光度法连续测定铝合金中的铜铁

本文介绍了在同一溶液中用二环已酮草酰双腙(BCO)光度法测定铜和磺基水扬酸(SaL)光度法测定铁的分析方法,铜和铁显色后的吸收峰分别是(?)=600nm,(?)=430nm,互不干扰,实现了连续测定.方法的精确度高,且稳定性和重现性好.其灵敏度分别为ε_(cu)=1.6×10~4.ε_(Fe)=9×10~3.1 试验部分1.1 试剂与仪器721A型分光光度计H_2O_2:30%柠檬酸铵、磺基水杨酸:50?O:0.025%,称取0.25g BCO溶于热乙醇100ml中,冷却后以水稀释至1L.铜和铁混合标准溶液:分别移取含铜、铁均为0.500mg.ml~(-1)的标液各25ml于250ml量瓶中,以水稀释至刻度,摇匀.此溶液中含铜和铁各50μg·ml~(-1).     

微量元素与帕金森病

帕金森病是世界公认的第二大神经系统疾病,我国目前的患病人数已超过245万,已成为影响我国人口健康水平的重大社会问题。帕金森病的病因至今不清。该文在分析该病流行状况、危险因素的基础上,探讨了微量元素与帕金森病的相关关系,以及微量元素组学研究用于该病预警和早期诊断的可能性。     

火焰原子吸收光谱法测定苦黄注射液及其中药材中五种金属元素

用硝酸和过氧化氢消化样品，通过基体改进剂，使用火焰原子吸收光谱法测定苦黄注射液及其中药材大黄、茵陈、柴胡、苦参中铜、铁、锌、钾和钠的含量。方法的回收率在92．6％～112．1％之间，相对标准偏差小于4％。     

重铬酸钾滴定法测定废杂铜中的铁含量

研究了废杂铜中铁含量的测定方法.试料采用盐酸、硝酸、高氯酸溶解,加入过量氨水生成氢氧化铁沉淀与铜、铬等干扰元素分离,沉淀用热盐酸溶解后,用氯化亚锡还原至溶液呈浅黄色,重铬酸钾滴定法测定铁含量.探讨了溶样方式、氯化铵用量、氨水过量的体积、硫磷混酸用量对测定结果的影响.对4个废杂铜样品中的铁含量进行测定,测定结果的相对标准...     

火焰原子吸收法测定癌细胞中的钙、镁、铜等金属元素

采用火焰原子吸收法直接测定一系列(食道、胃)癌细胞及其近旁的正常细胞中的钙、镁、铜等金属含量。结果表明，钙的变异系数为1．83％-4．19％，回收率为99．8％-104．0％；镁的变异系数为0．02％～1．18％，回收率为97．2％-98．5％；铜的变异系数为3．80％-6．68％，回收率为90．5％～99．7％；均得到较满意的结果，具有一定的参考价值。     

火焰原子吸收光谱法测定天佛参口服液及其原料药中五种金属元素

样品经硝酸和过氧化氢消化,用火焰原子吸收光谱法测定其中铜、铁、锌、钾和钠5种金属元素的含量。为克服共存组分的干扰,测定铁（Ⅲ）须在盐酸（2＋98）溶液中进行,测定锌（Ⅱ）则应在正丁醇-水（6＋94）溶液中进行,测定铜（Ⅱ）、钾（Ⅰ）及钠（Ⅰ）则在硝酸（2＋98）溶液中进行。上述各溶液的总体积均为250mL。应用此法分析...     

流动注射在线柱预富集-电感耦合等离子体原子发射光谱测定痕量金属元素

本文报道了流动注射在线柱预富集ICP光谱测定痕量金属的方法,以meso-四(4-磺基苯)卟啉为柱前衍生试剂,硅胶作固定相和盐酸作洗脱液,对痕量金属离子Cu、Mn、Ni、Fe、Pb、Cd进行在线预富集检测。在给定实验条件下,方法的富集倍数为9.3～11.3,检出限和测定的相对标准偏差(n=6)分别在0.32～26.8ng/ml和1.3％～3.0％范围内。方法用于小牛肝和西红柿叶样品分析,结果与参考值吻合。     

碘量法连续测定选矿废水中的铜铁

针对选矿废水中的铜离子和铁离子,在滴定铜离子含量的基础上,向滴定液中继续加入三氯化铝溶液作为解蔽剂将铁离子解蔽,此时溶液呈深棕色,以硫代硫酸钠标准溶液继续滴定铁,溶液深棕色消失转为奶白色即为滴定终点,避免了单独滴定铜铁含量的麻烦,且在滴定铁离子含量时无需除铜。经实验验证,对选矿废水中铁含量进行滴定与重铬酸钾滴定铁含量的结果一致,相对误差小于2.03%,加标回收率在95.8%~101.9%,相对标准偏差(RSD,n=10)在0.48%~1.5%。方法精密度高,重现性好,简便快捷,可以满足选矿废水中铜、铁含量的测定要求。     

Application of Synchrotron Radiation in Neuromicrobiology: Role of Iron in Parkinson's Disease

In order to understand the role of iron (Fe) in the oxidative stress underlying the pathogenesis of Parkinson's disease (PD) and parkinsonism–dementia complex (PDC), we investigate distributions and chemical states of Fe within a single neuron of the two disease cases, using synchrotron radiation (SR) micro beam. In the X-ray fluorescence (XRF) spectroscopic study, an excessive accumulation of Fe can be seen in the melanized neurons and free-neuromelanin (MN) aggregates in the substantia nigra tissue of both PD and PDC midbrains. X-ray absorption near-edge structure (XANES) analyses of PD revealed that the chemical state of Fe in the melanized neurons and free-MN aggregates shifted toward Fe³⁺ with a pre-edge peak at Fe K-edge due to a 1s 3d transition, indicating a breaking of the inversion symmetry around the Fe site. In PDC, however, the melanized neurons and free-MN aggregates showed mixed states of Fe²⁺ and Fe³⁺ without any pre-edge peak in the spectra. This tendency was also observed in the control case. These results suggest that the changes in distributions and chemical states of Fe may endogenously play a crucial role in the oxidative damage of the melanized neurons in PD, but through a different mechanism other than PDC.     

左旋多巴与帕金森氏病

帕金森氏病是一种典型的中老年疾病。本文介绍了左旋多巴的物化性质和分子的立体结构,概述了帕金森氏病的典型特征以及左旋多巴治疗帕金森氏病的机理和药理。     

Flavonoids in Treatment of Chronic Kidney Disease

Chronic kidney disease (CKD) is a progressive systemic disease, which changes the function and structure of the kidneys irreversibly over months or years. The final common pathological manifestation of chronic kidney disease is renal fibrosis and is characterized by glomerulosclerosis, tubular atrophy, and interstitial fibrosis. In recent years, numerous studies have reported the therapeutic benefits of natural products against modern diseases. Substantial attention has been focused on the biological role of polyphenols, in particular flavonoids, presenting broadly in plants and diets, referring to thousands of plant compounds with a common basic structure. Evidence-based pharmacological data have shown that flavonoids play an important role in preventing and managing CKD and renal fibrosis. These compounds can prevent renal dysfunction and improve renal function by blocking or suppressing deleterious pathways such as oxidative stress and inflammation. In this review, we summarize the function and beneficial properties of common flavonoids for the treatment of CKD and the relative risk factors of CKD.     

Thin Films of Molecular Metals TTF-TCNQ

We present recent results on the characterization of highly ordered polycrystalline thin films of the charge transfer salt TTF-TCNQ (TTF=tetrathiafulvalene, TCNQ=tetracyanoquinodimethane) prepared by thermal sublimation in high vacuum under different conditions. The increase in orientation and microcrystal size as a function of substrate and annealing temperatures is addressed. A consequence of such an increase is the reduction of the conductivity activation energy, which eventually leads to the observation of the Peierls transition by resistivity measurements. X-ray absorption near edge spectroscopy studies performed with synchrotron radiation reveal directly the influence of charge transfer on unoccupied states near the Fermi level.     

Noscapine Prevents Rotenone-Induced Neurotoxicity: Involvement of Oxidative Stress,Neuroinflammation and Autophagy Pathways

Parkinson’s disease is characterized by the loss of dopaminergic neurons in substantia nigra pars compacta (SNpc) and the resultant loss of dopamine in the striatum. Various studies have shown that oxidative stress and neuroinflammation plays a major role in PD progression. In addition, the autophagy lysosome pathway (ALP) plays an important role in the degradation of aggregated proteins, abnormal cytoplasmic organelles and proteins for intracellular homeostasis. Dysfunction of ALP results in the accumulation of α-synuclein and the loss of dopaminergic neurons in PD. Thus, modulating ALP is becoming an appealing therapeutic intervention. In our current study, we wanted to evaluate the neuroprotective potency of noscapine in a rotenone-induced PD rat model. Rats were administered rotenone injections (2.5 mg/kg, i.p.,) daily followed by noscapine (10 mg/kg, i.p.,) for four weeks. Noscapine, an iso-qinulinin alkaloid found naturally in the Papaveraceae family, has traditionally been used in the treatment of cancer, stroke and fibrosis. However, the neuroprotective potency of noscapine has not been analyzed. Our study showed that administration of noscapine decreased the upregulation of pro-inflammatory factors, oxidative stress, and α-synuclein expression with a significant increase in antioxidant enzymes. In addition, noscapine prevented rotenone-induced activation of microglia and astrocytes. These neuroprotective mechanisms resulted in a decrease in dopaminergic neuron loss in SNpc and neuronal fibers in the striatum. Further, noscapine administration enhanced the mTOR-mediated p70S6K pathway as well as inhibited apoptosis. In addition to these mechanisms, noscapine prevented a rotenone-mediated increase in lysosomal degradation, resulting in a decrease in α-synuclein aggregation. However, further studies are needed to further develop noscapine as a potential therapeutic candidate for PD treatment.     

Interactions of Isoquinoline Alkaloids with Transition Metals Iron and Copper

Data on alkaloid interactions with the physiologically important transition metals, iron and copper, are mostly lacking in the literature. However, these interactions can have important consequences in the treatment of both Alzheimer’s disease and cancer. As isoquinoline alkaloids include galanthamine, an approved drug for Alzheimer’s disease, as well as some potentially useful compounds with cytostatic potential, 28 members from this category of alkaloids were selected for a complex screening of interactions with iron and copper at four pathophysiologically relevant pH and in non-buffered conditions (dimethyl sulfoxide) by spectrophotometric methods in vitro. With the exception of the salts, all the alkaloids were able to chelate ferrous and ferric ions in non-buffered conditions, but only five of them (galanthine, glaucine, corydine, corydaline and tetrahydropalmatine) evoked some significant chelation at pH 7.5 and only the first two were also active at pH 6.8. By contrast, none of the tested alkaloids chelated cuprous or cupric ions. All the alkaloids, with the exception of the protopines, significantly reduced the ferric and cupric ions, with stronger effects on the latter. These effects were mostly dependent on the number of free aromatic hydroxyls, but not other hydroxyl groups. The most potent reductant was boldine. As most of the alkaloids chelated and reduced the ferric ions, additional experimental studies are needed to elucidate the biological relevance of these results, as chelation is expected to block reactive oxygen species formation, while reduction could have the opposite effect.     

Dopamine,Oxidative Stress and Protein–Quinone Modifications in Parkinson's and Other Neurodegenerative Diseases

Dopamine (DA) is the most important catecholamine in the brain, as it is the most abundant and the precursor of other neurotransmitters. Degeneration of nigrostriatal neurons of substantia nigra pars compacta in Parkinson's disease represents the best‐studied link between DA neurotransmission and neuropathology. Catecholamines are reactive molecules that are handled through complex control and transport systems. Under normal conditions, small amounts of cytosolic DA are converted to neuromelanin in a stepwise process involving melanization of peptides and proteins. However, excessive cytosolic or extraneuronal DA can give rise to nonselective protein modifications. These reactions involve DA oxidation to quinone species and depend on the presence of redox‐active transition metal ions such as iron and copper. Other oxidized DA metabolites likely participate in post‐translational protein modification. Thus, protein–quinone modification is a heterogeneous process involving multiple DA‐derived residues that produce structural and conformational changes of proteins and can lead to aggregation and inactivation of the modified proteins.     

Cyst Reduction by Melatonin in a Novel Drosophila Model of Polycystic Kidney Disease

Autosomal dominant polycystic kidney disease (ADPKD) causes progressive cystic degeneration of the renal tubules, the nephrons, eventually severely compromising kidney function. ADPKD is incurable, with half of the patients eventually needing renal replacement. Treatments for ADPKD patients are limited and new effective therapeutics are needed. Melatonin, a central metabolic regulator conserved across all life kingdoms, exhibits oncostatic and oncoprotective activity and no detected toxicity. Here, we used the Bicaudal C (BicC) Drosophila model of polycystic kidney disease to test the cyst-reducing potential of melatonin. Significant cyst reduction was found in the renal (Malpighian) tubules upon melatonin administration and suggest mechanistic sophistication. Similar to vertebrate PKD, the BicC fly PKD model responds to the antiproliferative drugs rapamycin and mimics of the second mitochondria-derived activator of caspases (Smac). Melatonin appears to be a new cyst-reducing molecule with attractive properties as a potential candidate for PKD treatment.     

肝豆状核变性病与人体内铜的关系

为探讨肝豆状核变性发病机理与人体内铜的关系，结合本实验室分析条件，用原子吸收分光光度法对509名患者的24小时尿铜、血清铜含量进行了检测。结果表明，109名患者的24小时尿铜含量远高于正常人水平，血清铜含量低于正常人水平，经诊断证实这些患者患有肝豆状核变性病。本文进一步对这些患者按不同年龄、不同性别进行了分析，为肝豆状核变性病的成因、发展、诊断及治疗提供参考依据。     

Acetyl-CoA Deficiency Is Involved in the Regulation of Iron Overload on Lipid Metabolism in Apolipoprotein E Knockout Mice

The role of dietary iron supplementation in the development of nonalcoholic fatty liver disease (NAFLD) remains controversial. This study aimed to investigate the effect of excess dietary iron on NAFLD development and the underlying mechanism. Apolipoprotein E knockout mice were fed a chow diet, a high-fat diet (HFD), or an HFD containing 2% carbonyl iron (HFD + Fe) for 16 weeks. The serum and liver samples were acquired for biochemical and histopathological examinations. Isobaric tags for relative and absolute quantitation were performed to identify differentially expressed proteins in different groups. Excess dietary iron alleviated HFD-induced NAFLD, as evidenced by significant decreases in serum/the hepatic accumulation of lipids and the NAFLD scores in HFD + Fe-fed mice compared with those in HFD-fed mice. The hepatic acetyl-CoA level was markedly decreased in the HFD + Fe group compared with that in the HFD group. Important enzymes involved in the source and destination of acetyl-CoA were differentially expressed between the HFD and HFD + Fe groups, including the enzymes associated with cholesterol metabolism, glycolysis, and the tricarboxylic acid cycle. Furthermore, iron overload-induced mitochondrial dysfunction and oxidative stress occurred in mouse liver, as evidenced by decreases in the mitochondrial membrane potential and antioxidant expression. Therefore, iron overload regulates lipid metabolism by leading to an acetyl-CoA shortage that reduces cholesterol biosynthesis and might play a role in NAFLD pathogenesis. Iron overload-induced oxidative stress and mitochondrial dysfunction may impair acetyl-CoA formation from pyruvate and β-oxidation. Our study provides acetyl-CoA as a novel perspective for investigating the pathogenesis of NAFLD.