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1.
【目的】肠道菌群通过"微生物-肠道-脑轴"影响中枢神经系统的功能,同时也与老年性痴呆的发生发展相关,特别是盲肠内微生物菌群的变化更为显著。肠道菌群可以产生和代谢甲醛,而肠道能够迅速吸收甲醛;体内甲醛含量与老年性痴呆病人的认知损害程度呈正相关。因此,本文比较了7月龄APP/PS1转基因老年性痴呆模型小鼠(简称APP/PS1转基因小鼠)与同月龄C57BL/6J野生型小鼠(简称C57BL/6J小鼠)肠道菌群产生甲醛的情况。【方法】取APP/PS1转基因小鼠(n=8)与C57BL/6J小鼠(n=9)的不同肠段(十二指肠、小肠、盲肠、结肠),采用2,4-Dinitrophenylhydrazi zne(DNPH)显色偶联高效液相色谱(HPLC coupled with DNPH)测定肠道消化物和肠壁组织的甲醛。【结果】APP/PS1转基因小鼠盲肠消化物内的甲醛含量,较C57BL/6J小鼠存在显著升高(P=0.036);而两者小肠和结肠消化物甲醛含量无显著差别。在两种小鼠之间,小肠壁内甲醛存在差异(P=0.052),而盲肠和结肠壁甲醛含量无显著差异(P0.05)。【结论】肠道菌群是小鼠体内甲醛的主要来源之一,无论肠道消化物,还是肠道壁组织均为盲肠的甲醛含量最高。这些结果表明,APP/PS1转基因小鼠肠道菌群存在甲醛代谢失调,从而导致其肠道消化物的甲醛含量升高。  相似文献   

2.
应用HPLC测定生物制品中甲醛含量的研究   总被引:3,自引:0,他引:3  
研究了直接用于液相色谱测定甲醛与2,4-二硝基苯肼的反应条件,使反应在菌疫苗类生物制品自身的pH范围内即弱酸性条件下,无需酸碱度调节,反应产物甲醛衍生物不需要有机溶剂萃取,避免损失,可直接用于液相色谱分析。在检出限及精确度方面更是优越于分光光度法。将样品用2,4-二硝基苯肼溶液衍生后,经C18化学键合硅胶为固定相,以乙睛∶水(60∶40,体积比)为流动相。紫外检测波长360 nm进行测定。方法的平均回收率为95.4%(n=5),两种生物制品6次独立测定的相对标准偏差分别为重组乙型肝炎疫苗(CHO)RSD=0.92%,吸附白喉破伤风联合疫苗RSD=3.92%。甲醛(0.6~3.0μg/mL)范围内,浓度与吸收面积值呈良好的线性关系。结果显示,该研究方法的色谱条件能准确定量、灵敏、准确、重复性好,优于药典的分光光度法,可用于实际检测分析。  相似文献   

3.
目的:建立直接测定中成药汞含量的无损分析方法.方法:采用一种新型冷原子吸收测仪,样品经添加辅助剂后直接测定.结果:本法检出限可达0.004 ng,检测范围为0.5~10 ng,加标回收率为98.7~104.3%,方法精密度为0.5%(n=6).结论:本法直接进样测定,极其简便、省时,用于两类中成药中汞含量测定,效果显著优于现行方法.  相似文献   

4.
目的:建立RP-HPLC测定乌头类双酯型生物碱水解产物苯甲酸含量的方法.方法:色谱柱:Waters C18(150×4.6 mm),流动相:甲醇-0.02 mol/L乙酸铵溶液(5∶95),检测波长:230 nm,流速:1.0 ml/min,柱温:30℃.结果:苯甲酸在0.432~3.888μg(r=0.9999)之间呈线性关系,苯甲酸加样回收率为98.62%(RSD=1.89%).结论:该方法简便、稳定、准确,可做为乌头类双酯型生物碱水解产物苯甲酸含量测定的方法.  相似文献   

5.
用二阶导数光谱法测定脑活素注射液中色氨酸的含量,可以消除该注射液中其它成份对其干扰。以水作为参比:波长选定282.0nm(峰):285.2nm(谷),色氨酸测定浓度0~0.05mg/ml,线性关系良好,回归方程D=94.585C—0.0111r=0.999.9平均回收率(%)100.6(n=5 CV(%)=1.2)  相似文献   

6.
GA3、6-BA对金钗石斛生长发育及生物碱含量的影响   总被引:1,自引:0,他引:1  
在金钗石斛(Dendrobium nobile Lindl.)高分蘖期前用GA3和6-BA进行浸根处理,分析GA3和6-BA对金钗石斛生长发育及生物碱含量的影响.结果表明:GA3、6-BA处理使金钗石斛SOD、POD活性升高,可溶性蛋白质和可溶性糖含量增加; 用0.5~1.0mg·L-1GA3和10 mg·L-16-BA处理可使金钗石斛的总生物碱含量分别增加6.7%~10.1%和3.4%;石斛碱的含量不受GA3和6-BA的影响.0.5~1.0 mg·L-1 GA3和10~50 mg·L-1 6-BA处理可使金钗石斛生物产量分别增加13.3%~30.7%和17.3%~40.0%,有效分蘖率提高63.2%~68.9%和63.1%~82.1%,GA3可显著促进茎的延长生长.内源IAA含量在5-8月份较高,其中以6月份含量最高(4.84 μg·g-1),1月份最低(2.97 μg·g-1);内源ABA含量在1月份达最高(0.61 μg·g-1).用含有1.0 mg·L-1 GA3和50 mg·L-1 6-BA的激素营养液处理可以显著提高金钗石斛生物产量(比CK增产38%),而且总生物碱含量也增加5.6%.  相似文献   

7.
利用Agilent高效液相色谱仪,建立了同时测定郁金香鳞茎中GA_3、IAA、ABA 3种植物内源激素的高效液相色谱检测方法和异丙醇提取方法。采用外标法,C_(18)反相柱,流动相A(甲醇)∶B(磷酸缓冲液pH=3. 5)=45∶55;流速1 mL·min~(-1);检测波长0~3. 2 min 265 nm,3. 0~4. 5 min 212 nm,4. 5~6. 5 min 218 nm,6. 5~13. 0 min265 nm;柱温20℃进行测定;以异丙醇提取剂和二氯甲烷低温摇床提纯鳞茎中内源激素。整个过程操作简单,只需2. 0~2. 5 h可完成激素提取测定,检测方法线性相关度均在0. 995以上,测出限GA_3200 ng·mL~(-1),IAA5 ng·mL~(-1),ABA 20 ng·mL~(-1);提取方法回收率为84. 812%~95. 679%,相对标准偏差为6. 432%~2. 831%。用此方法提取郁金香的内源激素做出的图基线平稳,准确度高,可得到满意的峰形,且操作简单,各环节激素的损失较少。  相似文献   

8.
核酸(DNA和RNA)甲基化/脱甲基是表观遗传调控的重要机制.甲醛参与DNA、RNA的甲基化/脱甲基过程,从而影响表观遗传的调节,包括学习记忆等认知功能.然而,甲醛代谢失调将影响核酸的甲基化与脱甲基,使动物的学习记忆能力下降,造成认知损伤.对北京地区604名老人(≥60岁)的调查显示,内源甲醛含量与被试受教育的年限相关,受教育程度越高,内源甲醛含量越低,反之亦然.这些结果表明,内源甲醛在人类学习记忆中扮演重要的角色,"活到老,学到老"可以延缓甲醛代谢失调引起的老年认知损伤.因此,研究内源甲醛代谢与核酸甲基化修饰之间的关系,对探索记忆储存及认知损伤等表观遗传学相关疾病的发生发展机制,具有一定的启示.  相似文献   

9.
薄层扫描法测定寡核苷酸含量   总被引:6,自引:4,他引:2       下载免费PDF全文
建立了薄层扫描测定寡核苷酸含量的新方法.与传统方法相比,该方法具有简单、微量、样品间无交叉污染等优点,该方法的线性方程 Y=-155.7+0.1428X),相关系数(r=0.9989),线性范围(10—3000ng),平均回收率(97.33%)及平均变异系数(5.5%)均属优良.  相似文献   

10.
超声提取-分光光度法测定远志总皂苷的含量   总被引:3,自引:0,他引:3  
目的:超声提取远志总皂苷,并用分光光度计进行总皂苷含量的测定.方法:超声提取远志总皂苷,以远志皂苷元为对照品,香草醛-冰醋酸-高氯酸为显色剂,采用分光光度法在585 nm处测定远志总皂甙含量.结果:对照品在28~63 μg范围内线性良好(r2=0.9984),平均回收率为100.45%,RSD=1.59%(n=5).超声提取和热回流提取的远志总皂苷含量分别为1.63%,1.50%.结论:超声提取法用时短,提取率高,能达到比传统回流法更理想的效果.分光光度法测定含量简便、快速、准确、可靠.  相似文献   

11.
内源性甲醛异常蓄积与记忆衰退   总被引:2,自引:1,他引:1       下载免费PDF全文
近期,本实验室报道了内源性甲醛浓度与认知功能损伤程度之间的关系(Neurobiol Aging,2011,32(1):31-41).观察到转基因痴呆小鼠(APP、APP/PS1)及衰老加速型(SAMP8)小鼠脑内甲醛浓度较对照组显著升高.参照痴呆鼠脑内甲醛浓度,实验人员对正常成年小鼠进行注射,导致其视觉空间记忆能力减退.注射甲醛消除剂可以降低老龄大鼠体内甲醛浓度、减少APP痴呆模型小鼠脑内的老年斑,且能观察到记忆功能的改善.临床观察显示,老年痴呆患者尿甲醛浓度与认知功能损伤程度之间呈正相关.甲醛的过量蓄积造成脑慢性损伤,可能是散发性老年记忆衰退的机制之一.  相似文献   

12.
Formaldehyde, one of the most toxic organic compounds, is produced and processed in human cells. The level of human endogenous formaldehyde is maintained at a low concentration (0.01–0.08 mmol L−1 in blood) under physiological conditions, but the concentration increases during ageing (over 65 years old). Clinical trials have shown that urine formaldehyde concentrations are significantly different between elderly Alzheimer’s patients (n=91) and normal elderly volunteers (n=38) (P<0.001). Abnormally high levels of intrinsic formaldehyde lead to dysfunction in cognition such as learning decline and memory loss. Excess extracellular and intracellular formaldehyde could induce metabolic response and abnormal modifications of cellular proteins such as hydroxymethylation and hyperphosphorylation, protein misfolding, nuclear translocation and even cell death. This cellular response called formaldehyde stress is dependent upon the concentration of formaldehyde. Chronic impairments of the brain resulted from formaldehyde stress could be one of the mechanisms involved in the process of senile dementia during ageing.  相似文献   

13.
1. When the binding of ethidium bromide to rRNA is measured both in the presence and in the absence of spermine, by spectrophotometric titrations, by gel filtration, or by the changes in fluorescence intensity, spermine competes with ethidium bromide for sites on the rRNA; under the conditions used in these experiments ethidium bromide is bound to the double-stranded regions of rRNA. 2. When an excess of ethidium bromide is added to ribosomes from Bacillus stearothermophilus approx. 80% of the endogenous spermine is displaced from the ribosomes. 3. [(14)C]Spermine is fixed to ribosomes by either formaldehyde or 1,5-difluoro-2,4-dinitrobenzene. Most of the [(14)C]spermine, fixed to ribosomes by 1,5-difluoro-2,4-dinitrobenzene, attaches to the ribosomal protein. 4. It is concluded that most of the endogenous spermine is bound to the double-stranded RNA in ribosomes, and that some of these double-stranded regions to which spermine is attached also have ribosomal proteins bound to them.  相似文献   

14.

Background

Chronic formaldehyde exposure leads to memory impairment and abnormal elevation of endogenous formaldehyde has been found in the brains of Alzheimer's disease (AD) patients. Hyperphosphorylated Tau protein with subsequent aggregates as neurofibrillary tangles (NFTs) is one of the typical pathological characteristics in AD brains. The mechanism underlying abnormally elevated concentrations of endogenous formaldehyde that induce Tau hyperphosphorylation is unknown.

Methods

N2a cells and mice were treated with formaldehyde for different time points, then Western blotting and immunocytochemistry were utilized to determine the phosphorylation and polymerization of Tau protein. HPLC was used to detect the concentration of formaldehyde in cell media.

Results

Under formaldehyde stress, Tau became hyperphosphorylated, not only in the cytoplasm, but also in the nucleus of neuroblastoma (N2a) cells, and mouse brains. Polymers of cellular phospho-Tau were also detected. Significant accumulation of glycogen synthase kinase-3β (GSK-3β) in the nucleus of N2a and mouse brain cells, and elevation of its phosphorylation at Y216, was observed under formaldehyde stress. Formaldehyde-induced Tau hyperphosphorylation was blocked in the presence of LiCl and CT99021, inhibitors of GSK-3β, and by RNAi interference.

Conclusions

Formaldehyde, which may cause age-related memory loss, can act as a factor triggering Tau hyperphosphorylation via GSK-3β catalysis and induces polymerization of Tau.

General significance

Investigation of formaldehyde-induced Tau hyperphosphorylation may provide novel insights into mechanisms underlying tauopathies.  相似文献   

15.
Methanol is a widely used solvent for organic compounds and a human toxicant. In our studies of the metabolism of aromatic amines in the Ames/Salmonella assay, we observed a rapid and quantitative conversion of the mutagenic and carcinogenic aromatic amine 2,4-diaminotoluene (2,4-DAT) to a single product. This product was only produced in the presence of methanol, and not other organic solvents. Isolation of this product showed that it was highly mutagenic in Salmonella TA98 with S9 activation. Characterization of the product of the interaction of methanol and 2,4-DAT indicated that methanol is activated to a reactive intermediate, probably formaldehyde, by the 9000 X g supernatant used in the Ames/Salmonella assay. The formaldehyde subsequently reacts with 2,4-DAT to form the mutagenic product, identified as bis-5,5'(2,4,2',4'-tetraaminotolyl)methane. Results of this study demonstrate that methanol may be an inappropriate solvent for mutation and metabolism studies of aromatic amines and possibly other chemicals, and that solvent-xenobiotic interactions may in some cases lead to the misinterpretation of results.  相似文献   

16.
The content of endogenous morphine-like substance in bovine pituitary and brain was determined by an opiate radioreceptor assay. The intermediate lobe was most concentrated in activity and the brain least concentrated. Most of the endorphin is obtained in a 120 000 g-min fraction from pituitary or brain homogenates.  相似文献   

17.
Summary Slices of the posterior salivary gland and of the superior buccal lobe of the brain of Octopus vulgaris take up 3H-5-hydroxytryptamine in vitro. By light and electron microscopical radioautography the uptake is localised in certain neuronal perikarya and axonal varicosities in the superior buccal lobe, and in nerves that end in the secretory tubules of the posterior salivary gland. These structures do not incorporate 3H-noradrenaline. After formaldehyde histochemistry, monoamine fluorescence is found in some neuronal perikarya of the superior buccal lobe, and in nerves entering the secretory tubules of the gland. The posterior salivary gland nerve, which originates in the superior buccal lobe and supplies the gland, shows a pronounced accumulation of fluorescence on the proximal side of a ligature applied in vivo. It is suggested that monoamines are transported from the brain to the gland by the posterior salivary gland nerves.J. B. would like to thank the Science Research Council, Great Britain, for financial support.  相似文献   

18.
Dimethylammonium 2,4-dichlorophenoxyacetate (2,4-D · DMA) induced strand breaks in PM2 DNA when incubated with CuCl2, whereas 2,4-D · DMA alone or CuCl2 alone did not show any or only a negligible effect. The formation of single strand breaks increased linearly with time and concentration of 2,4-D · DMA. Neocuproine, a specific Cu(I) chelator totally prevented strand break formation. So did catalase (up to 100mM 2,4-D · DMA), but DMSO had only a small protective effect. 2,4-Dichlorophenol, CO2 and formaldehyde were detected as reaction products of 2,4-D and CuCl2. From these results a redox reaction of Cu(II) and 2,4-D is proposed, which could explain the DNA damaging properties of CuCl2/2,4-D · DMA.  相似文献   

19.

Background

Bone cancer pain seriously affects the quality of life of cancer patients. Our previous study found that endogenous formaldehyde was produced by cancer cells metastasized into bone marrows and played an important role in bone cancer pain. However, the mechanism of production of this endogenous formaldehyde by metastatic cancer cells was unknown in bone cancer pain rats. Lysine-specific demethylase 1 (LSD1) is one of the major enzymes catalyzing the production of formaldehyde. The expression of LSD1 and the concentration of formaldehyde were up-regulated in many high-risk tumors.

Objective

This study aimed to investigate whether LSD1 in metastasized MRMT-1 breast cancer cells in bone marrows participated in the production of endogenous formaldehyde in bone cancer pain rats.

Methodology/Principal Findings

Concentration of the endogenous formaldehyde was measured by high performance liquid chromatography (HPLC). Endogenous formaldehyde dramatically increased in cultured MRMT-1 breast cancer cells in vitro, in bone marrows and sera of bone cancer pain rats, in tumor tissues and sera of MRMT-1 subcutaneous vaccination model rats in vivo. Formaldehyde at a concentration as low as the above measured (3 mM) induced pain behaviors in normal rats. The expression of LSD1 which mainly located in nuclei of cancer cells significantly increased in bone marrows of bone cancer pain rats from 14 d to 21 d after inoculation. Furthermore, inhibition of LSD1 decreased the production of formaldehyde in MRMT-1 cells in vitro. Intraperitoneal injection of LSD1 inhibitor pargyline from 3 d to 14 d after inoculation of MRMT-1 cancer cells reduced bone cancer pain behaviors.

Conclusion

Our data in the present study, combing our previous report, suggested that in the endogenous formaldehyde-induced pain in bone cancer pain rats, LSD1 in metastasized cancer cells contributed to the production of the endogenous formaldehyde.  相似文献   

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