煤烟导致非细胞体系DNA氧化应激损伤的机制

目的 探讨煤烟导致非细胞体系氧应激损伤的机理。方法 以N－乙酰半胱氨酸（NAC）和甘露醇等不同作用位点的抗氧化剂作为实验干预手段,采用溴乙锭荧光法观察煤烟所致非细胞体系的DNA交联形成作用。结果 甘露醇可以有效地降低煤烟经DNA染毒所致的小牛胸腺DNA和肺细胞NDA的交联作用;而NAC却没有观察到相类似的作用。结论 煤烟在不需要经过细胞酶代谢条件下,可以通过产生羟自由基的途径而导致DNA氧应激损伤。     

香烟烟雾对雄性小鼠睾丸细胞DNA损伤的研究

分别以二甲基亚砜 (DMSO)和磷酸缓冲液 (PBS)作为吸收液 ,用大气收集器 (U形多孔玻板吸收管 )采集香烟主流烟雾 ,制得 DMSO烟雾溶液和 PBS烟雾溶液。用彗星试验检测了这 2种烟雾溶液对小鼠睾丸细胞的 DNA损伤作用。结果显示 :2种烟雾溶液均含有 DNA损伤剂 ,可引起小鼠睾丸细胞的 DNA损伤 ,且 DMSO烟雾溶液的细胞毒性和遗传毒性均明显高于 PBS烟雾溶液。该研究为香烟的雄性生殖毒性评价提供了理论依据 ,同时也为香烟的研究提供了更为方便的手段。     

饮水氯化消毒副产物--3-氯-4-二氯甲基-5-羟基-2(5氢)-呋喃酮的DNA损伤作用研究

目的 研究饮水氯化消毒副产物——3—氯—4—二氯甲基—5—羟基—2(5氢)—呋喃酮(MX)的DNA损伤作用。方法 以人肝肿瘤细胞株HepG2为靶细胞，MX设10、30、100、300μmol／L(终浓度)4个剂量，以二甲基亚砜为溶剂对照，H2O2为阳性对照，应用单细胞凝胶电泳试验(彗星试验)研究MX对HepG2的DNA损伤作用。结果 MX在30、100、300μmol／L3个剂量均可引起HepG2 DNA链断裂，DNA迁移长度随MX浓度的增加而增加，且与溶剂对照相比差异均有显著性。结论 饮水氯化消毒副产物——MX对HepG2有明显的DNA损伤作用。     

二甲基亚砜拮抗烹调油烟冷凝物遗传毒性的研究

目的研究二甲基亚砜(DMSO)对烹调油烟冷凝物(COFC)致人支气管上皮细胞遗传毒性作用的影响。方法采用永生化人支气管上皮细胞系BEAS-2B细胞,分为空白对照组、DMSO对照组、试剂对照组(0.1%乙醇)、COFC染毒组(50、100、150mg/L)和相应的DMSO保护组(0.5%DMSO)。采用单细胞凝胶电泳和微核、多核实验研究COFC的遗传毒性及DMSO对烹调油烟损伤的防护作用。结果COFC染毒组可引起细胞DNA断裂,细胞拖尾率、彗星尾部DNA含量、尾长、尾部面积和尾距增加,微核多核率升高,DMSO对以上损伤有显著的拮抗作用。结论COFC对人支气管上皮细胞具有明显的遗传毒性作用,而DMSO对此有抑制作用。     

摩托车尾气对小鼠抗氧化作用及DNA损伤的影响

目的:了解摩托车尾气对机体抗氧化酶、脂质过氧化物及DNA损伤的作用。方法:选用40只健康昆明种成年小鼠,体重24.6~36.3 g,平均体重为(30.50±5.12)g,随机分为4组,染毒组分别将摩托车尾气吸收液按1∶2、1∶4、1∶16进行稀释后进行灌胃染毒,对照组用二甲基亚砜按1∶2用蒸馏水稀释后灌胃,每天1次,每周5 d,共计40 d。分别测定小鼠肝细胞匀浆SOD、GSH-Px活性和MDA、GSH含量、以及外周血淋巴细胞DNA单链损伤的变化。结果:摩托车尾气染毒各组可致肝细胞匀浆中MDA含量增高,GSH含量及SOD、GSH-Px活性降低,外周血淋巴细胞DNA单链断裂增多,存在剂量—效应关系,高浓度时表现更为明显,与对照组比较差异有统计学意义(P<0.01)。结论:本实验结果显示摩托车尾气对实验小鼠体内肝组织具有氧化损伤和DNA损伤毒作用。     

常用防腐剂对大鼠肝脏脂质过氧化的影响

[目的]探讨常用肪腐剂苯甲酸、苯甲酸钠、山梨酸钾、对羟基苯甲酸乙酯、氟化钠等对大鼠肝脏脂质过氧化(LEO)作用的影响.[方法]模拟苯甲酸、苯甲酸钠、山梨酸钾、对羟基苯甲酸乙睹、氟化钠等防腐剂在食物中的含量,配制一系列浓度,运用体外TBA比色法检测LPO的含量,了解常用防腐剂对大鼠肝脏的损害程度. [结果]在实验条件下苯甲暖在0.1～10.0 mmol/L、苯甲酸钠在0.1～10.0 mmol/L、山梨酸钾在1.0～20mmol/L、对羟基苯甲酸乙酯在1.0～10 mmol/L、氟化钠在0.3～1.0 mmol/L浓度范围内对大鼠肝脏LPO有显著的诱导作用. [结论]苯甲酸、苯甲酸钠、山梨酸钾、对羟基苯甲酸乙蹭、氟化钠对大鼠肝脏LPO具有不同程度的诱导作用,会加大对肝脏细胞的损伤.     

加氯消毒对水中有机提取物致人胎肝细胞DNA损伤的影响

目的探讨自来水加氯消毒对水中有机提取物致细胞DNA损伤的影响。方法于2007年7月(夏季)和2008年3月(春季)采集以长江为水源的某水厂的水源水、经加氯消毒处理后的出厂水和末梢水,以人胎肝细胞(L-02)为靶细胞,采用单细胞凝胶电泳技术,检测水样有机提取物诱导细胞DNA损伤的效应。水样有机提取物设4个染毒浓度(1.2、6、30、150ml/ml),阳性对照为苯并(a)芘(200μmol/L),溶剂对照为二甲基亚砜(DMSO,10μl/ml)。结果春季水源水、出厂水和末梢水以及夏季出厂水和末梢水水样有机提取物在低、中、高浓度(6、30、150ml/ml)引起的L-02细胞DNA损伤较溶剂对照组明显增加。春夏两季加氯消毒后的出厂水和末梢水有机提取物在低、中、高浓度(6、30、150ml/ml)引起的L-02细胞DNA损伤较水源水明显增强。春季的水样有机提取物对细胞DNA的损伤作用高于夏季。结论水源水、出厂水和末梢水有机提取物均能引起L-02细胞的DNA损伤,氯化消毒增加了水源水的遗传毒性,春季水样的遗传毒性大于夏季。     

饮料防腐剂可致帕金森病

随着炎炎夏日的到来,清凉爽口的饮料也蜂拥而入。但英国大学的一项研究发现,碳酸饮料中常见的防腐剂能够破坏DNA,最终可能导致肝硬化和帕金森等疾病。英国专家通过实验发现,碳酸饮料中用作防腐剂的苯甲酸钠可以破坏细胞的"能量站"——线粒体。这种化学物质能够严重损伤线粒体中的DNA,令它们完     

贫铀对支气管上皮细胞遗传毒性及DMSO的保护作用

目的 观察贫铀(DU)诱发的细胞遗传毒性及二甲基亚砜(DMS3)的保护作用.方法 采用彗星实验、HPRT基因突变检测、微核多核及染色体分析研究贫铀的遗传毒性作用及DMSO对其毒性的抑制作用.结果 BEAS-2B细胞经贫铀染毒后,可引起DNA链断裂,彗星尾部面积、尾长、尾部DNA含量、尾距随贫铀浓度增加而增加;DMSO对贫铀诱发BEAS-2B细胞产生的DNA链断裂有明显的抑制作用.贫铀诱发微核细胞、多核细胞增多,DMSO对微核细胞增多有抑制作用,而对多核细胞增多无明显的抑制作用.贫铀作用于BEAS-2B细胞后引起HPRT基因突变率增加,DMSO保护组能有效地降低HPRT基因突变率.染色体分析结果表明,经染毒后转化细胞可出现染色体稳定性和非稳定性畸变,DMSO对染色体畸变具有抑制作用.结论 贫铀染毒能造成细胞的遗传毒性,DMSO对贫铀所致细胞的DNA损伤具有保护作用.     

依达拉奉辅助治疗重症颅脑损伤的效果观察

目的探讨依达拉奉联合脑苷肌肽治疗重症颅脑损伤患者的效果。方法选取我院2014年1月至2018年7月收治的重症颅脑损伤患者352例,随机分为联合组和对照组,各176例。联合组给予依达拉奉联合脑苷肌肽治疗,对照组给予脑苷肌肽治疗。观察两组患者治疗前后的GCS评分、 ICP、颅脑损伤标记物(S-100B、 GFAP、 NSE、 UCH-L1)水平及不良反应情况。结果治疗后,两组患者的GCS评分显著高于治疗前,且联合组的GCS评分显著高于对照组(P均<0.05)。治疗后,两组患者的ICP、颅脑损伤标记物水平显著低于治疗前,且联合组的ICP、颅脑损伤标记物水平显著低于对照组(P均<0.05)。两组患者的不良反应发生率比较差异无统计学意义(P>0.05)。结论依达拉奉联合脑苷肌肽治疗重症颅脑损伤可显著提高患者的GCS评分,降低ICP,改善颅脑损伤,且安全性好,值得推广应用。     

Effects of carnosine and related compounds on the stability and morphology of erythrocytes from alcoholics

The effects of carnosine and related compounds on erythrocytes from alcoholics were studied. In their presence, erythrocytes showed an increased ability to resist haemolysis and showed a more normal morphology, with carnosine and N-acetyl-carnosine being the most effective compounds. These beneficial properties of the dipeptides do not appear to be directly related to their antioxidant or buffering properties.     

Carnosine concentration of ingested meat affects carnosine net release into the portal vein of minipigs

Because of its physiological effects, carnosine (beta-alanyl-L-histidine) can be considered as a bioactive food component. The objective of this study was to assess the quantitative significance of intact carnosine absorption after ingestion of different beef meats, using the minipig as animal model. In a preliminary experiment, we evaluated the level of dietary carnosine in intestinal digesta of pigs (n = 4) after a meat meal (0.94 g protein/kg body weight) of grilled top loin (TL) or stewed shoulder (S). In accordance with meat carnosine concentration (20.7 and 7.2 micromol/g for TL and S, respectively), intestinal carnosine concentration was greater for TL than S. For both meats, carnosine flow to mid-jejunum was almost completed in the first 3 h following intake, and about one-half of the ingested carnosine disappeared from the intestinal lumen before the mid-jejunum. In catheterized minipigs (n = 4), we assessed the portal net release of dietary carnosine after a meat meal (1.4 g protein/kg body weight) of TL, S, and a blend of grilled neck and brisket (NB; 12.2 micromol carnosine/g). Postprandial carnosine plasma concentration and portal net release were not affected after an S meal, but they increased, proportionally to meat carnosine content, with NB and TL. For these meats, carnosine net release throughout the whole postprandial period accounted for 22% of the ingested carnosine. These results indicated that meat carnosine can be absorbed across the intestinal wall and that carnosine bioavailability depends on carnosine content of cooked meat.     

High levels of dietary carnosine are associated with increased concentrations of carnosine and histidine in rat soleus muscle

The aims of this investigation were to: 1) determine the effect of a moderately high dose of carnosine on muscle concentrations of carnosine, histidine and vitamin E at deficient, minimally adequate and sufficient levels of dietary vitamin E and 2) compare the effects of moderately high and pharmacological doses of carnosine on muscle concentrations of carnosine, histidine and vitamin E when dietary vitamin E is minimally adequate. Muscle concentrations of carnosine, histidine and vitamin E were measured in the lateral gastrocnemius and red and white vastus lateralis; carnosine and histidine concentrations were also measured in soleus muscle. Male Sprague-Dawley rats (n = 12/group) were fed a basal vitamin E-deficient diet supplemented with either 0, 0.001 or 0.01% vitamin E and 0, 0.1 or 1.8% carnosine. After 8 wk, 1.8% carnosine resulted in significant fivefold increases in carnosine and twofold increases in histidine in the soleus muscle (P < or = 0.05). Muscle vitamin E concentrations were not significantly affected by dietary carnosine. Thus, very high levels of dietary carnosine are associated with increases in carnosine and histidine concentrations in rat soleus muscle.     

苯甲酸雌二醇对腹腔镜下腹膜阴道成形术后阴道上皮的影响

目的 观察苯甲酸雌二醇对腹腔镜下腹膜阴道成形术后阴道上皮的影响。方法 将2003年1月至2011年3月在邢台市人民医院行腹腔镜腹膜阴道成形术的40例患者随机分成实验组与对照组,每组各20例。实验组于人工成形的阴道内涂抹苯甲酸雌二醇软膏,每日1.5g,连用3个月;对照组不用任何雌激素类药物。结果 术后3个月阴道长度实验组为(9.1±0.4)cm,对照组为(9.0±0.6)cm,两组比较差异无统计学意义(P>0.05);但实验组阴道弹性好,并发症发生率低。实验组术后3个月阴道涂片结果为:可见大量复层鳞状上皮细胞,少量炎症细胞,阴道细胞成熟指数[Vaginalexfoliatecellmaturationindex,MI(%)]为(50.2±10.5)。对照组为:可见中等炎症细胞,少许鳞状上皮细胞。结论 苯甲酸雌二醇应用于腹腔镜腹膜阴道成形术后可增加阴道上皮弹性,促进人工阴道鳞状上皮化,减少并发症。     

The utilization of carnosine in rats fed on a histidine-free diet and its effect on the levels of tissue histidine and carnosine

Carnosine can support the growth of rats fed on a histidine-free diet. Rats fed on the histidine-free diet lost weight rapidly for a few days, then remained at a relatively constant weight for 2 weeks at least. However, rats fed on a 0.90% carnosine diet, which contains histidine equimolar to that in a 20% casein diet, increased their weight at the same rate as rats fed on a 20% amino acid diet simulated with casein. On the other hand, the growth of rats fed on a 5% carnosine diet was about 70% compared with that of control rats fed on the 20% amino acid diet for a 2-week experimental period. Carnosinase activity was not significantly affected in the kidney of rats fed on the histidine-free or the 5% carnosine diet. On the other hand, carnosinase activity in the small intestine of rats fed on the histidine-free diet was significantly increased. Histidine content of serum of rats fed on the histidine-free diet decreased to 1/3 of that of control rats, while that of rats fed on the 5% carnosine diet increased to about 14 times. Carnosine content of rat gastrocnemius muscle increased with carnosine content of diets, followed by an increase of histidine in the muscle. However, carnosinase activity of gastrocnemius muscle was not affected by carnosine in diets.     

甲基汞、电离辐射对小鼠胸腺DNA合成及适应性反应的影响

为了解环境理化因子作用对机体产生的生物效应,采用＾３Ｈ－ＴｄＲ掺入法研究了甲基汞和不同剂量的电离辐射对小鼠胸腺ＤＮＡ合成及适应性反应的影响。结果表明：甲基汞可以抑制胸腺细胞ＤＮＡ合成;低剂量的电离辐射（０．０７５Ｇｙ）对胸腺ＤＮＡ合成具有一定刺激作用,＾３Ｈ－ＴｄＲ掺入量明显高于对照组;而高剂量的电离辐射（２Ｇｙ）对胸腺细胞ＤＮＡ合成有抑制作用;经低剂量电离辐射预处理后再进行甲基汞染毒时比单独用甲     

Physiological role of carnosine in contracting muscle

High-intensity exercise leads to reductions in muscle substrates (ATP, PCr6, and glycogen) and a subsequent accumulation of metabolites (ADP, P, H(+), and Mg(+)) with a possible increase in free radical production. These factors independently and collectively have deleterious effects on muscle, with significant repercussions on high-intensity performance or training sessions. The effect of carnosine on overcoming muscle fatigue appears to be related to its ability to buffer the increased H(+) concentration following high-intensity work. Carnosine, however, has other roles such as an antioxidant, a metal chelator, a Ca(2+) and enzyme regulator, an inhibitor of protein glycosylation and protein-protein cross-linking. To date7comma; only 1 study has investigated the effects of carnosine supplementation (not in pure form) on exercise performance in human subjects and found no improvement in repetitive high-intensity work. Much data has come from in vitro work on animal skeletal muscle fibers or other components of muscle contractile mechanisms. Thus further research needs to be carried out on humans to provide additional understanding on the effects of carnosine in vivo.     

Carnosine as a histidine source: transport and hydrolysis of exogeneous carnosine by rat intestine

Transport and metabolism of L-carnosine (beta-alanyl-L-histidine) were studied in rat small intestine. Carnosine administered orally was found in rat serum as well as small intestine and liver, followed by an increase of histidine. At ten minutes after carnosine infusion per os, the carnosine content of the hepatic portal vein increased with the dose. On the other hand, the histidine content increased two-fold but did not vary with the dose. These results suggest that part of the carnosine administered orally is hydrolyzed to beta-alanine and histidine in the small intestine. Carnosinase activity was present in many rat tissues and was most active in kidney in the presence of Mn2+. However, in the absence of Mn2+ carnosinase activity in small intestine was found to be the same level as that of kidney. A study has been made of the distribution of carnosinase along the small intestine of adult rat. The dipeptidase was distributed along the whole length of the small intestine with maximum hydrolytic activity in the jejunum, and was localized in the cytosol of the intestinal mucosa. Antiserum prepared against carnosinase purified from kidney inhibited the activity of small intestine as well as that of kidney.     

Essentiality of histidine in adult mice

The difficulty in demonstrating a histidine deficiency in adult animals may be due in part to the histidine reserve in skeletal muscle in the form of carnosine. Mice are unusual among vertebrates in that their muscle is free of carnosine and its methylated analogue, anserine. When mice were fed a histidine-free diet, weight loss was noticeable within 3 d and continued over a period of 18 d. At this point the animals had lost 25-30% of their original weight. These results are compatible with the view that a dietary histidine deficiency can be offset by carnosine. Mice, whose muscle contains no carnosine, show early signs of a deficiency when deprived of histidine.     

Biochemical behaviour of norbixin during in vitro DNA damage induced by reactive oxygen species

Naturally occurring antioxidants such as carotenoids are extensively studied for their potential in reducing the risk for cancer and other chronic diseases. In the present study, the radical-scavenger activity of the food additive norbixin, a water-soluble carotenoid extracted from Bixa orellana seeds and commercialized as annatto, was evaluated under conditions of DNA damage induced by reactive oxygen species, particularly by hydroxyl radicals. The cell-free scavenger activity of norbixin was evaluated using plasmid DNA as target molecule and Sn2+ or Fe2+ as oxidant. The addition of H2O2 enhanced DNA breakage induced by metal ions, particularly Fe2+. Under these conditions, norbixin started to protect plasmid DNA against single- and double-strand breakage at a metal:norbixin ratio of 1:1 (Sn2+) and 1:10 (Fe2+). However, at lower ratios to Sn2+, norbixin enhanced Sn2+-induced DNA breakage (P < 0.05). The ability of norbixin to protect genomic DNA against oxidative damage was assessed in murine fibroblasts submitted to H2O2-induced oxidative stress and the results were evaluated by the comet assay. Under low serum conditions (2 % fetal bovine serum (FBS)), a protective effect of norbixin against H2O2-induced DNA breakage was inversely related to its concentration, a protection ranging from 41 % (10 microm) to 21 % (50 microm). At higher concentrations of norbixin, however, oxidative DNA breakage was still enhanced, even in the presence of a high serum concentration (10 % FBS). Under normal conditions, norbixin per se has no detectable genotoxic or cytotoxic effects on murine fibroblasts. The antimutagenic potential of norbixin against oxidative mutagens was also evaluated by the Salmonella typhimurium assay, with a maximum inhibition of 87 % against the mutagenicity induced by H2O2. Although plasmid DNA and Ames data indicated that norbixin can protect DNA against oxidative damage, it seems to be a risky guardian of genomic DNA as it can also increase the extent of oxidative damage.