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Melatonin and alcohol-related disorders.
Chronobiology International ( IF 2.8 ) Pub Date : 2020-05-18 , DOI: 10.1080/07420528.2020.1761372
Natalia Kurhaluk 1 , Halyna Tkachenko 1
Affiliation  

This review concerns the current knowledge of melatonin and alcohol-related disorders. Chronobiological effects of ethanol are related to melatonin suppression and in relation to inflammation, stress, free radical scavenging, autophagy and cancer risk. It is postulated that both alcohol- and inflammation-induced production of reactive oxygen species (ROS) alters cell membrane properties leading to tissue dysfunction and, subsequent further ROS production. Lysosomal enzymes are often used to assess the relationships between intensified inflammation states caused by alcohol abuse and oxidative stress as well as level of tissue damage estimated by the increased release of cellular enzymes into the extracellular space. Studies have established a link between alcoholism and desynchronosis (circadian disruption). Desynchronosis results from the disorganization of the body’s circadian time structure and is an aspect of the pathology of chronic alcohol intoxication. The inflammatory conditions and the activity of lysosomal enzymes in acute alcohol poisoning or chronic alcohol-dependent diseases are in most cases interrelated. Inflammation can increase the activity of lysosomal enzymes, which can be regarded as a marker of lysosomal dysfunction and abnormal cellular integrity. Studies show alcohol toxicity is modulated by the melatonin (Mel) circadian rhythm. This hormone, produced by the pineal gland, is the main regulator of 24 h (sleep-wake cycle) and seasonal biorhythms. Mel exhibits antioxidant properties and may be useful in the prevention of oxidative stress reactions known to be responsible for alcohol-related diseases. Naturally produced Mel and exogenous sources in food can act in free radical reactions and activate the endogenous defense system. Mel plays an important role in the normalization of the post-stress state by its influence on neurotransmitter systems and the synchronization of circadian rhythms. Acting simultaneously on the neuroendocrine and immune systems, Mel optimizes homeostasis and provides protection against stress.

Abbreviations: ROS, reactive oxygen species; Mel, melatonin; SRV, resveratrol; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; ANT, arylalkylamine-N-acetyltransferase; EC cells, gastrointestinal enterochromaffin cells; MT1, melatonin high-affinity nanomolecular receptor site; MT2, melatonin low-affinity nanomolecular receptor site; ROR/RZR, orphan nuclear retinoid receptors; SOD, superoxide dismutase; CAT, catalase; GPx, glutathione peroxidase; GR, glutathione reductase; GSH, reduced form of glutathione; GSSG, oxidized form of glutathione; TAC, total antioxidant capacity; ONOO∙, peroxynitrite radical; NCAM, neural cell adhesion molecules; LPO, lipid peroxidation; α-KG, α-ketoglutarate, HIF-1α, Hypoxia-inducible factor 1, IL-2, interleukin-2; HPA axis, hypothalamic-pituitary-adrenal axis; Tph1, tryptophan hydroxylase 1; AA-NAT, arylalkylamine-N-acetyltransferase; AS-MT, acetylserotonin O-methyltransferase; NAG, N-acetyl-beta-D-glucosaminidase; HBA1c glycated hemoglobin; LPS, lipopolysaccharide; AAP, alanyl-aminopeptidase; β-GR, β-glucuronidase; β-GD, β-galactosidase; LAP, leucine aminopeptidase.



中文翻译:

褪黑激素和酒精相关疾病。

这项审查涉及褪黑激素和酒精相关疾病的最新知识。乙醇的计时生物学作用与褪黑激素抑制有关,并且与炎症,压力,自由基清除,自噬和癌症风险有关。据推测,酒精和炎症诱导的活性氧物质(ROS)的产生都会改变细胞膜的性质,从而导致组织功能障碍,进而导致ROS的进一步产生。溶酶体酶通常用于评估酒精滥用和氧化应激引起的炎症状态加剧之间的关系,以及通过细胞酶向细胞外空间释放的增加而估计的组织损伤程度。研究已经建立了酗酒与失同步(昼夜节律紊乱)之间的联系。失同步是由于人体的昼夜节律时间结构混乱造成的,是慢性酒精中毒病理的一个方面。在大多数情况下,急性酒精中毒或慢性酒精依赖疾病的炎症状况和溶酶体酶的活性是相互关联的。炎症可增加溶酶体酶的活性,可将其视为溶酶体功能障碍和异常细胞完整性的标志。研究表明,酒精毒性受褪黑素(Mel)昼夜节律的调节。松果体产生的这种激素是24小时(睡眠-觉醒周期)和季节性生物节律的主要调节剂。梅尔具有抗氧化性能,可用于预防已知与酒精有关的疾病的氧化应激反应。天然产生的梅尔和食物中的外源性物质可参与自由基反应并激活内源性防御系统。Mel对神经递质系统的影响和昼夜节律的同步性在应激状态的正常化中起着重要作用。Mel同时作用于神经内分泌和免疫系统,可优化体内平衡并提供抗压力保护。

缩写: ROS,活性氧;梅尔,褪黑激素;SRV,白藜芦醇;NF-κB,活化的B细胞的核因子κ轻链增强剂;ANT,芳基烷基胺-N-乙酰基转移酶;EC细胞,胃肠道肠嗜铬细胞;MT1,褪黑激素高亲和力纳米分子受体位点;MT2,褪黑激素低亲和力纳米分子受体位点;ROR / RZR,孤儿核维甲酸受体;SOD,超氧化物歧化酶;CAT,过氧化氢酶;GPx,谷胱甘肽过氧化物酶;GR,谷胱甘肽还原酶;GSH,还原型谷胱甘肽;GSSG,谷胱甘肽的氧化形式;TAC,总抗氧化能力;ONOO∙ ,过氧亚硝酸根;NCAM,神经细胞粘附分子;LPO,脂质过氧化;α-KG,α-酮戊二酸,HIF-1α,缺氧诱导因子1- α,IL-2,白介素2;HPA轴,下丘脑-垂体-肾上腺轴;Tph1,色氨酸羟化酶1;AA-NAT,芳基烷基胺-N-乙酰基转移酶;AS-MT,乙酰5-羟色胺O-甲基转移酶;NAG,N-乙酰基-β-D-氨基葡萄糖苷酶;HBA1c糖化血红蛋白;LPS,脂多糖;AAP,丙氨酰氨基肽酶;β-GR,β-葡萄糖醛酸苷酶;β-GD,β-半乳糖苷酶;LAP,亮氨酸氨基肽酶。

更新日期:2020-05-18
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