单胺氧化酶与胚胎植入关系的研究进展

单胺氧化酶是一种参与胺类物质代谢的酶,其底物主要包括5-羟色胺、肾上腺素和去甲肾上腺素等生物活性胺。单胺氧化酶通过对其底物的代谢发挥生理作用,主要参与神经活动调节。然而在对胚胎植入和子宫内膜容受形成的研究中发现,在人子宫内膜容受窗期其亚型之一单胺氧化酶A表达明显上调,提示单胺氧化酶与胚胎植入有密切关系。随研究深入,越来越多的研究证实单胺氧化酶参与胚胎着床的调控,但其具体作用及作用机制目前还不清楚。综述有关单胺氧化酶与胚胎植入的相关研究。     

单胺氧化酶与胚胎植入关系的研究进展

单胺氧化酶是一种参与胺类物质代谢的酶,其底物主要包括5-羟色胺、肾上腺素和去甲肾上腺素等生物活性胺.单胺氧化酶通过对其底物的代谢发挥生理作用,主要参与神经活动调节.然而在对胚胎植入和子宫内膜容受形成的研究中发现,在人子宫内膜容受窗期其亚型之一单胺氧化酶A表达明显上调,提示单胺氧化酶与胚胎植入有密切关系.随研究深入,越来越多的研究证实单胺氧化酶参与胚胎着床的调控,但其具体作用及作用机制目前还不清楚.有关单胺氧化酶与胚胎植入的相关研究.     

化学物对单胺类神经递质及其受体的影响研究

单胺类神经递质由儿茶酚胺类和5羟色胺等组成,对单胺类神经递质及其受体的研究重点在单胺氧化酶和其它代谢酶上,目前的研究表明许多神经系统疾病与单胺类神经递质及其受体的异常有关,本文从单胺氧化酶和其它代谢酶方面对化学物影响单胺类神经递质及其受体的研究进行综述。     

矽肺与实验性矽肺的单胺氧化酶与5-羟基吲哚乙酸水平

单胺氧化酶不是一种单一的酶类,而是一组作用于不同单胺类(如酪胺、多巴胺、5-羟色胺等)的酶类,在氧的参与下生成醛,氨与过氧化氢(R-CH_2-NH_2+H_2O+O_2血清单胺氧化酶→CHO+H_2O_2+NH_3)。单胺氧化酶在胶原形成过程中参与分子内及分子间架桥,最后形成高分子不溶性胶原。 5-羟基吲哚乙酸为5-羟色胺的代谢产物。经粉尘激活的5-羟色胺,在单胺氧化酶的参与下生成5-羟色醛,再进一步氧化形成5-羟基吲哚乙酸。     

肺微粒体混合功能氧化酶与肺癌的关系

几个世纪以来,人们通常把肺看作是仅仅与气体交换有关的器官,现在应改变这种看法。据文献报导,肺与内分泌有密切关系,它参与肽、胺和前列腺素的释放、激活和抑制。另外,它还参与毒物的代谢转化。肺微粒体混合功能氧化酶所能催化的反应也是多种多样的,它的非特异性酶促反应的特点,特别是它所含的芳烃羟化酶(Aryl hydrocarbon hydroxylase)为解释多环芳烃的致肺癌性提供了有力的依据。这些研究对于阐明毒物在肺内代谢的过程,毒作用机理和寻找防治职业中毒的具体方法等均有很大的理论和实践意义。一、肺是一个具有代谢毒物能力的器官研究哺乳动物肺混合功能氧化酶和毒物代谢的关系是受到肝微粒体混合功能氧化酶系研究的启发。1963年Garfinkel详细比较了肺     

童年期虐待与单胺氧化酶A基因多态性在青少年反社会行为中的交互作用

青少年反社会行为给个人健康、家庭和社会都带来沉重的负担，引起了公众的广泛关注。目前，大多数研究已证实童年期虐待、单胺氧化酶A基因与反社会行为之间存在关联。然而，关于童年期虐待与单胺氧化酶A基因交互作用与反社会行为之间的关联性尚存在争议。本文旨在对童年期虐待与单胺氧化酶A基因交互作用与青少年反社会行为的最新研究成果及其可能的作用机制进行综述，发现童年期虐待与单胺氧化酶A基因可能通过影响大脑中特定的神经环路、改变情绪调节功能等交互作用于反社会行为。此外，本综述剖析了当前研究结果不一致的可能原因，为今后研究指明方向，也为青少年反社会行为的预防控制提供科学依据。     

尿酸在生物进化中的生理意义

摘要:尿酸是缺乏尿酸氧化酶的生物体内嘌呤代谢的终产物。尿酸氧化酶基因在进化过程中的缺失或保留导致不同的物种体内尿酸代谢途径和尿酸水平不同。下面就不同物种的尿酸水平（本文中均采用尿酸酶法）、相关代谢酶及生理功能方面阐述尿酸在生物进化过程中的意义。     

犬尿氨酸途径在认知功能障碍中的作用及机制

色氨酸(TRP)是人体的必需氨基酸,是许多信号分子形成的前体。犬尿氨酸途径是TRP代谢的主要途径,在吲哚胺2,3-双加氧酶的催化下,形成代谢产物犬尿喹啉酸和喹啉酸,他们通过不同机制作用于N-甲基-D-天冬氨酸受体,参与神经调节,影响认知过程,在许多中枢神经系统疾病的发生发展中起着重要作用。在生理和病理条件下,犬尿氨酸代...     

5-羟吲哚乙酸的研究进展

5-羟吲哚乙酸（5-HIAA）是色氨酸（TRP）-5-羟色胺（5-HT）代谢途径的终产物,由5-HT在单胺氧化酶（MAO）作用下转化而来。人体体液中5-HIAA含量测定对于多种疾病的诊断、治疗及机理研究有重要价值,本文对5-HIAA的生化特性、测定方法及临床意义的研究状况进行综述。     

肠道必需氨基酸代谢及其功能的研究进展

在肠道代谢过程中,食物必需氨基酸可不同程度地被肠道组织利用。这些必需氨基酸,除了用于合成肠黏膜蛋白质外,还可通过不同途径在肠上皮细胞内代谢。它们不仅是小肠黏膜的能量物质,同时还参与肠道内氨基酸、谷胱甘肽和多胺等多种生物活性物质的合成,对维持肠黏膜完整性和肠道功能有重要意义,对整个机体的代谢产生重要的影响。     

Targeting Dietary and Microbial Tryptophan-Indole Metabolism as Therapeutic Approaches to Colon Cancer

Tryptophan metabolism, via the kynurenine (Kyn) pathway, and microbial transformation of tryptophan to indolic compounds are fundamental for host health; both of which are altered in colon carcinogenesis. Alterations in tryptophan metabolism begin early in colon carcinogenesis as an adaptive mechanism for the tumor to escape immune surveillance and metastasize. The microbial community is a key part of the tumor microenvironment and influences cancer initiation, promotion and treatment response. A growing awareness of the impact of the microbiome on tryptophan (Trp) metabolism in the context of carcinogenesis has prompted this review. We first compare the different metabolic pathways of Trp under normal cellular physiology to colon carcinogenesis, in both the host cells and the microbiome. Second, we review how the microbiome, specifically indoles, influence host tryptophan pathways under normal and oncogenic metabolism. We conclude by proposing several dietary, microbial and drug therapeutic modalities that can be utilized in combination to abrogate tumorigenesis.     

Gut microbiota functions: metabolism of nutrients and other food components

The diverse microbial community that inhabits the human gut has an extensive metabolic repertoire that is distinct from, but complements the activity of mammalian enzymes in the liver and gut mucosa and includes functions essential for host digestion. As such, the gut microbiota is a key factor in shaping the biochemical profile of the diet and, therefore, its impact on host health and disease. The important role that the gut microbiota appears to play in human metabolism and health has stimulated research into the identification of specific microorganisms involved in different processes, and the elucidation of metabolic pathways, particularly those associated with metabolism of dietary components and some host-generated substances. In the first part of the review, we discuss the main gut microorganisms, particularly bacteria, and microbial pathways associated with the metabolism of dietary carbohydrates (to short chain fatty acids and gases), proteins, plant polyphenols, bile acids, and vitamins. The second part of the review focuses on the methodologies, existing and novel, that can be employed to explore gut microbial pathways of metabolism. These include mathematical models, omics techniques, isolated microbes, and enzyme assays.     

粗壮女贞提取物抗甲型H1N1流感病毒的细胞代谢组学初探

目的 基于代谢组学分析探讨粗壮女贞提取物抗甲型H1N1流感病毒感染细胞的可能机制。方法 粗壮女贞提取物预处理狗肾传代细胞（MDCK）24 h,加入甲型H1N1流感病毒稀释液作用1 h后换维持液孵育24 h设为实验干预组（CB_IVA24）,同时设置未经粗壮女贞提取物干预的病毒感染细胞为对照组（IVA24）,采集各组细胞上清,基于LC - MS技术对各组进行代谢组学分析,评估数据质量后,通过多元统计分析和生物信息手段挖掘代谢数据。结果 在正、负离子模式下,分别鉴定出代谢物469种和356种,其中上调的差异代谢物共45种（P＜0.05）,下调的差异代谢物共18种（P＜0.05）。代表性差异代谢物通路包括:甲烷代谢（P = 0.02）、不同环境中的微生物代谢（P = 0.02）、苯丙素的生物合成（P = 0.03）、GABA - A受体激动剂/拮抗剂（P = 0.05）。结论 粗壮女贞提取物抑制甲型H1N1流感病毒保护宿主细胞的作用可能与其改变宿主代谢有关。     

Borrelia burgdorferi hijacks cellular metabolism of immune cells: Consequences for host defense

Changes in cellular metabolism have proven to be important factors in driving cell behavior. It has been shown that cellular metabolism of immune cells changes when exposed to or infected by several pathogens: while this is often an adaptation of the host cells to the infection, sometimes it represents a mechanism through which the pathogens evade immune activation. Borrelia burgdorferi sensu lato, the causative agent of Lyme borreliosis, is a pathogen that highly depends on the host to survive, as the bacterium lacks many central metabolic pathways to generate its own nutrients. It is therefore quite likely that the bacterium interacts with host cells to obtain these metabolites and thereby affects metabolism in the host. Previously, several studies have assessed metabolic pathways in B. burgdorferi s.l. and how it adapts to its different host species. However, few studies have looked into how the interaction with the bacterium might affect the host cell metabolism. In this review we present the major metabolic pathways activated during Lyme borreliosis, viewed from both bacterium and host metabolism, and we discuss how these pathways interact with each other, and how they influence pathogenesis of Lyme borreliosis.     

睡眠剥夺小鼠肝脏代谢稳态变化的代谢组学分析

目的 探讨睡眠剥夺对小鼠肝脏中不同代谢物代谢稳态的影响及其关联的代谢通路,阐释睡眠不足对健康影响的代谢相关机制。方法 2月龄C57BL/6J小鼠随机分为睡眠剥夺组和正常对照组,每组4只,普通饲料喂养。睡眠剥夺组利用小鼠睡眠剥夺仪,每日剥夺睡眠20 h,连续10 d;对照组小鼠同样设备条件下自由睡眠10 d。采集动物肝脏,制取上清液,以液相色谱-质谱联用（LC - MS）法检测两组小鼠的肝脏代谢物谱,对差异代谢物进行主成分分析(PCA)和正交偏最小二乘法 - 判别分析(OPLS - DA),并通过MetPA数据库分析差异代谢物的代谢通路。结果 相较于对照组,睡眠剥夺组小鼠共检出11种差异代谢物。代谢通路的权重分析表明,睡眠剥夺对小鼠肝脏物质代谢通路影响较大的主要有嘧啶代谢、氨基酸代谢、谷胱甘肽代谢及花生四烯酸代谢。其关键差异代谢物依次为尿苷、谷氨酸、5’ - 甲基硫代腺苷(MTA)、谷胱甘肽和花生四烯酸。结论 短期睡眠剥夺即可引起机体谷胱甘肽代谢、嘧啶代谢、氨基酸代谢及花生四烯酸代谢等多重代谢紊乱,有损代谢健康。     

Effects of Sublethal Dose of Fipronil on Neuron Metabolic Activity of Africanized Honeybees

Fipronil is a neurotoxic insecticide that inhibits the gamma-aminobutyric acid receptor and can affect gustative perception, olfactory learning, and motor activity of the honeybee Apis mellifera. This study determined the lethal dose (LD₅₀) and the lethal concentration (LC₅₀) for Africanized honeybee and evaluated the toxicity of a sublethal dose of fipronil on neuron metabolic activity by way of histochemical analysis using cytochrome oxidase detection in brains from worker bees of different ages. In addition, the present study investigated the recovery mechanism by discontinuing the oral exposure to fipronil. The results showed that mushroom bodies of aged Africanized honeybees are affected by fipronil, which causes changes in metabolism by increasing the respiratory activity of mitochondria. In antennal lobes, the sublethal dose of fipronil did not cause an increase in metabolic activity. The recovery experiments showed that discontinued exposure to a diet contaminated with fipronil did not lead to recovery of neural activity. Our results show that even at very low concentrations, fipronil is harmful to honeybees and can induce several types of injuries to honeybee physiology.     

精子代谢与男性不育的相关性研究进展

精子发生和成熟中涉及到多种与代谢相关的过程,任何一种代谢异常都可引起精子活动力、受精能力等受损,最终导致男性不育的发生,如精子中活性氧簇过度产生引起的氧化应激反应,损害了精子的运动和获能;在临床上,男性不育症患者的精浆与正常男性相比,其代谢物成分表现出明显的变化,也可反映精子发育和成熟过程的异常,并间接表明这可能与男性不育相关。本文从精子代谢的相关途径、精子代谢组学检测与精子活动力及临床男性不育症的相关性等方面进行综述。     

Carnitine supplementation to obese Zucker rats prevents obesity-induced type I to type II muscle fiber transition and favors an oxidative phenotype of skeletal muscle

Lipid metabolic disorder is a critical risk factor for metabolic syndrome, triggering debilitating diseases like obesity and diabetes. Both obesity and diabetes are the epicenter of important medical issues, representing a major international public health threat. Accumulation of fat in adipose tissue, muscles and liver and/or the defects in their ability to metabolize fatty acids, results in insulin resistance. This triggers an early pathogenesis of type 2 diabetes (T2D). In mammals, lipid metabolism involves several organs, including the brain, adipose tissue, muscles, liver, and gut. These organs are part of complex homeostatic system and communicate through hormones, neurons and metabolites. Our study dissects the importance of mammalian Krüppel-like factors in over all energy homeostasis. Factors controlling energy metabolism are conserved between mammals and Caenorhabditis elegans providing a new and powerful strategy to delineate the molecular pathways that lead to metabolic disorder. The C. elegans intestine is our model system where genetics, molecular biology, and cell biology are used to identify and understand genes required in fat metabolism. Thus far, we have found an important role of C. elegans KLF in FA biosynthesis, mitochondrial proliferation, lipid secretion, and β-oxidation. The mechanism by which KLF controls these events in lipid metabolism is unknown. We have recently observed that C. elegans KLF-3 selectively acts on insulin components to regulate insulin pathway activity. There are many factors that control energy homeostasis and defects in this control system are implicated in the pathogenesis of human obesity and diabetes. In this review we are discussing a role of KLF in human metabolic regulation.     

Alcohol-histamine interactions.

Alcohol and histamine metabolic pathways in the body have the common enzymes aldehyde dehydrogenase and aldehyde oxidase. The metabolite of ethanol, acetaldehyde, can effectively compete with the metabolites of histamine, methylimidazole acetaldehyde, and imidazole acetaldehyde. At the periphery, alcohol and acetaldehyde liberate histamine from its store in mast cells and depress histamine elimination by inhibiting diamine oxidase, resulting in elevated histamine levels in tissues. Histamine mediates alcohol-induced gastric and intestinal damage and bronchial asthma as well as flushing in Orientals. On the other hand, alcohol provokes food-induced histaminosis and histamine intolerance, which is an epidemiological problem. There are many controversial reports concerning the effect of H2 receptor antagonists on ethanol metabolism and the activity of alcohol dehydrogenase in the stomach. In addition, alcohol affects histamine levels in the brain by modulating histamine synthesis, release, and turnover. Histamine receptor antagonists can affect ethanol metabolism and change the sensitivity of animals to the hypnotic effects of alcohol. In contrast to other neurotransmitters, the involvement of the brain histamine system in the mechanisms of the central actions of alcohol and in the pathogenesis of alcoholism is poorly studied and understood.