饮用水中过量铁和锰对蚕豆根尖细胞微核率的影响

目的 探讨饮用水中过量的铁和锰的致突变作用。方法 采用蚕豆根尖细胞微核技术。结果 当水中铁含量超过饮用水卫生标准3～10倍时，蚕豆根尖细胞微核率升高，且微核率与铁剂量间存在着明显的剂量-反应关系。锰对蚕豆根尖细胞微核率升高的作用不明显，只有在剂量高达卫生标准1000倍时，才会使蚕豆根尖细胞微核率有所增加。结论 过量的铁有致突变作用。     

Dopamine transporter density is decreased in parkinsonian patients with a history of manganese exposure: What does it mean?

Manganese (Mn) exposure can cause parkinsonism. Pathological changes occur mostly in the pallidum and striatum. Two patients with a long history of occupational Mn exposure presented with Mn-induced parkinsonism. In one patient, magnetic resonance imaging (MRI) showed findings consistent with Mn exposure, and Mn concentration was increased in the blood and urine. However, this patient's clinical features were typical of idiopathic Parkinson disease (PD). Previous pathological and positron emission tomography studies indicate that striatal dopamine transporter density is normal in Mn-induced parkinsonism, whereas it is decreased in PD. Therefore, we performed [(123)I]-(1r)-2 beta-carboxymethoxy-3beta-(4-iodophenyl)tropane ([(123)I]-beta-CIT) single-photon emission computed tomography. Severe reduction of striatal beta-CIT binding was indicated, which is consistent with PD. We propose three interpretations: (1) the patients have PD, and Mn exposure is incidental; (2) Mn induces selective degeneration of presynaptic dopaminergic nerve terminals, thereby causing parkinsonism; or (3) Mn exposure acts as a risk of PD in these patients. Our results and careful review of previous studies indicate that the axiom that Mn causes parkinsonism by pallidal lesion may be over-simplified; Mn exposure and parkinsonism may be more complex than previously thought. Further studies are required to elucidate the relationship between Mn and various forms of parkinsonism.     

ICR 小白鼠脏器中铜,锌锰含量

对40只正常成年远交系 ICR 小白鼠的主要脏器,用 WFX—Ⅱ型双光束原子吸收分光光度计测定了各脏器中铜、锌、锰含量.结果表明,主要脏器中铜、锌、锰含量大小顺序不一,铜含量最多的脏器是心,锌、锰含量最多的脏器是肝,在雌雄之间均无显著性差异.     

Progressive motor syndrome in a welder with pallidal T1 hyperintensity on MRI: A two-year follow-up.

Chronic exposure to manganese (Mn) fume during welding may lead to mainly extrapyramidal syndrome that is resistant to treatment. We present a 32-year-old patient who developed severe postural instability, Parkinsonism, dystonia, and pyramidal signs in the 10th year of welding. The neurological condition of the patient worsened markedly in the following 3 years, resulting in severe disability rendering him to be assisted in all his daily activities and he did not benefit from any dopaminergic agent. T1 sequences of the MRI of the brain showed pallidal hyperintensity symmetrically. Welders in our country often protect their eyes but ignore to use tools that protect them from inhalation of the fume. Since chronic Mn toxicity may cause serious disability and irreversible neurological disturbances, we strongly believe that it is necessary to inform welders and their employers about this potential hazard.     

茶叶中微量锰的新催化光度法测定

利用于氨三乙酸存在下，锰（Ⅱ）对高碘酸钾氧化二甲苯蓝ＦＦ的催化效应，建立了一个新的测定微量锰的动力学分光光度法。该法检出限为６×１０￣（－２）ｎｇ·ｍｌ￣（－１），线性范围为０．２～８．０ｎｇ·２．５ｍｌ￣（－１），常见离子基本不干扰测定。用于直接测定健齿茶和茉莉花茶中的锰含量，结果发现，锰含量分别为２２１４μｇ·ｇ￣（－１）及６４８μｇ·ｇ￣（－１）。此法简便易行，灵敏度高。     

示波极谱法测定植物中痕量锰

本文介绍在乙二胺介质中用JP-2型示波极谱仪测定植物中痕量锰的方法.锰量在2～500ng/ml范围内与催化极谱电流呈线性关系,常见20多种元素不干扰测定.本法简便、快速、炅敏,准确.回收率在90～110%之间.用本法测定植物中锰的结果与原子吸收法和分光光度法的测定结果非常吻合.     

老人自发与黑发中铜、锰、铁、锌、镁含量的比较

本文用原子吸收光谱法测定了延边地区65岁～108岁健康老人110人头发中的铜、锰、铁、锌及镁的含量,比较了66人的白发与44人的黑发中这些元素的含量差异.结果表明,白发中的锰和镁的含量明显低于黑发,但铜、锌、铁的含量则无明显差异.这些差别在男性很明显,但在女性则不甚明显.     

The Potential Roles of Blood–Brain Barrier and Blood–Cerebrospinal Fluid Barrier in Maintaining Brain Manganese Homeostasis

Manganese (Mn) is a trace nutrient necessary for life but becomes neurotoxic at high concentrations in the brain. The brain is a “privileged” organ that is separated from systemic blood circulation mainly by two barriers. Endothelial cells within the brain form tight junctions and act as the blood–brain barrier (BBB), which physically separates circulating blood from the brain parenchyma. Between the blood and the cerebrospinal fluid (CSF) is the choroid plexus (CP), which is a tissue that acts as the blood–CSF barrier (BCB). Pharmaceuticals, proteins, and metals in the systemic circulation are unable to reach the brain and spinal cord unless transported through either of the two brain barriers. The BBB and the BCB consist of tightly connected cells that fulfill the critical role of neuroprotection and control the exchange of materials between the brain environment and blood circulation. Many recent publications provide insights into Mn transport in vivo or in cell models. In this review, we will focus on the current research regarding Mn metabolism in the brain and discuss the potential roles of the BBB and BCB in maintaining brain Mn homeostasis.     

Infusion of pH 2.0 d-chiro-inositol glycan insulin putative mediator normalizes plasma glucose in streptozotocin diabetic rats at a dose equivalent to insulin without inducing hypoglycaemia

Summary We compared the effects of infusing a chemically defined chiro-inositol glycan putative insulin mediator with an equivalent dose of insulin in low-dose (45 mg/kg) streptozotocin diabetic rats. Insulin decreased plasma glucose levels from 17.32±0.17 to 3.96±0.064 mmol/l (p<0.0002) in 120 min, a decrease of 77.13%, while the putative mediator promoted a decrease in plasma glucose from 14.85±0.084 to 7.22±0.13 mmol/l (p<0.007) in 60 min. The putative mediator maintained euglycaemia over the ensuing 60 min with a plasma glucose level of 7.01±0.10 mmol/l at 120 min. Thus, insulin further reduced the plasma glucose from euglycaemia at 60 min to produce hypoglycaemia at 120 min. The lack of production of hypoglycaemia by the putative mediator can be explained by its inhibition of glucose-stimulated insulin secretion by the islet beta cells, thus providing a potential negative feedback regulatory mechanism; or by its selective action on muscle to increase glycogen synthesis. The significance of these results in terms of future directions in drug design is herein considered.Abbreviations STZ Streptozotocin - PDH pyruvate dehydrogenase