类脂过氧化对竹红菌甲素引起膜蛋白光敏交联的影响

本文研究了丙二醛与红细胞膜温育后所形成的交联。当丙二醛浓度在5×10~-4mol/L以上时,膜蛋白发生交联,并且在460nm处有荧光特征峰出现。而甲素光敏所致膜蛋白的交联,在460nm处没有荧光峰,光敏所产生的内源丙二醛量很少,不足以引起红细胞膜反应形成交联。我们还研究了BHT和Vit E两种抗氧化剂对甲素光敏作用的影响。BHT能抑制类脂过氧化,不能抑制膜蛋白巯基的变化和膜蛋白的交联。而Vit E仅不能抑制膜蛋白的交联。以上结果均说明甲素光敏所致膜类脂过氧化是不参与膜蛋白交联的。     

The effects of bisulfite on growth and macromolecular synthesis in Escherichia coli

Bisulfite reversibly inhibits the growth of a variety of microorganisms and has been used as a preservative in foods and beverages for that reason. We have now measured macromolecule synthesis in Escherichia coli K12 after bisulfite treatment. RNA synthesis, the synthesis of total protein, and of an inducible enzyme, beta-galactosidase, stopped almost immediately upon addition of 2 mM (or higher concentrations) of bisulfite. These functions resumed after a lag whose duration depended on the concentration of bisulfite added. The synthesis of DNA was slowed upon bisulfite addition, but did not stop entirely. The inhibition of RNA synthesis by bisulfite took place in both stringent and relaxed strains of E. coli and was not relieved upon addition of chloramphenicol. Stringent control was therefore not involved in this effect. No effect on protein synthesis was observed in the cell-free system of E. coli (using poly(U) or MS2 RNA as messenger) at bisulfite concentrations up to 10 mM. Protein synthesis inhibition in vivo was apparently not due to a reaction of bisulfite with a component of this system. In additional experiments, RNA polymerase was not impaired by bisulfite, and the growth inhibition effect was shown to proceed in the presence of inhibitors of free radical chain reactions.     

Effect of thyroidectomy and adrenalectomy on changes in liver glutathione and malonaldehyde levels after acute ethanol injection

At low concentrations ethanol is metabolized largely by alcohol dehydrogenase to acetaldehyde, while at higher concentrations a microsomal ethanol oxidising system (MEOS) is involved, namely cytochrome P450 IIE1, which also probably generates free radical species. In hyperthyroidism hepatic glutathione stores are depleted and net superoxide anion production occurs. In contrast, in hypothyroidism hepatic glutathione may be increased and thus renders the liver less sensitive to alcohol generated free radical production. Steroid hormones inhibit lipid peroxidation. Sixty male Wistar rats either underwent thyroidectomy, adrenalectomy, or sham procedures. Twenty control animals were pair fed with thyroidectomized animals, whilst another twenty fed ad libitum. An intraperitoneal injection of alcohol (75 mmol/kg) was given 2.5 h prior to sacrifice to half the animals in each group, the remainder receiving saline. The total hepatic glutathione contents of the pair fed and the ad libitum groups were not different, but were significantly increased by thyroidectomy (p = <0.001). This effect was significantly reduced by alcohol (p < 0.01). The sham procedures and dietary restrictions had no effect. The ethanol alone reduced total hepatic glutathione, but this only reached statistical significance in the thyroidectomized and sham-adrenalectomized groups. Hepatic malonaldehyde (MDA) levels were significantly reduced in the thyroidectomy group but alcohol had no effect on them. We conclude that hypothyroidism increased hepatic glutathione status, presumably by reducing radical production by enzyme systems, which would otherwise consume this important scavenger. Long term exposure to ethanol with induction of MEOS is probably required for it to generate toxic levels of free radical species.     

维生素E与左乙拉西坦对癫痫患者的临床疗效及血浆T-Aoc，MDA水平的影响

目的:探讨维生素E(VE)辅助左乙拉西坦(LEV)治疗癫痫的临床疗效及对患者血浆总抗氧化能力(T-Aoc)、丙二醛(MDA)水平的影响。方法:选取我院2013年6月~2015年9月收治的134例癫痫患者,随机分为两组。对照组予LEV治疗,观察组在此基础上给予VE治疗。记录比较两组临床疗效,治疗前后脑电图背景活动,血浆T-Aoc、MDA水平;并评价两组用药的安全性。结果:观察组总有效率为88.1%,较对照组(74.6%)明显升高(P0.05)。与治疗前相比,两组治疗后脑电图指标δ、θ波频率均明显增快(P0.05);α波频率均明显减慢(P0.05),且观察组治疗后脑电图指标改善效果均明显优于同期对照组(P0.05)。与治疗前比较,观察组血浆T-Aoc水平显著升高、MDA水平显著降低(P0.01),而对照组血浆T-Aoc水平有所上升、MDA水平略有下降,但差异无统计学意义(P0.05)。观察组不良反应发生率为10.4%,与对照组(7.5%)相比差异无统计学意义(P0.05)。结论:VE辅助LEV治疗癫痫能更有效降低发作频率,改善脑电图背景活动,平衡机体氧化/抗氧化系统,且安全性高。     

醒脑静联合古拉定对急性酒精中毒患者血清H2O2、SOD、MDA及iNOS水平的影响

目的:探讨醒脑静联合古拉定治疗急性酒精中毒的疗效及对患者血清过氧化氢(H_2O_2)、超氧化物歧化酶(SOD)、丙二醛(MDA)和诱导型一氧化氮合酶(i NOS)水平的影响。方法:选取我院2015年4月至2017年4月收治的80例急性酒精中毒患者,采用随机数字表法分为两组。对照组40例,采用醒脑静治疗;观察组40例,采用醒脑静联合古拉定治疗。记录比较两组症状改善时间,治疗前后肝功能及血清学指标变化,临床疗效与不良反应的发生情况。结果:观察组血压与心率恢复正常及清醒时间均较对照组显著缩短(P0.01)。与治疗前相比,两组治疗后血清谷酰转肽酶(GGT)、谷草转氨酶(AST)和谷丙转氨酶(ALT)水平均显著下降(P0.01),且观察组以上指标均显著低于对照组(P0.01)。治疗4、8 h后,两组血清H_2O_2、MDA、iNOS水平均较治疗前显著下降(P0.01),血清SOD水平较治疗前显著升高(P0.01),且观察组以上指标改善较对照组更显著(P0.01)。观察组治疗后总有效率达97.50%,较对照组(90.00%)略高,但差异无统计学意义(P0.05)。观察组苏醒后不适率为27.50%,较对照组显著降低(67.50%,P0.01)。结论:采用醒脑静及古拉定治疗急性酒精中毒患者可更快速、有效消除临床症状,改善肝功能,减少患者不适感,疗效更显著,可能与其有效降低血清MDA、i NOS水平并升高血清SOD水平有关。     

Improved procedure for the determination of malonaldehyde by gas-chromatography with electron-capture detection as 2,4,6-trichlorophenylhydrazine derivative

A previously described derivatization method using trichlorophenylhydrazine was developed for the estimation of malonaldehyde measured by gas-chromatography (GC) with electron-capture detection. The precision and reliability of the procedure are improved here by the use of methylmalonaldehyde as internal standard and by the introduction of a diverter valve at the end of the capillary column to protect the electron-capture detector, respectively.The method was applied to determine malonaldehyde content in bovine plasma samples.     

Relationship between the hemolytic action of heavy metals and lipid peroxidation

It is well known that some of the heavy metals have a hemolytic action, but the mechanisms responsible for this effect are not well established. In order to elucidate whether or not the hemolytic action of heavy metal ions is associated with the peroxidation of membrane lipids, the relationship between metal-induced hemolysis and the generation of malonaldehyde has been studied.The results obtained show that metal-induced hemolysis is associated with the development of peroxidative processes in erythrocyte membranes. The peroxidation is caused by metals with and without pro-oxidant catalytic action. The level of the malonaldehyde products rises before the appearance of hemolysis which proves that the development of peroxidative processes precedes but does not result from hemolysis.The suggestion has been made that the peroxidation of membrane lipids is a possible mechanism of damage to the red cell membrane in metal-induced hemolysis.     

Neutrophil elastase inhibitor, sivelestat sodium hydrate prevents ischemia–reperfusion injury in the rat bladder

In the present study, we evaluated the effect of neutrophil elastase inhibitor, sivelestat sodium hydrate on ischemia–reperfusion injury in the rat bladder. Rat abdominal aorta was clamping with a small clip to induce ischemia–reperfusion injury in the bladder. Eight-week-old male Sprague Dawley rats were divided into four groups; sham-operated control rats, 30 min ischemia–60 min reperfusion (IR) rats, and IR rats treated with 15 or 60 mg/kg of sivelestat sodium hydrate. Sixty minutes prior to induction of ischemia, sivelestat sodium hydrate was administrated intraperitoneally. Real-time monitoring of blood flow and nitric oxide (NO) release were measured simultaneously with a laser Doppler flowmeter and an NO-selective electrode, respectively. The NO₂–NO₃ and malonaldehyde (MDA) concentrations were measured in the experimental urinary bladders. Clamping of the abdominal aorta, blood flow was rapidly decreased and NO release was gradually increased. After removing the clip, blood flow was rapidly increased and NO release was gradually returned to the basal level. These movements of blood flow and NO release were inhibited by treatment with sivelestat sodium hydrate in a dose-dependent manner. Both NO₂–NO₃ and MDA concentrations in the bladder were increased by induction of IR, and NO₂–NO₃ and MDA concentrations were decreased by treatment with high dose of sivelestat sodium hydrate significantly. Our data indicated that sivelestat sodium hydrate could inhibit increasing NO₂–NO₃ and MDA concentrations by IR, and it has potentiality protective effects on IR injury in the rat urinary bladder.