Phototransformations of 5-aminolevulinic acid-induced protoporphyrin IX in vitro: a spectroscopic study

Human adenocarcinoma cells of the line WiDr were incubated with 5-aminolevulinic acid to induce protoporphyrin IX (PpIX) and then exposed to laser light of wavelength 635 nm. The PpIX fluorescence decreased with increasing exposure. The decay rate was slightly dependent on the initial PpIX concentration. The PpIX fluorescence was halved by a fluence of about 40 J/cm2. Several fluorescing photoproducts were formed. The main one, supposedly the chlorine-type photoprotoporphyrin (Ppp), had a fluorescence excitation spectrum stretching out to about 680 nm with a maximum at around 668 nm. The formation kinetics of this product was dependent on the initial PpIX concentration. Moreover, it was selectively bleached by exposure to light at 670 nm. A photoproduct with an emission maximum at 652 nm, different from Ppp, remained after this exposure. Traces of a photoproduct(s) with fluorescence emission slightly blue-shifted compared with that of PpIX, supposedly water-soluble porphyrins, were also detected after light exposure.     

三角波交流示波极谱的研究(Ⅰ)——示波极谱图的性质

用三角波电流代替正弦波电流,进行交流示波极谱滴定,所得示波极谱图与正弦波结果相似。对一些离子的滴定表明,两法所得结果均在定量分析允许误差范围以内。报道了三角波交流示波极谱图的一些性质。     

Interaction between sodium tanshinone IIA sulfonate and the adriamycin semiquinone free radical: A possible mechanism for antagonizing adriamycin-induced cardiotoxity

Adriamycin (ADR) is a powerful and widely used antitumor drug, but its dose dependent cardiotoxicity limits its application. This side effect is believed to be caused by the adriamycin semiquinone free radical (ASFR). The primary focus of this work is to test effects of sodium tanshinone IIA sulfonate (STS) on ASFR and adriamycin–induced lipid peroxidation. It was found that ADR, whether in the system of heart homogenate, heart mitochondria or heart submitochondria, with NADH as the substrate or in xanthine/xanthine oxidase under anaerobic conditions, all produced ASFR rapidly. STS was shown to effectively scavenge ASFR in all these systems and postpone the appearance of ASFR. The delayed time was proportional to the amount of STS. Under aerobic conditions, ASFR could be oxidized to generate oxygen free radicals. STS could not scavenge these oxygen free radicals, but it could effectively scavenge lipid free radicals generated from membrane lipid peroxidation of heart mitochondria. STS could significantly reduce mitochondrial swelling and lipid peroxidation induced by ADR. Animal experiments show that treatment of STS could inhibit endogenous lipid peroxidation caused by ADR. Here, a protective mechanism of STS is suggested that STS can rapidly and univalently oxidize ASFR, causing the cycle of adriamycin between its quinone form and semiquinone form and inhibiting the accumulation of ASFR. Under aerobic condition, STS can protect heart mitochondria by scavenging lipid free radicals generated from adriamycin-induced mitochondrial lipid peroxidation. This investigation shows that STS may be a physiological drug to antagonize the cardiotoxicity of ADR.     

The trigonal–bipyramidal triiodo­thallium(III) complex [TlI3{(CH3)2SO}2]

The title compound, bis(dimethyl sulfoxide)triiodo­thallium(III), [TlI₃(C₂H₆OS)₂], was crystallized from equimolar amounts of Tl^II and I₂ in a dimethyl sulfoxide (DMSO) solution. After the initial redox reaction, the thallium(III)–iodo complex forms and precipitates as a DMSO solvate. In the crystal structure, Tl is surrounded by three iodide ligands in the equatorial plane and two O‐coordinated DMSO mol­ecules in the axial positions, forming a slightly distorted trigonal bipyramid. The complex lies on a twofold rotation axis, making the DMSO mol­ecules and two of the I atoms crystallographically equivalent.     

Splenectomy improves liver fibrosis via tumor necrosis factor superfamily 14 (LIGHT) through the JNK/TGF-β1 signaling pathway

Splenectomy has been reported to improve liver fibrosis in patients with cirrhosis and hypersplenism. However, the mechanisms remain unclear. Tumor necrosis factor superfamily 14 (TNFSF14; also known as LIGHT) is highly expressed in the context of fibrosis and promotes disease progression in patients with fibrotic diseases such as pulmonary and skin fibrosis. Here, we determined whether splenectomy controls the production of LIGHT to improve liver fibrosis. Splenectomy reduced serum LIGHT levels in cirrhotic patients with hypersplenism and a ConA-induced liver fibrosis mouse model. Blocking LIGHT resulted in the downregulation of TGF-β1 in RAW264.7 cells. LIGHT treatment of RAW264.7 and JS1 cells in coculture regulated transforming growth factor-β1 (TGF-β1) expression through the activation of JNK signaling. Small interfering RNA-mediated silencing of lymphotoxin β receptor (LTβR) in macrophages resulted in pronounced decreases in the levels of fibrosis and αSMA in JS1 cells. These results indicated that LIGHT bound to LTβR and drove liver fibrosis in vitro. Blocking TGF-β1 abolished the effect of LIGHT in vitro. Furthermore, the administration of recombinant murine LIGHT protein-induced liver fibrosis with splenectomy, while blocking LIGHT without splenectomy improved liver fibrosis in vivo, revealing that the decrease in fibrosis following splenectomy was directly related to reduced levels of LIGHT. Thus, high levels of LIGHT derived from the spleen and hepatic macrophages activate JNK signaling and lead to increased TGF-β1 production in hepatic macrophages. Splenectomy attenuates liver fibrosis by decreasing the expression of LIGHT.Subject terms: Tumour-necrosis factors, Liver fibrosis, Hepatic stellate cells, Liver cirrhosis, Experimental models of disease     

C2H4-K体系中振动态至电子态传能的研究

用TEA CO_2激光将C_2H_4分子激发到高振动激发态，高振动激发态的C_2H_4分子与基态的K原子碰撞发生振动态→电子态（V→E）传能过程，根据提出的能级组模型，对测得的时间分辨原子荧光信号进行处理，获得温度在453－663 K范围内，C_2H_4-K体系中V→E传能速率的数量级为10~(-10)/cm~3·molecule~(－1)·s~(－1)，对应的碰撞传能截面约为0.30～0.80 nm．随着反应温度升高，V→E传能截面减小．上述实验结果表明碰撞体间吸引相互作用在这种非共振的V→E传能过程中起主要作用．利用多极相互作用势下的碰撞络合物模型对实验结果进行了讨论．     

Kinetics of thermal decomposition of Co3O4 powder and single crystals

Kinetics of thermal decomposition in vacuum of Co₃O₄ powder as well as single crystals has been investigated. Discrepancies with the results of previous authors have been discussed. Decomposition of Co₃O₄ proceeds through formation of a compact layer of CoO and hence diffusion is the rate-limiting factor. The experimental curves α(t) be described for 0.05 < α < 0.85 using a modified Ginstling-Brounshtein equation: 1 ? 2α/3 ? (1 ? α)^2/3 = ktⁿ where the activation energy varies with the degree of decomposition.     

Fast electron transfer repair of oxidizing OH adduct of dGMP by chlorogenic acid

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Unusual regioselectivity of Pd(0)-catalyzed coupling reaction of electron-deficient alkenyl halides with allenic/propargylic zinc reagents. Highly selective synthesis of 6-phenylhex-5-yn-2(or 3)-enoates/enitrile and 4-phenyl-6-substituted-hexa-2,4,5-trienoates

The Pd(0)-catalyzed coupling reaction of electron-deficient alkenyl halides with the organozinc formed by the subsequent treatment of 1-phenylalk-1-yne with n-BuLi and ZnBr2 with or without a catalytic amount of HgCl2 was studied. Both the allene-formation- and the alkyne-formation-type coupling reactions were observed with high regio- and stereoselectivity: the reaction of 1-phenylprop-1-yne afforded 6-phenylhex-5-yn-2(or 3)-enoates and -enitriles, while the reaction of 1-phenylhex-1-yne formed 4-phenyl-6-substituted-hexa-2,4,5-trienoates. A plausible explanation for the regioselectivity was discussed. The double bonds in 6-phenylhex-5-yn- 2-enoates were prone to migrate to the position conjugated with the carbon-carbon triple bonds to form 6-phenylhex-5-yn-3-enoates at higher temperature. The migration did not occur in absence of an excess amount of allenic/propargylic zinc reagent or at low temperature.     

合成气制乙醇的铑基催化剂中助剂铁,锂的作用本质研究

催化活性测试表明,助剂Fe具有显著提高乙醇生成选择性及铑催化活性的双重作用;助剂Li具有显著提高乙醇选择性的作用,对铑催化活性影响不大。基于H_2/D_2同位素效应结果及CO化学吸附、IR、XRD、XPS等的表征结果,认为助剂Fe经活化处理后大部分与Rh形成RhFe合金,使Rh分散度显著提高,从而提高了乙醇的选择性;Rh分散度的提高以及小部分以Fe~(2+)(Fe~(3+))形式存在的助剂Fe促进甲酰基的生成及随后的氢解断C-O键反应是助剂Fe促使铑催化活性提高的两个因素。Li的主要作用在于通过与C_2含氧中间体乙烯酮氧端的弱亲合作用,促进了乙醇前驱体的生成,从而使乙醇生成选择性提高。