of TPP may be required for maximal activity of PDHC in some patients with lactic acidaemia. The assay of PDHC activity, performed at a low concentration of TPP (1 × 10−4 mM) allows selection of patients with thiamine-responsive lactic acidaemia. Received: 21 January 1997 / Accepted: 3 March 1998  相似文献   
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