缺氧对大鼠大脑皮层细胞过氧化物及巯基含量影响

采用荧光分光光度法，检测缺氧大鼠的大脑皮层细胞脂质过氧化物和巯基含量的变化及金属硫蛋白对神经细胞的保护作用。结果表明：缺氧组细胞中脂质过氧化物的含量明显高于对照组（Ｐ＜０．０１）；巯基含量显著低于对照组（Ｐ＜０．０１）；金属硫蛋白能抑制脂质过氧化物的生成，使巯基含量升高。结果提示：缺氧可引发大脑皮层细胞脂质过氧化，抗氧化剂金属硫蛋白对细胞脂质过氧化损伤有一定的保护作用。     

三七中人参三醇甙对大鼠离体心脏缺血再灌注损伤及心律失常的保护作用

三七中人参三醇甙(PTS)5,50μg·ml~(-1)灌流对离体大鼠Langendorff心脏缺血再灌注所致心律失常具有明显的保护作用,可降低室颤发生率,并可保护心肌组织中超氧化物歧化酶的降低,PTS 50μg·ml~(-1)还可抑制心肌丙二醛的产生,对缺血再灌注所致心肌乳酸脱氩酶和磷酸肌酸激酶的漏出亦有明显的抑制作用。     

冠心病不同临床类型患者血浆、血小板脂质过氧化损伤与TXA_2/PGI_2平衡的研究

作者观察98例正常人和109例不同临床类型冠心病人血浆、血小板LPO、SOD,SeGSHP_x,RBC—SOD及血浆TXB_2、6-keto-PGF_(1α)的变化,发现各型冠心病组均有LPO、PL—LPO、TxB_2、TxB_2/6-keto-PGF_(1α)比值明显升高,6-keto-PGF_(1α),SOD、PLSOD、RBC-SOD,SOD/LPO及SeGSHPX/LPO比值明显降低。但各型程度不同,以急性心肌梗塞和不稳定性心绞痛改变突出。血浆LPO与6-keto-PGF_(1α)呈显著负相关。提示脂质过氧化损伤与TXA_2/PGI_2平衡密切相关。认为SOD/LPO、SeGSHPx/LPO,TXB_2/6-keto-PGF_(1α)比值在冠心病诊断中是重要有意义的指标,血小板SOD/LPO比值能更敏感地反映冠心病人氧化与抗氧化能力的平衡状态。     

提高H2O2/甲酸体系选择性氧化抽提脱硫效率的研究

为了降低焦化蜡油(CGO)-甲酸／H2O2选择性氧化体系中H2O2的无效分解速度，屏蔽重金属离子对H2O2分解的催化效应，考察了造纸行业中常用的硅酸钠、硅酸镁和乙二胺四乙酸(EDTA)等稳定剂和螯合剂的加入对有机溶剂抽提后CGO中含硫量的影响。实验结果表明，EDTA可以很好地和重金属离子螯合，氧化后CGO抽余油中硫含量大幅降低。     

用神经网络法预测药物在体透过人皮肤的渗透性

目的：预测药物在体透过人皮肤的渗透性。方法：以正辛醇／水分配系数(logP)、分子体积(V)、氢键酸度(∑β2^H)和氢键碱度(∑β2^H)等理化参数作为输入层神经元，以药物在一定时间内在体透过人皮肤的透过比的对数值(R，透过量／未透过量)作为输出层神经元，建立起合适的BP(Back—propagation)神经网络。结果：17个药物在一定时间内在体透过人皮肤的透过比的神经网络计算值和实测值均相当符合。结论：用BP神经网络法可以较好地预测药物在体透过人皮肤的渗透性。     

超氧化物歧化酶和脂质过氧化物与溃疡病发病关系

目的：观察超氧化物歧化酶（ＳＯＤ）和脂质过氧化物（ＬＰＯ）在消化性溃疡（ＰＵ）治疗前后变化，以探索其对ＰＵ发病和愈合作用。方法：用ＳＵＮ法和于树玉法分别测定ＰＵ患者血及组织中铜锌超氧化物歧化酶（Ｃｕ ＺｎＳＯＤ）活性和ＬＰＯ含量。结果：１８０例十二指肠溃疡（ＤＵ）和４２例胃溃疡（ＧＵ）患者粘膜和红细胞中Ｃｕ ＺｎＳＯＤ活性比正常组显著降低（Ｐ＜０．０１～０．００１）。１３６例ＤＵ组织及血中和１５例ＧＵ组织中ＬＰＯ含量比正常组显著升高（Ｐ＜００１～０．００１）。用呋喃唑酮、雷尼替丁和洛赛克分别治疗５０、２０和２４例ＤＵ患者两周后组织中Ｃｕ ＺｎＳＯＤ活性比治疗前明显升高（Ｐ＜０．０１～０．００１）。组织中ＬＰＯ含量比治疗前明显降低（Ｐ＜０００５～０．００１）。组织和红细胞中Ｃｕ ＺｎＳＯＤ活性从活动期→愈合期→瘢痕期逐渐升高，而ＬＰＯ含量则逐渐降低。结论：粘膜组织中Ｃｕ ＺｎＳＯＤ活性和ＬＰＯ含量升降与消化性溃疡的愈合和发病密切相关。     

振动对急性缺氧小鼠肺损伤的影响

本文观察了频率为20Hz、振幅为0．67mm和作用时间为40min的振动预处理对急性缺氧小鼠肺损伤的影响。结果发现实验组的肺组织匀浆脂质过氧化物LghdPeroxde（LPO）、支气管肺泡灌洗液（BALF）中蛋白含量和白细胞数明显低于对照组（P＜0．05）。这表明在特定率数的振动作用下能明显减轻急性缺氧小鼠肺的损伤。     

硒对二乙基亚硝胺诱发大鼠肝癌生长的抑制作用的观察

观察硒对二乙基亚硝胺诱发大鼠肝癌的影响。方法；在诱癌过程中，大鼠分别投予含０．２，１．０，３．０×１０＾－６硒的饲料，检测血，肝组织ＬＰＯ，ＧＳＨ－ＰＸ活性，观察诱癌率及癌结节面积。结果：补Ｓｅ后对诱癌率无显著影响，但补充３．０×１－０＾－６Ｓｅ可使癌结节面积显著减少。补Ｓｅ可显著地减轻诱癌早期血和肝组织中ＬＰＯ的形成及诱癌过程中血和肝组织中ＧＳＨ－ＰＸ活性的降低。     

Monoamine oxidase inhibition as a sequel of hydrogen sulfide intoxication: increases in brain catecholamine and 5-hydroxytryptamine levels

Administration of sodium hydrosulfide (NaHS), an alkali salt of hydrogen sulfide (H₂S) at doses of 10 and 30 mg/kg, corresponding to sublethal and lethal doses (0.66 and 2.0 X LD₅₀) resulted in significant increases in regional catecholamine levels of the rat brain only after the dose of 2.0 × LD₅₀ of NaHS. Whereas the cortex and the cerebellum showed little or no change in catecholamine content, the hippocampus, striatum and brainstem all showed increases in noradrenaline and adrenaline. Additional analysis also showed that brainstem dopamine and 5-hydroxytryptamine levels (5-HT) increased as well. In vitro testing of sulfide for inhibition of monoamine oxidase (MAO) activity showed the anion to be inhibitory with an IC₅₀ of 39.1±3.6 M. Inhibition of MAO activity ex vivo could be demonstrated at a dose of 100 mg/kg but not at the lower dose of 30 mg/kg NaHS. Inhibition of enzyme activity could not be demonstrated at this lower dose, possibly due to the well known rapid intramitochondrial metabolism of sulfide. Correlation of synaptosomal and mitochondrial sulfide levels with enzyme inhibition data suggests that inhibition of MAO may be an important contributing factor to the mechanism(s) underlying loss of central respiratory drive after fatal intoxication with H₂S.     

In vivo and in vitro models demonstrate a role for caveolin-1 in the pathogenesis of ischaemic acute renal failure

Caveolae and their proteins, the caveolins, transport macromolecules; compartmentalize signalling molecules; and are involved in various repair processes. There is little information regarding their role in the pathogenesis of significant renal syndromes such as acute renal failure (ARF). In this study, an in vivo rat model of 30 min bilateral renal ischaemia followed by reperfusion times from 4 h to 1 week was used to map the temporal and spatial association between caveolin-1 and tubular epithelial damage (desquamation, apoptosis, necrosis). An in vitro model of ischaemic ARF was also studied, where cultured renal tubular epithelial cells or arterial endothelial cells were subjected to injury initiators modelled on ischaemia-reperfusion (hypoxia, serum deprivation, free radical damage or hypoxia-hyperoxia). Expression of caveolin proteins was investigated using immunohistochemistry, immunoelectron microscopy, and immunoblots of whole cell, membrane or cytosol protein extracts. In vivo, healthy kidney had abundant caveolin-1 in vascular endothelial cells and also some expression in membrane surfaces of distal tubular epithelium. In the kidneys of ARF animals, punctate cytoplasmic localization of caveolin-1 was identified, with high intensity expression in injured proximal tubules that were losing basement membrane adhesion or were apoptotic, 24 h to 4 days after ischaemia-reperfusion. Western immunoblots indicated a marked increase in caveolin-1 expression in the cortex where some proximal tubular injury was located. In vitro, the main treatment-induced change in both cell types was translocation of caveolin-1 from the original plasma membrane site into membrane-associated sites in the cytoplasm. Overall, expression levels did not alter for whole cell extracts and the protein remained membrane-bound, as indicated by cell fractionation analyses. Caveolin-1 was also found to localize intensely within apoptotic cells. The results are indicative of a role for caveolin-1 in ARF-induced renal injury. Whether it functions for cell repair or death remains to be elucidated.