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Melatonin in yeast and fermented beverages: analytical tools for detection, physiological role and biosynthesis 酵母和发酵饮料中的褪黑素:检测、生理作用和生物合成的分析工具
Pub Date : 2020-06-01 DOI: 10.32794/mr11250053
Sara Muñiz-Calvo, Ricardo Bisquert, J. Guillamón
The recently established relation between the metabolism of aromatic amino acids of yeast and the production of different bioactive molecules during fermentation opens up new and interesting research topics. Among these molecules, melatonin has drawn researchers’ attention in the last decade given its potential benefits for human health. This review summarizes melatonin production in fermented beverages, and conventional and current methods for detecting melatonin in yeast-derived samples. In addition, the role of melatonin in yeast is discussed and the biosynthetic pathway of melatonin is presented in Saccharomyces cerevisiae.
近年来,酵母芳香氨基酸代谢与发酵过程中不同生物活性分子的产生之间的关系开辟了新的有趣的研究课题。在这些分子中,褪黑素在过去十年中引起了研究人员的注意,因为它对人类健康有潜在的好处。本文综述了发酵饮料中褪黑素的生产,以及酵母衍生样品中检测褪黑素的传统和当前方法。此外,还讨论了褪黑素在酵母中的作用,并介绍了褪黑素在酿酒酵母中的生物合成途径。
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引用次数: 2
Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease 褪黑素在调节神经发生中的作用:对阿尔茨海默病的神经退行性病理和类似治疗的影响
Pub Date : 2020-06-01 DOI: 10.32794/mr11250059
M. Shukla, Areechun Sotthibundhu, P. Govitrapong
The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.   
成人大脑神经发生的发现证实了大脑具有很强的可塑性,神经元可以在海马神经发生区产生,而海马神经发生与学习和记忆过程有关。成人神经发生的各个方面在脑功能稳态、衰老和认知方面具有重要意义,揭示了丰富的机制关联,从而进一步帮助促进了阿尔茨海默病(AD)神经退行性过程发展的治疗方法。阿尔茨海默病伴海马功能受损和认知缺陷的神经发生受损非常明显。褪黑素(松果体吲哚胺)增强神经发生,并与阿尔茨海默病的发展有关,因为其水平随着疾病进展而降低。在这篇综述中,我们讨论和评价了褪黑素在病理生理条件下调节神经发生的机制,这将揭示这种情况下的分子基础及其在内源性脑修复中的作用。此外,其成分作为胚胎和成人大脑中神经干和祖细胞增殖和分化的关键调节因子,将有助于强调该吲哚胺在预防和治疗AD方面的治疗意义。
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引用次数: 4
High doses of melatonin confer abiotic stress tolerance to phytopathogenic fungi grown in vitro 高剂量褪黑素使体外培养的植物病原真菌具有非生物应激耐受性
Pub Date : 2020-06-01 DOI: 10.32794/mr11250056
A. Madigan, Christopher Harris, Frank Bedon, A. Franks, K. Plummer
Melatonin is a secondary metabolite produced in all domains of life. Exogenous melatonin triggers defence mechanisms in plants that enhance abiotic stress tolerance. However, knowledge regarding the role of melatonin as a signal or an antioxidant in microbes is lacking. We investigated the in vitro growth responses of three phytopathogenic fungi, Sclerotinia sclerotiorum, Botrytis cinerea and Fusarium oxysporum f.sp. vasinfectum, to abiotic stress (2.5% ethanol with/without cold priming) under varying concentrations of melatonin. Melatonin at high concentrations (1000 – 2000 µM) partially restored fungal growth under stress, compared to controls, suggesting a role for melatonin in alleviating the impacts of stress exposure. Understanding how melatonin impacts fungal growth during stress conditions will be important for future applications using melatonin as a tool for crop protection.
褪黑素是一种次生代谢物,在生命的各个领域都会产生。外源性褪黑素触发植物的防御机制,增强非生物胁迫耐受性。然而,关于褪黑素在微生物中作为信号或抗氧化剂的作用的知识是缺乏的。研究了菌核菌(Sclerotinia sclerotiorum)、灰霉病菌(Botrytis cinerea)和尖孢镰刀菌(Fusarium oxysporum f.sp) 3种植物病原真菌的体外生长反应。在不同浓度的褪黑激素下,对非生物应激(2.5%乙醇带/不带冷启动)的血管感染。与对照组相比,高浓度褪黑激素(1000 - 2000µM)可以部分恢复真菌在胁迫下的生长,这表明褪黑激素在减轻应激暴露的影响中起作用。了解褪黑激素在逆境条件下对真菌生长的影响,将对褪黑激素作为作物保护工具的未来应用具有重要意义。
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引用次数: 4
Biorhythmic and receptor mediated interplay between melatonin and insulin: its consequences on diabetic erythrocytes 褪黑素和胰岛素之间的生物节律和受体介导的相互作用:其对糖尿病红细胞的影响
Pub Date : 2020-06-01 DOI: 10.32794/mr12250060
Adrita Banerjee, A. Chattopadhyay, D. Bandyopadhyay
Diabetes mellitus, one of the crucial epidemics of this country has snatched the sleep of mankind with a steep slope of 108 million in 1980 to more than 460 million in today’s world. The global statistics based on numerological information from World Health Organization (WHO) proposed alarmingly about 642 million affected individuals by 2040. Type 1 diabetes is due to damaged pancreatic β-cells while type 2 diabetes is a result of insulin insensitivity associated with hyperglycaemia. Hyperglycaemia is a principal symptom of diabetes. As a result, the circulatory erythrocytes [red blood cells (RBCs)] become the first and most vulnerable victims to confront such a stressful environment. The RBCs possess many components including haemoglobin, membrane proteins and lipids. They prefer to interact with glucose and form glycated haemoglobin and membrane phospholipid asymmetry which alters RBC adherence. These alterations trigger intracellular reactive oxygen species (ROS) formation and oxidative damage in diabetic erythrocytes. Melatonin, an indoleamine, ameliorates oxidative stress in various tissues and has the capacity of shielding erythrocytes from deleterious stress. A crucial relationship between melatonin and insulin indicates their interplay in occurrence of diabetes. Biorhythm entrained and receptor mediated action of melatonin on pancreatic β-cells in the context of hyperglycaemia are discussed for the first time in the review. Since melatonin protects against erythrocytes, as well as beneficial to diabetes, it is worthy to address proficiency of this indoleamine to the diabetic erythrocytes. In summary, this review has discussed the fostering role of melatonin in hyperglycaemia and encouraged further investigation related to the molecular pathways of melatonin on glucose metabolism. 
糖尿病,这个国家的主要流行病之一,夺走了人类的睡眠,从1980年的1.08亿急剧上升到今天的4.6亿多。基于世界卫生组织(世卫组织)数字学信息的全球统计表明,到2040年,受影响的人数将达到令人震惊的6.42亿人。1型糖尿病是由于胰腺β细胞受损,而2型糖尿病是胰岛素不敏感与高血糖相关的结果。高血糖是糖尿病的主要症状。因此,循环红细胞[红细胞(rbc)]成为面对这种压力环境的第一个也是最脆弱的受害者。红细胞含有许多成分,包括血红蛋白、膜蛋白和脂质。它们倾向于与葡萄糖相互作用,形成糖化血红蛋白和膜磷脂不对称,从而改变红细胞粘附性。这些改变触发细胞内活性氧(ROS)的形成和糖尿病红细胞的氧化损伤。褪黑素是一种吲哚胺,可以改善各种组织中的氧化应激,并具有保护红细胞免受有害应激的能力。褪黑激素和胰岛素之间的重要关系表明它们在糖尿病发生中的相互作用。本文首次讨论了在高血糖情况下褪黑素对胰腺β细胞的生物节律调控和受体介导作用。由于褪黑素对红细胞有保护作用,并且对糖尿病有益,因此值得解决这种吲哚胺对糖尿病红细胞的熟练程度。综上所述,本文讨论了褪黑素在高血糖中的促进作用,并鼓励进一步研究褪黑素对葡萄糖代谢的分子途径。
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引用次数: 1
Melatonin supplementation protects against the benzo(e)pyrene cytotoxicity and optic cup formation disruption in chicken embryos 褪黑素补充可防止鸡胚胎苯并(e)芘细胞毒性和视杯形成破坏
Pub Date : 2020-06-01 DOI: 10.32794/mr11250058
Felipe Teixeira Soares, Hiroyuki Otsuki Guimarães, Paulo Marcelo Silva da Silveira, Antonilde Marcelina Arruda de Sá, L. Sampaio
Benzo(e)pyrene is a cytotoxic chemical to the eyes, while neurohormone melatonin may exhibit protective effects on this cytotoxicity. In the current study, we have investigated the cytotoxic effects of benzo(e)pyrene on the chicken embryonic optic cups formation and whether melatonin supplementation protects chicken embryos against this xenobiotic toxicity. Fertilized chicken eggs were incubated for 48 h and then, they were divided into different groups. These groups included basal (without any treatment), control (distilled water), benzo(e)pyrene, melatonin and benzo(e)pyrene + melatonin groups, respectively. The 10 µl of distilled water or same volume of solution containing treatment compounds were injected into the air sac of the chicken egg. After an additional 18 h of incubation, the chicken embryos were excised and analyzed. The cytotoxicity was measured by a colorimetric whole chick embryo trypan blue assay. In embryos from basal, control and melatonin (0.01, 1 and 100 µM) groups, the frequency of the embryos with normal optic cups was 100% and had no increase in the embryonic cell death observed in post excision. In contrast, the frequency of normal optic cups in the benzo(e)pyrene (0.02 to 1200 µM) groups was significantly reduced (log IC50= -4.24 ± 0.02, R2= 0.98) with concentration-responsive manner. In addition, an increase in the embryonic cell death was also observed (log IC50 = -7.23 ± 0.28; R2 = 0.63). Melatonin treatment dose-responsively inhibited the benzo(e)pyrene-induced optic cups abnormality by 22.35 ± 4.06, 76.38 ± 3.30 and 100 % at the concentrations of 0.01, 1 and 100 µM, respectively. This same phenomenon was also observed in benzo(e)pyrene-induced embryonic cell death, i.e., melatonin suppressed the embryonic cell death by 16.67 ± 4.17, 54.17 ± 4.17 and 100 % with the abovementioned concentrations, respectively. Thus, melatonin supplementation injected into the chicken eggs protected against the benzo(e)pyrene embryotoxicity. Different pathways can be involved in melatonin’s protective effects. 
苯并(e)芘是一种对眼睛具有细胞毒性的化学物质,而神经激素褪黑激素可能对这种细胞毒性具有保护作用。在目前的研究中,我们研究了苯并(e)芘对鸡胚胎视神经杯形成的细胞毒性作用,以及褪黑激素是否能保护鸡胚胎免受这种外源毒性的影响。将受精卵孵育48 h,然后将其分成不同的组。各组分别为基础组(未经处理)、对照组(蒸馏水)、苯并芘组、褪黑素组和苯并芘+褪黑素组。将10µl蒸馏水或等量含处理化合物的溶液注入鸡蛋的气囊中。再孵育18小时后,切除鸡胚进行分析。采用全鸡胚台盼蓝比色法测定细胞毒性。在基底、对照和褪黑素(0.01、1和100µM)组的胚胎中,正常视杯的胚胎频率为100%,并且在切除后观察到的胚胎细胞死亡没有增加。相比之下,苯并(e)芘(0.02 ~ 1200µM)组正常光杯的频率显著降低(对数IC50= -4.24±0.02,R2= 0.98),呈浓度响应方式。此外,还观察到胚胎细胞死亡的增加(log IC50 = -7.23±0.28;R2 = 0.63)。在浓度为0.01、1和100µM时,褪黑素对苯并芘诱导的视杯异常的抑制作用分别为22.35±4.06、76.38±3.30和100%。在苯并芘诱导的胚胎细胞死亡中也观察到同样的现象,即褪黑素在上述浓度下对胚胎细胞死亡的抑制作用分别为16.67±4.17、54.17±4.17和100%。因此,向鸡蛋中注射褪黑激素可以防止苯并(e)芘的胚胎毒性。褪黑素的保护作用可能涉及不同的途径。
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引用次数: 2
Protective effects of melatonin on mitochondrial injury and neonatal neuron apoptosis induced by maternal hypothyroidism 褪黑素对母亲甲状腺功能减退所致线粒体损伤及新生儿神经元凋亡的保护作用
Pub Date : 2019-12-15 DOI: 10.32794/mr11250040
Mariyah Hidayat, S. Khaliq, Abdullah Khurram, K. Lone
In the current study, we reported the beneficial effects of melatonin in preventing neonatal neuronal apoptosis induced by maternal hypothyroidism. During the gestation and early lactation stages, the mother rats were given propylthiouracil (PTU) to inhibit their thyroid gland activity which resulted in the increased serum TSH and reduced T4 levels. This maternal hypothyroidism caused neuronal apoptosis of their pups, particularly in the CA3 area of hippocampus. Melatonin administration preserved function of thyroid gland and significantly reduced the apoptosis. Further studies have uncovered the potentially protective mechanisms of melatonin, that is, as a mitochondrial targeted antioxidant, melatonin preserves the mitochondrial outer membrane, inhibits the release of cytochrome C from mitochondria to cytoplasm and down regulates the gene expressions of Bax, along with caspases 3 and 9. Thus, melatonin breaks the mitochondria related apoptotic pathway to suppress the neuronal apoptosis induced by the maternal hypothyroidism.  Considering the limited remedies to effectively treat hypothyroidism associated neonatal brain damage, melatonin may provide an alternative method for this disorder.
在目前的研究中,我们报道了褪黑素在预防母亲甲状腺功能减退引起的新生儿神经元凋亡中的有益作用。在妊娠期和哺乳期早期给予丙硫尿嘧啶(PTU)抑制母鼠甲状腺活性,使其血清TSH升高,T4降低。母体甲状腺功能减退导致幼鼠神经元凋亡,尤其是海马CA3区神经元凋亡。褪黑素可保护甲状腺功能,显著减少细胞凋亡。进一步的研究揭示了褪黑素的潜在保护机制,即作为线粒体靶向抗氧化剂,褪黑素保护线粒体外膜,抑制细胞色素C从线粒体向细胞质的释放,下调Bax、caspases 3和caspases 9的基因表达。由此可见,褪黑素可破坏线粒体相关凋亡通路,抑制母体甲状腺功能减退所致的神经元凋亡。考虑到有效治疗甲状腺功能减退相关新生儿脑损伤的方法有限,褪黑激素可能为这种疾病提供了一种替代方法。
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引用次数: 0
Understanding the role of melatonin in cancer metabolism 了解褪黑素在癌症代谢中的作用
Pub Date : 2019-08-31 DOI: 10.32794/11250032
J. Mayo, R. Cernuda, Isabel Quirós, Pablo Luque Rodríguez, Joselyn García, D. Hevia, R. Sainz
Oncogenes alters metabolic pathways while the resulted metabolites, in turn, modifies the expression and production of oncogenes or tumor suppressors. Metabolic reprogramming has been considered as a consequence of oncogenes’ activity more than a phenotypic change of cancer cells. Currently, three different metabolic alterations for cancer cells, i.e. an increased ability to acquire nutrients, preferred metabolic pathways or differentiation pathways, have been described. Melatonin is a molecule which has been extensively investigated since it was discovered more than 60 years ago. From the aggregation of melanophores to antioxidant chain reactions, melatonin has been proposed to be an important molecule affecting the physiology of mammals but also the biology of unicellular organisms. Thus, the decrease in melatonin synthesis in humans with age has been related to several diseases including neurodegeneration and cancer. For many years, it has been believed that melatonin crosses biological membranes easily to exert its functions. However, this notion has been challenged by recent discovery that majority of melatonin might cross biological membranes through glucose transporters. This initial observation has generated a new important idea about melatonin’s function, that is, the membrane transportation of melatonin and glucose by the same transporter in cancer cells would be a new promising mechanism of this indole by either reprogramming glucose metabolism, impeding nutrients uptake or assigning preferred metabolic pathways in cancer cells. In this review, we will focus the role of melatonin as an antiproliferative agent, and its connection with metabolic changes due to melatonin competition with glucose.
癌基因改变代谢途径,而产生的代谢物反过来又改变癌基因或肿瘤抑制因子的表达和产生。代谢重编程被认为是癌基因活性的结果,而不是癌细胞的表型变化。目前,已经描述了癌细胞的三种不同的代谢改变,即获得营养物质的能力增加,首选代谢途径或分化途径。褪黑素是一种分子,自60多年前被发现以来,人们对其进行了广泛的研究。从黑色素细胞聚集到抗氧化链式反应,褪黑素已被认为是影响哺乳动物生理和单细胞生物生物学的重要分子。因此,随着年龄的增长,褪黑激素合成的减少与包括神经变性和癌症在内的几种疾病有关。多年来,人们一直认为褪黑素很容易穿过生物膜发挥作用。然而,这一观点受到了最近发现的挑战,即大多数褪黑激素可能通过葡萄糖转运体穿过生物膜。这一初步观察产生了关于褪黑激素功能的一个新的重要观点,即在癌细胞中,通过相同的转运体对褪黑激素和葡萄糖的膜运输可能是这种吲哚的一个新的有希望的机制,通过重新编程葡萄糖代谢,阻碍营养物质的摄取或在癌细胞中分配优先的代谢途径。在这篇综述中,我们将重点介绍褪黑激素作为一种抗增殖药物的作用,以及褪黑激素与葡萄糖竞争引起的代谢变化。
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引用次数: 8
Melatonin as a potential therapeutic molecule against myocardial damage caused by high fat diet (HFD) 褪黑素作为抗高脂饮食心肌损伤的潜在治疗分子
Pub Date : 2019-08-31 DOI: 10.32794/mr11250030
G. Bose, A. Ghosh, A. Chattopadhyay, P. Pal, D. Bandyopadhyay
     High fat diet (HFD) has been implicated as an independent risk factor for cardiovascular diseases since the second half of the last century. The HFD causes various pathogeneses and progressions of cardiovascular diseases. The oxidative stress and pro-inflammatory reactions induced by the HFD are probably the major risk factors of myocardial damage. In this review we highlight the roles of different dietary fats on cardiovascular diseases and the protective effects of melatonin as a potent antioxidant and anti-inflammation molecule on the pathology induced by HFD. The focus will be given to the molecular mechanisms. The protective effects of melatonin on HFD induced myocardial damage are mediated by multiple pathways. These include that melatonin suppresses the oxidative stress, preserves the normal fat and glucose metabolisms and reduces the pro-inflammatory reactions. Melatonin downregulates the expressions of pro-inflammatory genes of TLR4, NF-κB and NLRP3-Caspase1 but upregulates the expressions of anti-inflammatory genes of Sirt3, CTRP3 and RISK. All of these render melatonin as a powerful protector against cardiovascular diseases caused by the HFD. This review suggests that melatonin can be used as a therapeutic agent in this specific condition.  
自上世纪下半叶以来,高脂肪饮食(HFD)已被认为是心血管疾病的独立危险因素。HFD引起心血管疾病的各种发病机制和进展。HFD诱导的氧化应激和促炎反应可能是心肌损伤的主要危险因素。本文综述了不同膳食脂肪在心血管疾病中的作用,以及褪黑素作为一种有效的抗氧化剂和抗炎症分子对HFD诱导的病理的保护作用。重点将放在分子机制。褪黑素对HFD诱导心肌损伤的保护作用是通过多种途径介导的。其中包括褪黑素抑制氧化应激,保持正常的脂肪和葡萄糖代谢,减少促炎反应。褪黑素下调促炎基因TLR4、NF-κB和NLRP3-Caspase1的表达,上调抗炎基因Sirt3、CTRP3和RISK的表达。所有这些都使褪黑素成为对抗由HFD引起的心血管疾病的强大保护器。这一综述表明,褪黑激素可以作为一种治疗这种特殊情况的药物。
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引用次数: 2
Protective mechanisms of melatonin on caprine spleen injury induced by cadmium (Cd): an in vitro study 褪黑素对镉(Cd)致山羊脾损伤保护机制的体外研究
Pub Date : 2019-08-31 DOI: 10.32794/11250031
R. Majumder, M. Datta, P. Pal, B. Bhattacharjee, A. Chattopadhyay, D. Bandyopadhyay
Current study explores the potential mechanisms of melatonin on cadmium-induced spleen tissue injury of goat. Spleen tissues were incubated with different concentrations (50, 100, 200, 400 and 600 µM) of cadmium acetate (Cd), respectively and the lipid peroxidation of the tissue was measured. It was found that Cd at the level of 400 µM induced maximum spleen damage among other concentrations. Thus, Cd 400 µM was selected to examine whether melatonin treatment can protect against this damage. The results showed that Cd increased the oxidative stress in the spleen tissue either by elevating pro-oxidant enzymes, or, by suppressing the variety of antioxidant enzymes and thus, to increase the intracellular reactive oxygen species (ROS). Melatonin treatment at the concentrations of 0.25, 0.5 and 1 mM significantly reduced all these alterations, respectively. At the level of cellular organelles, Cd caused mitochondrial morphological and functional injuries. These include mitochondrial surface distortion and inhibitions of glycolytic, Krebs cycle, and respiratory chain enzymes. Melatonin at a concentration of 0.5 mM almost completely preserved Cd induced mitochondrial pathological alterations. Cd pollution is a cause of serious health hazard world wide, particularly in the developing areas and currently, there is no specific remedy for Cd toxicities. The results suggest that melatonin is a promising therapeutic agent to combat Cd-induced oxidative stress and it deserves further investigation clinically. 
本研究旨在探讨褪黑素在镉致山羊脾组织损伤中的作用机制。分别用不同浓度(50、100、200、400、600µM)的醋酸镉(Cd)孵育脾脏组织,测定组织脂质过氧化水平。结果表明,Cd在400µM水平对脾脏的损伤最大。因此,选择Cd 400µM来检查褪黑激素治疗是否可以防止这种损伤。结果表明,Cd或通过提高促氧化酶水平,或通过抑制抗氧化酶的多样性,从而增加细胞内活性氧(ROS),从而增加脾脏组织的氧化应激。褪黑素浓度为0.25、0.5和1 mM的处理分别显著降低了所有这些变化。在细胞器水平,镉引起线粒体形态和功能损伤。这些包括线粒体表面畸变和糖酵解、克雷布斯循环和呼吸链酶的抑制。褪黑素浓度为0.5 mM时,几乎完全保存Cd诱导线粒体病理改变。Cd污染是世界范围内严重危害健康的一个原因,特别是在发展中地区,目前没有针对Cd毒性的具体补救措施。结果表明,褪黑素是一种很有前景的抗cd诱导氧化应激的治疗药物,值得进一步的临床研究。
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引用次数: 3
Inhibition of mitochondrial pyruvate dehydrogenase kinase: a proposed mechanism by which melatonin causes cancer cells to overcome cytosolic glycolysis, reduce tumor biomass and reverse insensitivity to chemotherapy 抑制线粒体丙酮酸脱氢酶激酶:褪黑素引起癌细胞克服胞质糖酵解、减少肿瘤生物量和逆转对化疗不敏感的一种被提出的机制
Pub Date : 2019-08-31 DOI: 10.32794/mr11250033
R. Reiter, Ramaswamy Sharma, Q. Ma, S. Rosales‐Corral, D. Acuña-Castroviejo, G. Escames
This review presents a hypothesis to explain the role of melatonin in regulating glucose metabolism in cancer cells.  Many cancer cells use cytosolic glycolysis (the Warburg effect) to produce energy (ATP).  Under these conditions, glucose is primarily converted to lactate which is released into the blood in large quantities. The Warburg effect gives cancer cells advantages in terms of enhanced macromolecule synthesis required for accelerated cellular proliferation, reduced cellular apoptosis which enhances tumor biomass and a greater likelihood of metastasis.  Based on available data, high circulating melatonin levels at night serve as a signal for breast cancer cells to switch from cytosolic glycolysis to mitochondrial glucose oxidation and oxidative phosphorylation for ATP production. In this situation, melatonin promotes the synthesis of acetyl-CoA from pyruvate; we speculate that melatonin does this by inhibiting the mitochondrial enzyme pyruvate dehydrogenase kinase (PDK) which normally inhibits pyruvate dehydrogenase complex (PDC), the enzyme that controls the pyruvate to acetyl-CoA conversion. Acetyl-CoA has several important functions in the mitochondria; it feeds into the citric acid cycle which improves oxidative phosphorylation and, additionally, it is a necessary co-factor for the rate limiting enzyme, arylalkylamine N-acetyltransferase, in mitochondrial melatonin synthesis.  When breast cancer cells are using cytosolic glycolysis (during the day) they are of the cancer phenotype; at night when they are using mitochondria to produce ATP via oxidative phosphorylation, they have a normal cell phenotype. If this day:night difference in tumor cell metabolism is common in other cancers, it indicates that these tumor cells are only cancerous part of the time.  We also speculate that high nighttime melatonin levels also reverse the insensitivity of tumors to chemotherapy.
本文提出了一种假说来解释褪黑激素在调节癌细胞葡萄糖代谢中的作用。许多癌细胞利用胞质糖酵解(Warburg效应)来产生能量(ATP)。在这种情况下,葡萄糖主要转化为乳酸,并大量释放到血液中。在加速细胞增殖所需的增强大分子合成方面,Warburg效应赋予癌细胞优势,减少细胞凋亡,增加肿瘤生物量和更大的转移可能性。根据现有数据,夜间高循环褪黑激素水平是乳腺癌细胞从胞质糖酵解转向线粒体葡萄糖氧化和氧化磷酸化以产生ATP的信号。在这种情况下,褪黑素促进丙酮酸合成乙酰辅酶a;我们推测褪黑素通过抑制线粒体酶丙酮酸脱氢酶激酶(PDK)来实现这一点,PDK通常抑制丙酮酸脱氢酶复合物(PDC),这种酶控制丙酮酸转化为乙酰辅酶a。乙酰辅酶a在线粒体中有几个重要的功能;它进入柠檬酸循环,改善氧化磷酸化,此外,它是线粒体褪黑激素合成中限速酶芳基烷基胺n -乙酰转移酶的必要辅助因子。当乳腺癌细胞使用胞质糖酵解时(白天),它们具有癌症表型;在晚上,当它们利用线粒体通过氧化磷酸化产生ATP时,它们具有正常的细胞表型。如果这种肿瘤细胞代谢的昼夜差异在其他癌症中是常见的,这表明这些肿瘤细胞只是部分时间癌变。我们还推测夜间高褪黑素水平也能逆转肿瘤对化疗的不敏感。
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引用次数: 49
期刊
Melatonin Research
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