稀土苯多酸络合物的合成及其性质的研究

苯多酸作为配体，因有多个可参与配位的羧基，因此，可以和稀土离子生成不同配比而结构特殊的化合物，同时这类化合物具有一系列有趣的性质。本论文选择1,2,4,5-苯四酸（H_4L），1,3,5-苯三酸（H_3L_I），1,2,4-苯三酸（H_3L_(II)）和1,2,3-苯三酸（H_3L_(III)）作为配体，合成了除P_m以外的十四个镧系元素和Y的络合物。对于稀土和均苯四酸的络合物，除得到了文献曾报导过的4:3组成外，还合成了一个新的系列，其组成为1:1的络合物：Ln·HL·nH_2O(Ln = La-Gd，Er，Y)和Ln·L·NH_4·nH_2O(Ln=Eu，Tb-Lu)。培养出了未见文献报导的稀土Er与均苯四酸络合物的单晶，晶体结构分析指出其组成为[ Er·L·3H_2O]·NH_4·4H_2O，中心离子和配体形成八配位络阴离子，呈畸变的四方反棱柱结构。对所合成的稀土苯多酸络合物（除稀土和1,2,3-苯三酸络合物外），进行了热分析研究，结果表明这类络合物具有很高的热稳定性，空气中，除Ce外，其分解温度均大于420 ℃。指出了络合物热分解机理，对于绝大部分稀土苯多酸络合物。分解分两步进行，第一步络合物脱水，第二步分解为氧化物。镧的苯多酸络合物其分解过程经碱式碳酸盐（LaO）_2 CO_3，最后分解为La_2O_3。络合物DTA分解峰温随稀土原子序有规律地变化，且不同的苯多酸系列络合物呈类似的变化规律，变价元素处于曲线峰谷的位置。测定Ln_4L_3·nH_2O系列络合物的脱水热及脱水和分解表观活化能。系统地研究了络合物在4000-100cm~(-1)范围内的FT-IR光谱，通过对羧基反对称和对称伸缩振动的分析，指出了络合物中羧基的可能配位形式。对组成为Ln·HL·nH_2O(Ln=La-Gd，Y)，Ln·L·NH_4·nH_2O (Ln=Tb-Lu)，LnL_I·nH_2O (Ln = La-Ho)和LnL_(II)·nH_2O (Ln=Pr-Tm)的络合物，指认了Ln-O链伸缩振动，其振动频率随稀土离子总角动量量子数呈类似“斜W”效应的变化。对于Ln_4L_3·nH_2O，LnL_I·nH_2O和LnL_(II)·nH_2O络合物，随着配体的不同，羧基反对称和对称伸缩振动频率差ΔV以ΔV_(1,3,5)BTA > ΔV_(PMA) > ΔV_(1,2,4)BTA的规律变化。研究了Eu和Tb苯多酸铬合物的萤光相对亮度及其萤光光谱，对Tb络合物，其萤光相对亮度随配体结构的变化有如下变化规律：PMA > 1,2,4 BTA≥1,2,3 BTA > 1,3,5 BTA。Tb的PMA络合物由于其发光强度较大，有可能在实际中得到应用。

Hydrothermal synthesis of the two-dimensional coordination polymer {[Fe(phen)(OH)](bta)(0.5)}(n) (phen=1,10-phenanthroline, bta=benzene-1,2,4,5-tetracaboxylate)

The title two-dimensional coordination polymer was synthesised and characterised by X-ray diffraction analysis.

Chronic Morphine Treatment Impaired Hippocampal Long-Term Potentiation and Spatial Memory via Accumulation of Extracellular Adenosine Acting on Adenosine A(1) Receptors

Chronic exposure to opiates impairs hippocampal long-term potentiation (LTP) and spatial memory, but the underlying mechanisms remain to be elucidated. Given the well known effects of adenosine, an important neuromodulator, on hippocampal neuronal excitability and synaptic plasticity, we investigated the potential effect of changes in adenosine concentrations on chronic morphine treatment-induced impairment of hippocampal CA1 LTP and spatial memory. We found that chronic treatment in mice with either increasing doses (20-100 mg/kg) of morphine for 7 d or equal daily dose (20 mg/kg) of morphine for 12 d led to a significant increase of hippocampal extracellular adenosine concentrations. Importantly, we found that accumulated adenosine contributed to the inhibition of the hippocampal CA1 LTP and impairment of spatial memory retrieval measured in the Morris water maze. Adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine significantly reversed chronic morphine-induced impairment of hippocampal CA1 LTP and spatial memory. Likewise, adenosine deaminase, which converts adenosine into the inactive metabolite inosine, restored impaired hippocampal CA1 LTP. We further found that adenosine accumulation was attributable to the alteration of adenosine uptake but not adenosine metabolisms. Bidirectional nucleoside transporters (ENT2) appeared to play a key role in the reduction of adenosine uptake. Changes in PKC-alpha/beta activity were correlated with the attenuation of the ENT2 function in the short-term (2 h) but not in the long-term (7 d) period after the termination of morphine treatment. This study reveals a potential mechanism by which chronic exposure to morphine leads to impairment of both hippocampal LTP and spatial memory.

HORMONAL-REGULATION OF TISSUE-TYPE PLASMINOGEN-ACTIVATOR AND PLASMINOGEN-ACTIVATOR INHIBITOR TYPE-1 IN CULTURED MONKEY SERTOLI CELLS

Sertoli cells play a central role in the control and maintenance of spermatogenesis. Isolated Sertoli cells of mouse and rat testes have been shown to secrete plasminogen activator (PA) and a plasminogen activator inhibitor type-1 (PAI-1) in culture. In this study, we have investigated the hormonal regulation of PA and PAI-1 activities in cultured monkey Sertoli cells. Sertoli cells (5x10(5) cells/well) isolated from infant rhesus monkey testes were preincubated at 35 degrees C for 16 h in 24-well plates precoated with poly(D-lysine) (5 mu g/cm(2)) in 0.5 mi McCoy's 5a medium containing 5% of fetal calf serum and further incubated for 48 h in 0.5 mi serum-free medium with or without various hormones or other compounds, PA as well as PAI-1 activities in the conditioned media were assayed by fibrin overlay and reverse fibrin autography techniques respectively. The Sertoli cells in vitro secreted only tissue-type PA (tPA), no detectable amount of urokinase-type PA (uPA) could be observed, Monkey Sertoli cells were also capable of secreting PAI-1, Immunocytochemical studies indicated that both tPA and PAI-1 positive staining localized in the Sertoli cells, spermatids and residual bodies of the seminiferous epithelium; Northern blot analysis further confirmed the presence of both tPA and PAI-1 mRNA in monkey Sertoli cells. Addition of follicle-stimulating hormone (FSH) or cyclic adenosine monophosphate (cAMP) derivatives or cAMP-generating agents and gonadotrophin-releasing hormone (GnRH) agonist or phorbol ester (PMA) to the cell culture significantly increased tPA activity. PAI-1 activity in the culture was also enhanced by these reagents except 8-bromo-dibutyryl-cAMP, forskolin and 3-isobutyl-1-methylxanthin (MIX) which greatly stimulated tPA activity, whereas decreased PAI-1 activity, implying that neutralization of PAI-1 activity by tile high level of tPA in the conditioned media may occur. These data suggest that increased intracellular signals which activate protein kinase A (PKA), or protein kinase C (PKC) can modulate Sertoli cell tPA and PAI-1 activities, The concomitant induction of PA and PAI-1 by the same reagents in the Sertoli cells may reflect a finely tuned regulatory mechanism in which PAI-1 could limit the excession of the proteolysis.