Effect of beta-amyloid peptide fragment 25-35 on nonselective permeability of mitochondria

Beta-Amyloid peptide fragment 25-35 potentiated phosphate- and calcium-induced opening of mitochondrial channels and caused swelling of mitochondria (even without exogenous calcium and phosphate). These changes were accompanied by accumulation of lipid peroxidation products in mitochondria. Specific inhibitors of mitochondrial channels ADP and cyclosporine A prevented beta-amyloid peptide-induced swelling of mitochondria. Our findings suggest that potentiation of mitochondrial channel opening is an important component of the neurodegenerative effect of beta-amyloid.     

Plasma insulin and lipid levels in untreated obstructive sleep apnoea and snoring; their comparison with matched controls and response to treatment

SUMMARY  Obstructive sleep apnoea (OSA), and snoring are associated with coronary heart disease. To assess whether OSA or snoring may contribute to this by raising fasting lipid or insulin levels, venous fasting total cholesterol, triglyceride, very-low-density lipoprotein, low-density lipoprotein, high-density lipoprotein, and insulin were measured in 15 untreated OSA patients and 18 snorers. Each of these subjects was individually matched to a control of the same sex, age ± 10%, body index ± 15%, smoking and drinking habits. This produced study groups which did not differ significantly by any of these criteria. Fasting venous blood samples were collected at 06.30 hours following polysomnography, and analysed blind of the subjects respiratory status. The OSA patients were then treated with nasal continuous positive airway pressure. In 10 of these subjects lipid and insulin levels were repeated after more than three months treatment. Lipid and insulin levels were also remeasured in the controls matched to these 10 subjects. The end points were compared with paired t -tests.
There was no difference in any of the end points when the untreated OSA patients and the snorers were compared to their matched controls ( P >0.25 for all comparisons), and none of the indices changed when OSA was corrected with nasal continuous positive airway pressure ( P > 0.25 for all comparisons).
Patients with obstructive sleep apnoea or snoring do not have significant fasting hyperlipidaemia or hyperinsulinaemia when compared to carefully matched controls. These factors are therefore unlikely to be the cause of the excess cardiovascular mortality experienced by this patient group.     

活性氧对红细胞膜流动性影响的研究

目的 :研究活性氧诱导红细胞发生氧化溶血的机制。方法 :用不同浓度的 H2 O2 作用于离体正常红细胞 ,分别用比色法、硫代巴比妥酸荧光法、荧光偏振法测定红细胞溶血度、红细胞膜脂质过氧化物 (L PO)、红细胞膜微粘度。结果 :5 0 ,10 0 ,12 0 mm ol/ L 浓度的 H2 O2 作用于红细胞后 ,均引起红细胞发生氧化溶血 ,红细胞溶血度、红细胞膜 L PO、红细胞膜微粘度均明显增加 ;H2 O2 在 5 0～ 12 0 mm ol· L- 1浓度范围内 ,红细胞溶血度、红细胞膜 L PO、红细胞膜微粘度的增加与 H2 O2 有明显的量效关系 ;红细胞膜微粘度与红细胞溶血度呈明显正相关 ,红细胞膜 L PO与红细胞膜微粘度呈明显正关。结论 :活性氧引发红细胞膜脂质过氧化导致红细胞膜流动性降低在活性氧诱导红细胞发生氧化溶血的机制中起一定的作用     

中华眼镜蛇毒F组分对沙鼠脑缺血再灌注损伤的保护作用

目的：研究中华眼镜它毒F组分脑缺血再灌注损伤的保护作用,方法：结扎沙鼠双侧颈总动脉1h,造成前脑缺血模型,用比色法测定脑匀浆过氧化脂质的最终产物丙二醛（MDA）的含量及超氧化物歧化酶（SOD）的活性,结果：F组分0．9,0．3,0．1mg/kg可显著抑制脑内脂质过氧化,降低MDA的含量,并提高超化物歧化酶的活,性且呈一定的量效关系,同缺血再灌组比较P＜0．05,同阳性对照药尼莫通比较,P＞0．05,结论：中华眼镜蛇毒F组分对脑缺血再灌注损伤有保护作用,可能与抑制自由基的生成和促进自由基的清除有关。     

低铅染毒大鼠体内脂质过氧化及抗氧化水平改变

目的：观察低剂量铅染毒后大鼠体内脂质过氧化水平改变,为铅的毒作用机制研究提供依据。方法：以醋酸铅为受试物,雄性Wistar大鼠为受试对象,分别观察其脏器脂质过氧化水平改变。结果：低铅染毒后,大鼠各脏器超氧化物歧化酶（SOD）、谷胱苷肽过氧化物酶（GSH－Px）及过氧化脂质（LPO）均有不同程度改变（P＜0.05,P＜0.01）,而巯基（－SH）含量仅肝脏变化较明显。结论：较低剂量的铅即可引起体内脂质过氧化水平的改变,而这种变化可能是铅的毒作用途径之一。     

血脂与体外血栓形成的关系

应用国产ＤＪＨ－Ｉ型调速单型血栓形成仪，对４７４名４５岁以上成人体外血栓形成进行了检测，同时检查血脂水平。另外对部分隐性体外血栓阳性者及正常人的红细胞膜荧光偏振度（Ｐ）和微粘度（η）进行比较。结果表明：隐性体外血栓阳性者中血脂增高者为５７／１０９（５４．１２％），其中一级血栓３２／７５（４２．６％），二级血栓１１／１６（６８．７％），三级血栓１４／１８（７７．７％）。红细胞膜Ｐ和η在隐性体外血栓阳性者与正常人之间有显著差异（Ｐ＜０．０５）。提示：隐性体外血栓检测对临床心脑血管的血栓性疾病的早期预防、治疗有较大的参考价值