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991.
Recent interest in the neurotoxicity of haloperidol is based on its oxidation in rodents to the pyridinium derivative, HPP+, a structural analog of the neurotoxin, 1-methyl-4-phenylpyridinium (MPP+). Recently, we reported that HPP+ and a newly identified reduced pyridinium, RHPP+, were present in blood and urine of haloperidol-treated schizophrenics and that the concentrations of RHPP+ exceeded those of HPP+. In this study, we examined pathways for formation of RHPP+ in subcellular fractions of human liver (n=5) and brain (basal ganglia;n=5). The major pathway was reduction of HPP+ (20 µM) to RHPP+ in cytosol (0.17–0.39 and 0.03–0.07 µM RHPP+/g cytosolic protein per h in liver and brain, respectively). The reactions were inhibited significantly by menadione and in brain also by daunorubicin. The inhibition profile, cytosolic location and strict NADPH dependence suggest that the enzymes involved are ketone reductases. A second pathway was oxidation of reduced haloperidol (50 µM), a major metabolite of haloperidol in blood and brain, to RHPP+. In liver microsomes, 0.17–0.63 µmol RHPP+ was formed /g microsomal protein per h. A potent inhibitor of the pathway was ketoconazole (IC50, 0.8 µM), which suggests that P-450 3A isozymes could be involved. In brain mitochondria but not microsomes, reduced haloperidol (120 µM) was oxidised to RHPP+ at a small but significant rate (0.005–0.020 µmol RHPP+/g mitochondrial protein per h) which was not attenuated by SKF 525A, quinidine, ketoconazole, or monoamine oxidase inhibitors. Further studies are warranted to establish the biological importance of these metabolites in vivo. 相似文献
992.
Recent studies have shown that tetrafluoroethylene is a renal and hepatic carcinogen in the rat. In this study, we have examined
the ability of a single i.p. dose of 1,1,2,2-tetrafluoroethyl-l-cysteine (TFEC), a major metabolite of tetrafluoroethylene, to produce hepatic and renal injury in male and female rats.
We have also examined the effect of blocking the renal organic anion transport system with probenecid and of inhibiting the
activity of cysteine conjugate β-lyase with aminooxyacetic acid on the extent of renal injury produced by TFEC. Doses of ≥12.5 mg/kg
TFEC produced renal tubular necrosis to the pars recta of the proximal tubules within 24 h in both male and female rats. This
was associated with an increased kidney to body weight ratio and plasma urea at doses of ≥25 mg/kg. No consistent evidence
of liver injury was seen at doses up to 50 mg/kg TFEC in rats of either sex, although occasional vacuolation of hepatocytes
and a small dose-related increase in liver to body weight ratio was observed. Prior treatment of female rats with probenecid
completely prevented the renal injury produced by either 25 or 50 mg/kg TFEC as judged by plasma urea and histopathology.
However, prior treatment of female rats with aminooxyacetic acid afforded no protection against the nephrotoxicity produced
by either TFEC or the cysteine conjugate of hexachloro-1,3-butadiene. Thus no major sex difference in nephrotoxicity in the
rat was seen with TFEC, while accumulation of TFEC, or its N-acetyl derived metabolite, into renal proximal tubular cells
via a probenecid sensitive transport system appears to be a key event in the mechanism of nephrotoxicity. The lack of protection
observed with the cysteine conjugate β-lyase inhibitor, aminooxyacetic acid, may reflect the inability to completely inhibit
the mitochondrial form of this enzyme and thereby prevent the formation of the reactive metabolite. Our acute studies provide
no insight concerning the liver carcinogenicity of tetrafluoroethylene.
Received: 8 December 1997 / Accepted: 3 February 1998 相似文献
993.
A new method is presentd for the quantitative determination of regional blood volumes in vivo. It is based on rapid quantitative T1 mapping by Snapshot FLASH MRI combined with the injection of an intravascular MR contrast agent. Regional blood volumes in four different tissues of the rat (skeletal muscle, heart, liver, kidney) were determined in an In vivo experiment. 相似文献
994.
Schmidt S.; Giessel R.; Bergis K. H.; Strojek K.; Grzeszczak W.; Ganten D.; Ritz E.; the Diabetic Nephropathy Study Group 《Nephrology, dialysis, transplantation》1996,11(9):1755-1761
BACKGROUND.: There is agreement that a family history of hypertension (HT),is a predictor for the risk of diabetic nephropathy (DN) inpatients with type 2 diabetes, and possibly also type 1 diabetes.It follows that genes related to the risk of hypertension mustalso be considered candidate genes for DN. The 235T allele ofthe angiotensinogen gene was found to be related to primaryHT. METHODS.: To examine whether it is predictive for DN as well, we examinedthe angiotensinogen gene polymorphism in 230 healthy local controls,423 patients with type 1 diabetes (n=180 with DN; n=243 withoutDN) and 663 patients with type 2 diabetes (n=310 with DN; n=353without DN). The angiotensinogen gene M235T polymorphism wasdetermined using PCR amplification. RESULTS.: The following results were obtained (i) no significant differenceof genotype distribution (type 1: MM/MT/TT(%) 27.6/57.2/15.2vs. 27.2/56.1/16.7 (P=0.92); type 2: MM/MT/TT (%) 31.7/48.2/20.1vs. 32.9/46.8/20.3 (P=0.93)) or allele frequencies (type 1:M 0.56 vs. 0.55 (P=0.795); type 2: M 0.56 vs. 0.56 (P=0.86))was found, between diabetic patients with or without DN, (ii)no difference was found between normotensive and hypertensivediabetic patients. CONCLUSION.: The data argue against a role of the angiotensinogen gene M235Tpolymorphism in the manifestation of diabetic nephropathy orhypertension in diabetic patients. 相似文献
995.
The binding of type I collagen to its receptor initiates platelet aggregation, but the relationship of the receptor to other signal transduction components is not yet established. Correlation of platelet aggregation and anti-type I collagen receptor antibody immunoprecipitation of type I collagen treated [32PO4]-labeled platelets showed that there are two phosphoproteins (Mr 53 kDa and 21 kDa) that coprecipitated with the 65 kDa platelet type I collagen receptor. In the present investigation, we have identified one of the phosphoproteins. A soluble component the 100,000×g supernatant fraction of 53 kDa protein is recognized by polyclonal anti-PP1 antibody. The activity of the precipitated phosphatase is inhibited by okadaic acid and inhibitor 1, suggesting that it is protein phosphatase 1 (PP 1). Phosphorylation decreases PP 1 activity as was found with [32PO4]-phosphorylase b as the substrate. The immunocoprecipitation of the type-1 collagen receptor and PP 1 inot the result of cross reactivity of the anti-type I collagen receptor antibody with the PP I protein. These results indicate that the platelet type I collagen receptor, PP 1, and unidentified 21 kDa protein are in close association with the platelet type I collagen receptor upon the binding of type I collagen by the receptor. Copyright © 1996 Elsevier Science Ltd 相似文献
996.
997.
BORIS STRASBERG SHIMON ABBOUD JAIRO KUSNIEC SHULA INBAR NILI ZAFRIR AVIV MAGER ALIK SAGIE SAMUEL SCLAROVSKY 《Pacing and clinical electrophysiology : PACE》1993,16(11):2118-2126
One hundred consecutive patients recovering from an acute myocardiai infarction underwent, prior to home discharge, signal-averaged electrocardiography (ECG), left ventriculography. and 24-hour Holter ECG recording. The signal-averaged ECG was recorded and analyzed using two procedures: the orthogonal bipolar XYZ lead configuration with a bidirectional filter: and a precordial unipolar lead configuration with a uonrecursive digital filter. An abnormal signal-averaged ECG was seen in 40% of patients with the XYZ system and in 30% of patients in the precordial method, abnormal ejection fraction (< 40%) in 24% of patients and high grade ectopy activity in 22%. During the 24-month follow-up period, 12 patients (12%) had an arrhythmic event defined as either sudden death (11 patients) or sustained ventricular tachycardia (1 patient). Neither the signal-averaged ECG with the XYZ configuration, the abnormal ejection fraction, nor the high grade ectopy were able to statistically predict a higher arrhythmic event rate. The signal-averaged ECG with the precordial configuration was able to statistically predict a higher arrhythmic event rate, P < 0.03; odds ratio = 3.96. The combination of the orthogonal XYZ configuration signal-averaged ECG with the ejection fraction (P < 0.01, odds ralio = 7.33), or with ejection fraction and Holter monitoring (P < 0.06. odds ratio = 6.17) was able to predict a higher arrhythmic event rate. The combination of the precordial configuration signal-averaged ECG with the ejection fraction (P < 0.002, odds ratio = 14.4), or with ejection fraction and Holter monitoring (P < 0.06. odds ratio =10) was able to better predict a higher arrhythmic event rate. The combination of a normal or abnormal signal-averaged ECG and ejection fraction gave a sensitivity, specificity, positive, or negative value prediction of arrhythmic events of 60%, 90.6%, 37.5%, and 96%, respectively. It must be emphasized that the number of arrhythmic events during the 2-year follow-up was small and further study is required to determine the true predictive value of each method for arrhythmic events. 相似文献
998.
NO与PGE1对肺动脉高压犬血流动力学影响的对比研究 总被引:5,自引:0,他引:5
对比研究了吸入NO与静脉输注PGE1治疗肺微血管栓塞肺动脉高压犬的血流动力学效果,结果表明,NO与PGE1均显著降低肺动脉压和肺循环阻力,但PGE1显著影响体循环,而NO组心率、血压和体循环阻力均无明显变化,提示NO比PGE1更具有肺血管扩张选择性,治疗肺动脉高压NO明显优于PGE1。 相似文献
999.
目的 调查农村5岁以下儿童肺炎死亡相关的社会危险因素.方法1995年11月—1997年2月在湖北恩施和建始两个贫困地区对5岁以下儿童肺炎死亡的危险因素进行病例—对照研究,死亡病例组226例,肺炎对照组 452例.结果 引起儿童肺炎死亡的社会-经济危险因素有:家庭的人均年收入少于 450元、母亲没有立即带孩子看病的理由是没钱看病或交通不便、家中曾有过一个孩子死亡、家长和村医生的文化程度低、父亲的职业是农民、居室内有火炉、母亲对疾病的认识不够、医生的专业培训不足等.结论 除生物相关因素外,社会危险因素同样是农村5岁以下儿童肺炎死亡的重要因素.它们中某些因素是可以借助对父母的健康教育和急性呼吸道感染病例标准管理而得到控制. 相似文献
1000.
Theodore A. Henderson Robert W. Rhoades Carol A. Bennett-Clarke Pat A. Osborne Eugene M. Johnson Mark F. Jacquin 《The Journal of comparative neurology》1993,336(2):243-260
Prior studies indicate that neonatal nerve injury kills many trigeminal (V) first- and second-order cells, and interrupts pattern formation in the brainstem and cerebral cortex. Yet it is not known whether effects upon cell survival and pattern formation are causally related. To determine whether axotomized V ganglion cells can be rescued by an exogenous trophic agent, rats received 5 mg/kg of nerve growth factor (NGF) prior to, and every day after, infraorbital nerve section on the day of birth until sacrifice on postnatal day (PND) 1, 3, 5, 7, or 14. Other animals received identical lesions without NGF. Ganglion cell numbers were significantly reduced by PNDl in pups not given NGF, while NGF-treated rats displayed no significant cell loss through PND7. However, NGF did not permanently rescue V neurons because ganglion cell numbers were reliably reduced by PND14. Cell numbers in V nucleus principalis were reduced by PNDl in pups not given NGF, while NGF-treated animals displayed no cell loss through PND14. NGF's rescue of second-order cells is probably an indirect effect of NGF actions upon V ganglion cells because, in other newborns, NGF failed to maintain principalis cells after direct lesion of the left V ganglion. To determine whether preventing cell death permits whisker-related pattern formation, other rats also received NGF prior to and after infraorbital nerve section at birth. After 3–14 days, patterns were assessed in the brainstem and cortex with cytochrome oxidase histochemistry and serotonin immunocytochemistry. Whisker-related patterns failed to develop as in cases not given NGF. These data indicate that communication with the periphery is necessary for the maintenance of central whisker-related patterns. They also suggest that V ganglion cells can be rescued, albeit temporarily, from rapid injury-induced death by NGF, thereby delaying injury-induced cell death in nucleus principalis. However, the mechanism(s) responsible for injury-induced pattern alterations in the developing V system remains to be elucidated. © 1993 Wiley-Liss, Inc. 相似文献