乙醇 | 64-17-5

• 物质功能分类: 原料药 - 人工合成抗感染类药 - 消毒防腐药
• 分子结构分类: 有机化合物 - 有机氧化合物
• 中文名称: 乙醇
• 中文别名: 绝对酒精；乙醇(发醇法)；食用酒精；无水乙醇；食用乙醇；变性酒精；调香级食用酒精；酒精；变性乙醇；无水酒精；无水乙醇(药用)
• 英文名称: ethanol
• 英文别名: Ethyl alcohol；EtOH；aqueous ethanol；alcohol
• CAS: 64-17-5
• 化学式: C₂H₆O
• mdl: MFCD00003568
• 分子量: 46.069
• InChiKey: LFQSCWFLJHTTHZ-UHFFFAOYSA-N

物化性质

• 熔点：
  -114°C
• 沸点：
  78°C
• 密度：
  0.789 g/mL at 20 °C
• 蒸气密度：
  1.59 (vs air)
• 闪点：
  12°C
• 溶解度：
  水：可溶（完全）
• 最大波长(λmax)：
  λ: 240 nm Amax: 0.40λ: 250 nm Amax: 0.30λ: 260 nm Amax: 0.30λ: 270 nm Amax: 0.10λ: 340 nm Amax: 0.10
• 暴露限值：
  TLV-TWA 1900 mg/m3 (1000 ppm) (ACGIH).
• 介电常数：
  24.3（25℃）
• LogP：
  -0.19
• 物理描述：
  Ethanol appears as a clear colorless liquid with a characteristic vinous odor and pungent taste. Flash point 55°F. Density 6.5 lb / gal. Vapors are heavier than air.
• 颜色/状态：
  Clear, colorless, very mobile liquid
• 气味：
  Pleasant
• 味道：
  Burning
• 蒸汽密度：
  1.59 (NTP, 1992) (Relative to Air)
• 蒸汽压力：
  VP: -73 °C at 1 Pa; -56 °C at 10 Pa; -34 °C at 100 Pa; -7 °C at 1 kPa (all extrapolated); 29.2 °C at 10 kPa; 78.0 °C at 100 kPa
• 亨利常数：
  Henry's Law constant = 5X10-6 atm-cu m/mol at 25 °C
• 大气OH速率常数：
  3.27e-12 cm3/molecule*sec
• 稳定性/保质期：

  1. 化学性质：乙醇是醇类的代表物质，化学性质如下：

     • 生成金属衍生物：乙醇与钠、钾等碱金属反应生成乙醇化物；低级醇容易发生此反应，有时有着火危险。高级醇反应较慢，特别是高级仲醇、叔醇反应速度小，不容易生成醇化物。铝、镁、钙、钡等金属与醇一起煮沸也能生成醇化物。

       2C2H5OH + 2Na→2C2H5ONa + H2

     • 生成酯：乙醇与有机酸、无机酸反应时脱水生成酯，该反应是可逆的。常用强酸、金属盐、离子交换树脂等作催化剂；甲醇的反应性最大，C2~C5的伯醇反应速度大致相等；仲醇、叔醇的反应性小，在酸性介质中容易脱水生成烯烃，一般用间接的方法制备叔醇的酯。酰氯和酸酐与醇更易进行酯化反应。

       C2H5OH + RCOOH→RCOOC2H5 + H2O

     • 生成卤代烷：乙醇与卤代氢、亚硫酰氯或卤化磷反应时，羟基被卤原子置换，生成卤代烷。叔醇的反应速度最快，仲醇、伯醇的反应速度依次降低；卤化氢以碘化氢最快，氯化氢最慢。

     • 脱水反应：醇的脱水有分子间脱水和分子内脱水两种方式。分子间脱水生成醚，分子内脱水生成烯烃。反应的方式取决于醇的结构和条件；一般高温有利于生成烯烃，低温有利于生成醚；叔醇易脱水成烯，难以得到醚。反应常在催化剂存在下进行，常用的催化剂有硫酸、磷酸、三氧化二铝、磷酸铝等。

     • 缩醛的生成：乙醇在室温下与醛反应生成半缩醛，并放出热量。在酸性催化剂如HCl、H2SO4或CaCl2存在下，进一步与1mol醇反应生成缩醛。

     • 氧化反应：伯醇氧化生成醛，醛再继续氧化成羧酸；仲醇氧化生成酮；叔醇难氧化，在剧烈的条件下氧化生成碳原子数较叔醇少的产物。常用的氧化剂有重铬酸钠、硫酸或三氧化铬和冰乙酸。乙醇氧化生成乙醛或乙酸。

     • 脱氢反应：伯醇或仲醇的蒸气在高温下通过脱氢催化剂如铜、银、镍或铜-氧化铬时，则脱氢生成醛或酮；叔醇不能脱氢，只能脱水成烯烃。

     • 其他反应：乙醇易与乙烯酮、环氧乙烷、异氰酸酯等发生反应，分别生成乙酸酯、烷氧基醇和氨基甲酸乙酯。乙醇用漂白粉溶液氧化生成氯仿；用碘和氢氧化钾氧化生成碘仿；与不含亚硝酸的硝酸作用生成硝酸乙酯；与汞和过量的硝酸作用生成雷酸汞Hg(ONC)2；与氧化汞和氢氧化钠一起加热生成爆炸性物质C2Hg6O4H2。

  2. 与其他化学品反应剧烈，易发生爆炸。易挥发且极易燃烧，火焰呈淡蓝色。蒸气能与空气形成爆炸混合物，其爆炸极限为4.3%~19.0%(体积百分比)。具有吸湿性，并能与水形成共沸混合物。微毒。

  3. 稳定性：稳定

  4. 避免接触强氧化剂、酸类、酸酐、碱金属及胺类。

  5. 不会发生聚合反应。

• 自燃温度：
  685 °F (363 °C)
• 粘度：
  1.074 mPa.s at 25 °C
• 燃烧热：
  1336.8 kJ/mol at 25 °C
• 汽化热：
  42.32 kJ/mol at 25 °C
• 表面张力：
  21.97 mN/m at 25 °C
• 电离电位：
  10.47 eV
• 气味阈值：
  Odor Threshold Low: 49.0 [mmHg]; Odor Threshold High: 716.0 [mmHg]; Detection odor threshold from AIHA (mean = 180 ppm)
• 折光率：
  Index of refraction: 1.3611 at 20 °C/D
• 解离常数：
  15.9 (at 25 °C)
• 保留指数：
  443.2 ;443.8 ;443 ;444.7 ;444.7 ;436 ;446 ;446 ;446 ;416 ;432 ;457.4 ;459.2 ;463.6 ;457.4 ;459.2 ;463.6 ;440 ;414.4 ;496 ;427 ;423 ;427 ;439 ;421 ;458 ;454 ;472 ;493 ;440 ;493 ;462 ;439 ;440 ;442.2 ;428.2 ;455 ;450 ;428.8 ;433.5 ;443 ;440 ;427 ;436 ;443 ;443 ;428 ;440 ;421 ;427 ;440 ;406 ;411 ;411 ;415 ;427 ;443 ;421

计算性质

• 辛醇/水分配系数(LogP)：
  -0.1
• 重原子数：
  3
• 可旋转键数：
  0
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  20.2
• 氢给体数：
  1
• 氢受体数：
  1

ADMET

代谢

肝脏的。由细胞色素P450酶CYP2E1代谢。

Hepatic. Metabolized by cytochrome P450 enzyme CYP2E1.

来源:DrugBank

代谢

乙醇在肝细胞中的代谢会导致活性氧种类的生成、内质网应激以及线粒体能量和氧化还原代谢的改变。在乙醇暴露引起的肝病中，自噬不仅作为清洁剂去除受损的细胞器和细胞溶质组分，而且还选择性地清除特定的目标，如脂滴和受损的线粒体。此外，乙醇似乎在某些浓度下在保护肝细胞免受凋亡中发挥作用。本文描述了自噬在乙醇暴露肝病中的证据、功能以及潜在机制，以及乙醇对自噬影响的争议。

Ethanol metabolism in hepatocytes causes the generation of reactive oxygen species, endoplasmic reticulum stress and alterations in mitochondrial energy and REDOX metabolism. In ethanol-exposed liver disease, autophagy not only acts as a cleanser to remove damaged organelles and cytosolic components, but also selectively clears specific targets such as lipid droplets and damaged mitochondria. Moreover, ethanol appears to play a role in protecting hepatocytes from apoptosis at certain concentrations. This article describes the evidence, function and potential mechanism of autophagy in ethanol-exposed liver disease and the controversy surrounding the effects of ethanol on autophagy.

来源:Hazardous Substances Data Bank (HSDB)

代谢

法庭上有人声称，创伤受害者血乳酸升高可能会导致血清乙醇检测呈假性升高。大多数医院使用间接的方法来测量乙醇，即将血清样本添加到酒精脱氢酶和氧化烟酰胺腺嘌呤二核苷酸（NAD+）的混合物中。这允许患者血清中的任何乙醇被代谢为乙醛，在这个过程中导致NAD+还原为NADH。然后使用分光光度法测量NADH。法庭上的指控源于这样一个概念，即乳酸通过乳酸脱氢酶（LDH）氧化为丙酮酸会导致摩尔对摩尔的NAD+还原为NADH，因此理论上可能导致乳酸和LDH升高的患者出现假性乙醇浓度升高。为了提供可能的测试标本，确定了2015年4月20日至2015年12月13日到大学医院就诊的乳酸和LDH浓度升高的患者。如果血清量足够，样本将用于重新运行乳酸和LDH浓度的同时进行酶促乙醇检测。在这次重新检测中，乳酸和LDH浓度升高，并且产生阳性乙醇浓度的任何样本都被送去进行乙醇浓度的确认气相色谱测试。对照组包括20个乳酸和LDH正常的样本。最终分析中包括了37个样本。只有4名患者的酶促乙醇浓度升高，这4名患者也有可测量的GC乙醇浓度。这个数据集中的乳酸范围从2.4到24.2 mmol/L，平均值为6.53 mmol/L（正常值0.5-2.2）。LDH范围从242到8838 U/L，平均值为1695 U/L（正常值122-225 U/L）。在乳酸和LDH正常的患者上运行了20个对照样本，没有一个产生阳性的酶促乙醇结果。这些数据不支持乳酸和LDH升高会导致急诊科就诊的活体患者通过酶促乙醇检测产生假阳性血清乙醇结果的观点。

There have been allegations in the courtroom that elevated serum lactic acid in trauma victims can yield a falsely elevated serum ethanol assay. Most hospitals utilize an indirect method of ethanol measurement where a serum sample is added to a mix of alcohol dehydrogenase and oxidized nicotinamide adenine dinucleotide (NAD+). This allows any ethanol in the patient's serum to be metabolized to acetaldehyde, and in the process results in the reduction of NAD+ to NADH. NADH is then measured using spectrophotometry. The courtroom allegation stems from the concept that oxidation of lactate to pyruvate by lactate dehydrogenase (LDH) results in the same molar-for-molar reduction of NAD+ to NADH, and could therefore theoretically cause patients with elevated lactate and LDH to have a falsely elevated ethanol concentration. Patients with elevated lactic acid and LDH concentrations who presented to a university hospital from 20 April 2015 to 13 December 2015 were identified to provide possible test specimens. If a sufficient amount of serum was available, the sample was used to re-run the lactate and LDH concentration simultaneously with an enzymatic ethanol assay. Any samples that had elevated lactic acid and LDH concentrations on this retesting, and also yielded a positive ethanol concentration, were sent for confirmatory gas chromatography testing of ethanol concentrations. A control group of 20 samples with normal lactate and LDH were included. A total of 37 samples were included in the final analysis. Only 4 patients had an elevated enzymatic ethanol concentration, and all 4 also had a measurable GC ethanol concentration. The lactate in this dataset ranged from 2.4 to 24.2 mmol/L, with a mean of 6.53 mmol/L (normal value 0.5-2.2). The LDH ranged from 242 to 8838 U/L with a mean of 1695 U/L (normal value 122-225 U/L). Twenty control samples were run on patients with normal lactate and LDH, none of which yielded a positive enzymatic ethanol result. This data does not support the contention that an elevated LDH and lactate can yield a false positive serum ethanol result as run by enzymatic ethanol assay in live patients presenting to the emergency department.

来源:Hazardous Substances Data Bank (HSDB)

代谢

乙醇主要通过肝脏的连续氧化代谢，首先在醇脱氢酶（ADE）的作用下转化为乙醛，然后在醛脱氢酶（ALDH）的作用下转化为乙酸。每个代谢步骤都需要NAD+；因此，将1摩尔乙醇（46克）氧化为1摩尔乙酸在肝脏中需要2摩尔NAD+；实际上，NAD+的可用性限制了乙醇的代谢，大约为每小时8克或10毫升（大约170毫摩尔），对于一个70公斤的成年人来说，或者大约为每小时120毫克/公斤。因此，与达到的高血醇水平（BELs）相比，肝脏乙醇代谢功能在相对较低的血液水平时就达到了饱和，乙醇代谢是一个零级过程（单位时间内恒定数量）。少量的乙醇通过尿液、汗液和呼吸排出，但代谢为醋酸的部分占到摄入乙醇的90-98%，这主要归因于ADH和ADLH的肝脏代谢。

Ethanol is metabolized largely by sequential hepatic oxidation, first to acetaldehyde by alcohol dehydrogenase (ADE) and then to acetic acid by aldehyde dehydrogenase (ALDH). Each metabolic step requires NAD+; thus oxidation of 1 mol ethanol (46 g) to 1 mol acetic acid requires 2 mol NAD+ in the liver; indeed, NAD+ availability limits ethanol metabolism to about 8 gr or 10 mL (approximately 170 mmol) per hour in a 70-kg adult, or approximately 120 mg/kg per hour. Thus hepatic ethanol metabolism functionally saturates at relatively low blood levels compared with the high blood ethano levels (BELs) achieved, and ethanol metabolism is a zero-order process (constant amount per unit time). Small amounts of ethanol are excreted in urine, sweat, and breath, but metabolism to acetate accounts to 90-98% of ingested ethanol, mostly owing to hepatic metabolism by ADH and ADLH.

来源:Hazardous Substances Data Bank (HSDB)

代谢

乙醇、丙醇、异丙醇、丁醇、异丁醇、仲丁醇和叔丁醇在兔子口服给药后的代谢进行了研究。血液pH在丙醇、丁醇和异丁醇的情况下偏酸性，在异丙醇和仲丁醇的情况下偏碱性，而在乙醇和叔丁醇的情况下没有观察到变化。丁醇和异丁醇的尿排泄率最低。乙醛和醋酸被检测为乙醇和丙醇的尿代谢物，而异丁醛和戊酸是异丁醇的代谢物。

Metabolism of ethanol, propanol, isopropanol, butanol, isobutanol, sec-butanol, and tert-butanol was studied after oral administration in rabbits. Blood pH was on the acid side with propanol, butanol, and isobutanol, and on the alkaline side with isopropanol and sec-butanol, but no change was observed with ethanol and tert-butanol. Butanol and isobutanol had the lowest rate of urinary excretion. Acetaldehyde and acetic acid were detected as the urinary metabolites of ethanol and propanol, whereas isobutyraldehyde and isovaleric acid were the metabolites of isobutanol.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 毒性总结

识别和使用：乙醇是一种清澈、无色、非常流动的液体。它以适当的稀释用于酒精饮料中，并作为合成有机化学和色谱中的试剂，以及工业和实验室有机溶剂。其他用途包括制造变性酒精、药品（摩擦剂、乳液、补品、古龙水）和香水。在汽油中作为辛烷增强剂。药物助剂（溶剂）。 人体研究：乙醇是一种中枢神经系统（CNS）抑制剂。它增强了γ-氨基丁酸（GABA）在GABA-A受体上的抑制效应，并竞争性地抑制甘氨酸在N-甲基-D-天冬氨酸受体上的结合（它破坏兴奋性谷氨酸能神经传递）。乙醇还刺激其他抑制性神经递质的释放，如多巴胺和血清素。乙醇中毒最常见的临床体征是共济失调、嗜睡、呕吐和躺卧。在更严重的情况下，可能会出现低体温、定向障碍、发声、低血压、震颤、心动过速、酸中毒、腹泻、呼吸抑制、昏迷、惊厥和死亡。酒精直接刺激胃并引起呕吐。高乙醇血水平也会刺激呕吐。中毒时呕吐的担忧在于，在高血乙醇浓度下，控制喉头盖的肌肉反应迟钝甚至麻痹。这增加了吸入风险。乙醇中毒减少了外周氧气输送和代谢，并导致线粒体氧化功能障碍，可能导致急性中毒患者出现休克或低氧血症。低体温可能由多种机制引起。外周血管扩张、中枢抑制、乙醇干扰体温调节机制和/或对寒冷环境的适应性反应受损，所有这些都会导致体温降低。适量饮酒似乎可以降低心肌梗死和其他心脏病的风险。然而，大量饮酒与女性癌症死亡率增加有关。饮用酒精饮料（尤其是啤酒）与直肠癌风险增加有关，但与结肠癌无关。啤酒是育龄成人普遍消费的酒精饮料。喝啤酒的男性增加怀孕损失的风险。妇女在怀孕前后喝啤酒。暴饮似乎是一种常见的饮酒行为，暴饮者增加胎儿生长受损和后代行为异常的风险。哺乳期妇女饮用啤酒可能会暂时影响哺乳婴儿的运动功能。乙醇代谢率因人而异。双胞胎研究表明，乙醇代谢率的个体间差异可能受遗传控制。人类乙醇氧化的主要途径是通过酒精脱氢酶途径转化为乙醛。乙醛通过乙醛脱氢酶进一步氧化为乙酸。亚洲人已知对乙醇的健康影响敏感；这种敏感性归因于乙醛脱氢酶的不同形式。亚洲人摄入酒精后，血液乙醛水平显著升高，范围从0.4到3 mg/L，个体因血液乙醛水平升高而出现面部潮红和心动过速。动物研究：将全强度乙醇滴入兔眼会引起可逆性损伤，24小时后仅评为10分之3。将70%的酒精应用于兔角膜会损伤并暂时松动角膜上皮，但恢复是完整的。当大鼠通过口服灌胃以8至15克/千克/天的剂量给予乙醇，并喂食含有25%总热量的脂肪的饮食，持续4个月时，肝脏观察到局部坏死、炎症和纤维化。九只喂食乙醇占50%总热量的狒狒发展成脂肪肝，四只动物在9到12个月内发展成肝炎。将家兔暴露于饱和乙醇蒸气中，持续25至365天，发展成肝硬化。在大鼠单次腹腔注射二乙基亚硝胺后，通过饮用含有乙醇的水进行治疗，持续12至18个月。乙醇是肝肿瘤的有效促进剂。在妊娠第20-150天每天给予绒猴最多5克/千克体重乙醇，显示怀孕损失（流产和死产）增加，但没有结构畸形或面部变化。乙醇，而不是乙醛，被怀疑是实验室动物胎儿毒性的原因。在妊娠第10天，将100毫克/千克的4-甲基吡唑（一种酒精脱氢酶抑制剂）与6克/千克的乙醇腹腔内给药联合口服，显著增加了乙醇在小鼠中的胚胎毒性。在含有或不含有代谢活化系统的沙门氏菌TA 97、TA 98、TA 100、TA 1535、TA 1537或TA 1538菌株中，乙醇不是致突变剂。在存在代谢活化系统的条件下，乙醇对被认为对氧自由基有反应的沙门氏菌TA 102菌株有轻微的致突变性。乙醇未诱导小鼠淋巴瘤L5178Y TK +/-细胞突变，也未在缺乏代谢活化系统的中国仓鼠V79细胞中诱导微核。在中国仓鼠卵巢细胞处理乙醇时，未观察到染色体畸变或姐妹染色单体交换。生态毒理学研究：斑马鱼从囊胚阶段开始暴露于不同浓度的乙醇（对照组、0.01%、0.1%和1%），持续至孵化后144小时。除了1%乙醇组在108-120 hpf期间遭受89%的死亡率外，未观察到存活影响

IDENTIFICATION AND USE: Ethanol is a clear, colorless, very mobile liquid. It is used in alcoholic beverages in suitable dilutions, and as a reagent in synthetic organic chemistry and chromatography, as well as industrial and laboratory organic solvent. Other uses are in manufacture of denatured alcohol, pharmaceuticals (rubbing compounds, lotions, tonics, colognes), in perfumery. Octane booster in gasoline. Pharmaceutic aid (solvent). HUMAN STUDIES: Ethanol is a central nervous system (CNS) depressant. It enhances the inhibitory effects of gamma-aminobutyric acid (GABA) at the GABA-A receptor and competitively inhibits the binding of glycine at the N-methyl-d-aspartate receptor (it disrupts excitatory glutaminergic neurotransmission). Ethanol also stimulates release of other inhibitory neurotransmitters, such as dopamine and serotonin. The most common clinical signs of ethanol toxicosis are ataxia, lethargy, vomiting, and recumbency. In more severe cases, hypothermia, disorientation, vocalization, hypotension, tremors, tachycardia, acidosis, diarrhea, respiratory depression, coma, seizures, and death may occur. Alcohol is directly irritating to the stomach and causes vomiting. High ethanol blood levels also stimulate emesis. The concern with vomiting during intoxication is that at high blood ethanol concentrations, the muscles that control the epiglottis become slow to react or even paralyzed. This increases the risk for aspiration. Ethanol intoxication reduces peripheral oxygen delivery and metabolism and causes mitochondrial oxidative dysfunction, potentially resulting in shock or hypoxia in an acutely intoxicated patient. Hypothermia may result from multiple mechanisms. Peripheral vasodilation, CNS depression, ethanol interference with the thermoregulator mechanism, and/or impaired behavioral responses to a cold environment all lead to a lowered body temperature. Moderate ethanol intake appears to reduce the risk of myocardial infarction and other heart diseases. However, high spirits consumption was associated with increased risk of cancer mortality in women. Consumption of alcoholic beverages (beer, in particular) is associated with an increased risk for rectal but not colon cancer. Beer is a commonly consumed alcoholic beverage among reproductive-age adults. Beer drinking males have an increased risk of contributing to pregnancy waste. Women consume beer before and after pregnancy recognition. Binge drinking appears to be a common drinking behavior, and those who binge drink have an increased risk of impaired fetal growth and offspring behavior. Beer consumption by lactating women might temporarily impair motor function of nursing infants. The rate of ethanol metabolism varies among individuals. Studies of twins indicate that interindividual variability in the rate of ethanol metabolism may be genetically controlled. The main pathway for ethanol oxidation in humans is to acetaldehyde via alcohol dehydrogenase pathway. Acetaldehyde is oxidized further to acetic acid by aldehyde dehydrogenase. Asians are known to be sensitive to the health effects of ethanol; the sensitivity has been attributed to different forms of the enzyme acetaldehyde dehydrogenase. Alcohol ingestion by Asians resulted in marked elevations of blood acetaldehyde levels ranging from 0.4 to 3 mg/L, and individuals developed facial flushing and tachycardia as a direct consequence of elevated blood acetaldehyde levels. ANIMAL STUDIES: A drop full-strength ethanol on rabbit eyes causes reversible injury graded only 3 on a scale of 10 after 24 hr. Application of 70% alcohol to rabbit corneas injures and temporarily loosens the corneal epithelium, but the recovery is complete. When rats were dosed with ethanol by oral gavage with 8 to 15 g/kg/day over 4 months and fed a diet containing 25% of total calories as fat, focal necrosis, inflammation, and fibrosis were observed in the liver. Nine baboons fed ethanol at 50% of total calories developed fatty liver, and four animals developed hepatitis within 9 to 12 months. Rabbits exposed to saturated vapors of ethanol for periods ranging from 25 to 365 days developed cirrhosis of the liver. Rats were given a single intraperitoneal dose of diethylnitrosamine followed by treatment with ethanol in drinking water for 12 to 18 months. Ethanol was an effective promoter of liver tumors. Cynomolgus monkeys administered up to 5 g/kg bw ethanol daily on gestation days 20-150 revealed an increase in pregnancy wastage (abortions and still births) but no structural malformation or facial change. Ethanol, and not acetaldehyde, has been implicated as the causative agent of the teratogenic effects in laboratory animals. Oral coadministration of 100 mg/kg of 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, with 6 g/kg of ethanol intraperitoneally on gestation day 10 dramatically increased the embryotoxicity of ethanol in mice. Ethanol is not mutagenic in Salmonella typhimurium strains TA 97, TA 98, TA 100, TA 1535, TA 1537, or TA 1538 in the presence or absence of metabolic activation. In the presence of a metabolic activation system, ethanol is slightly mutagenic to Salmonella strain TA 102, a strain considered to respond to the presence of oxygen radicals. Ethanol did not induce mutations in mouse lymphoma L5178Y TK+/- cells and did not induce micronuclei in Chinese hamster V79 cells in the absence of metabolic activation. No chromosomal aberrations or sister chromatid exchanges were observed in Chinese hamster ovary cells treated with ethanol. ECOTOXICITY STUDIES: The zebrafish were exposed to different concentrations (control, 0.01, 0.1, and 1%) of ethanol from blastula stage to 144 hour-post-fertilization (hpf). No effect on survival was observed except the 1% ethanol group suffered 89% mortality during 108-120 hpf. No developmental defects were observed at the 0.01 and 0.1% concentrations, but significantly higher deformity rates occurred with 1% ethanol. Hyperactivity and less tortuous swimming paths were observed in all ethanol concentrations.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 毒性总结

酒精与GABA(A)受体（delta亚单位）、NMDA受体、甘氨酸受体、血清素受体、乙酰胆碱受体、L型钙通道和GIRK通道结合。乙醇主要通过结合GABAA受体在中枢神经系统中发挥作用，增加抑制性神经递质GABA的效果。人体内的乙醇被酒精脱氢酶转化为乙醛。乙醛与酒精的多数临床效应有关，它已被证明会增加发展为肝硬化以及多种癌症的风险。在通过相应的脱氢酶代谢酒精时，NAD（烟酸腺嘌呤二核苷酸）被转化为还原型NAD。通常，NAD用于在肝脏中代谢脂肪，因此酒精与这些脂肪竞争使用NAD。长期接触酒精意味着肝脏中的脂肪积累，导致所谓的“脂肪肝”。持续的摄入（如酗酒）会导致肝细胞死亡，因为脂肪储存会减少细胞功能直至死亡。这些细胞随后被瘢痕组织取代，导致称为肝硬化的状况。

Alcohol binds to the GABA(A) receptors (delta subunit), NMDA receptors, Glycine receptors, Serotonin receptors, Acetylcholine receptors, L-channel calcium channels and GIRK channels. Ethanol acts in the central nervous system primarily by binding to the GABAA receptor, increasing the effects of the inhibitory neurotransmitter GABA. Ethanol within the human body is converted into acetaldehyde by alcohol dehydrogenase. Acetaldehyde is linked to most of the clinical effects of alcohol. It has been shown to increase the risk of developing cirrhosis of the liver and multiple forms of cancer. During the metabolism of alcohol via the respective dehydrogenases, NAD (Nicotinamide adenine dinucleotide) is converted into reduced NAD. Normally, NAD is used to metabolise fats in the liver, and as such alcohol competes with these fats for the use of NAD. Prolonged exposure to alcohol means that fats accumulate in the liver, leading to the term 'fatty liver'. Continued consumption (such as in alcoholism) then leads to cell death in the hepatocytes as the fat stores reduce the function of the cell to the point of death. These cells are then replaced with scar tissue, leading to the condition called cirrhosis.

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 致癌性证据

A3；已确认对动物有致癌性，但对人类的相关性未知。

A3; Confirmed animal carcinogen with unknown relevance to humans.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 致癌物分类

国际癌症研究机构致癌物：酒精饮料中的乙醇

IARC Carcinogenic Agent:Ethanol in alcoholic beverages

来源:International Agency for Research on Cancer (IARC)

毒理性

• 致癌物分类

国际癌症研究机构（IARC）致癌物分类：1类：对人类致癌

IARC Carcinogenic Classes:Group 1: Carcinogenic to humans

来源:International Agency for Research on Cancer (IARC)

吸收、分配和排泄

• 吸收

迅速吸收。

Rapidly absorbed.

来源:DrugBank

吸收、分配和排泄

口服给药后，乙醇会从胃和小肠迅速吸收进入血液，并分布到全身水分中（0.5-0.7升/千克）。空腹摄入乙醇后，大约30分钟血液中的乙醇浓度达到峰值。由于乙醇从小肠吸收的速度比从胃快，胃排空延迟（例如，由于食物的存在）会减慢乙醇的吸收。... 口服摄入酒精后，胃和肝脏中的酒精脱氢酶酶的首次通过代谢会导致比静脉给药相同剂量时更低的血液酒精水平。

After oral administration, ethanol is absorbed rapidly into the bloodstream from the stomach and small intestines and distributes into total body water (0.5-0.7 L/kg). Peak blood levels occur about 30 minutes after ingestion of ethanol when the stomach is empty. Because absorption occurs more rapidly from the small intestine than from the stomach, delays in gastric emptying (owing, e.g., to the presence of food) slow ethanol absorption. ... After oral consumption of alcohol, first-pass metabolism by gastric and liver alcohol dehydrogenase enzymes leads to lower blood alcohol levels than would be obtained if the same dose were administered intravenously.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

酒精在肺泡空气和血液之间的分布取决于其扩散速度，以及其在当前温度下和肺毛细血管中酒精浓度下的蒸汽压。经验性测定已经得出这个分布比率的不同值，但一个普遍接受的值是1:2100。

The distribution of alcohol between alveolar air and blood depends on its speed of diffusion, and its vapor pressure at the prevailing temp and concentration of alcohol in the lung capillaries. Empirical determinations have yielded rather different values for this distribution ratio, but a commonly accepted value is 1:2100.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

静脉血（眼眶窦）和脑内乙醇水平在给予乙醇后前30分钟内对长睡眠和短睡眠小鼠进行了测量（剂量为2.5至6.0克/千克）。乙醇通过腹腔注射或灌胃给药。对于两种小鼠品系和每个剂量，脑内乙醇浓度在前6分钟内显著高于血液乙醇水平（高达100毫克/分升），血液和脑内乙醇水平在给药后4至6分钟达到峰值。血液和脑内浓度达到平衡大约需要6至10分钟（取决于剂量和小鼠品系）。在失去翻正反射能力时，脑内乙醇水平显著高于血液乙醇水平。这些结果表明，在给药后前6分钟内，血液乙醇水平不适合用于评估脑内乙醇含量。

Venous blood (orbital sinus) and brain ethanol levels were measured in long sleep and short sleep mice within the first 30 min following ethanol administration (2.5 to 6.0 g/kg). Ethanol was administered ip or intragastrically. For both lines of mice and for every dose, brain ethanol concentrations were significantly greater (as much as 100 mg/dL) than blood ethanol levels for the first 6 min, and peak blood and brain ethanol levels were reached 4 to 6 min after dosing. Approx 6 to 10 min (depending on dose and line of mouse) was required for blood and brain concn to reach equilibrium. At the time of loss of the righting response brain ethanol levels were significantly higher than blood ethanol levels. These results indicate that within the first 6 min after administration of ethanol, blood ethanol level is not suitable for the assessment of brain ethanol content.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

波霍雷茨基和布里克的测定大鼠呼出空气中乙醇浓度方法经过修改。给雌性Sprague Dawley大鼠注射不同剂量的乙醇（1至2克/千克），并在给药后不同时间间隔（15至120分钟）收集动脉血和呼出空气样本。动脉血中乙醇浓度与呼出空气中乙醇浓度之间存在良好的相关性（r=0.96）；血/呼吸转换因子为3241 ± 55。

The method of Pohorecky and Brick was modified for determination of ethanol concn in rebreathed air of rats. Female Sprague Dawley rats were injected with different doses (1 to 2 g/kg) of ethanol and both arterial blood and rebreathed air samples were collected at various time intervals (15 to 120 min) after administration. A good correlation (r= 0.96) was found between ethanol concn in arterial blood and in rebreathed air; the blood/breath conversion factor was 3241 + or - 55.

来源:Hazardous Substances Data Bank (HSDB)

安全信息

• 职业暴露等级：
  A
• 职业暴露限值：
  TWA: 1000 ppm (1900 mg/m3)
• TSCA：
  Yes
• 危险等级：
  3
• 立即威胁生命和健康浓度：
  3,300 ppm [10% LEL]
• 危险品标志：
  F
• 安全说明：
  S16,S24/25,S26,S36,S36/37,S45,S61,S7
• 危险类别码：
  R11
• 海关编码：
  2207200010
• 危险品运输编号：
  1170
• 危险类别：
  3
• RTECS号：
  KQ6300000
• 包装等级：
  II
• 危险标志：
  GHS02,GHS07,GHS08
• 危险性描述：
  H225,H302,H319,H371
• 危险性防范说明：
  P210,P260,P280,P308 + P311,P337 + P313,P403 + P235
• 储存条件：
  储存时应注意以下事项：存放在阴凉、通风良好的库房内，远离火源和热源，库温不宜超过37℃。保持容器密封，并与氧化剂、酸类、碱金属、胺类等分开存放，切忌混储。使用防爆型照明和通风设施，并禁止使用可能产生火花的机械设备和工具。储存区应配备泄漏应急处理设备和合适的收容材料。

SDS

第一部分：化学品名称

制备方法与用途

根据给出的信息，乙醇（酒精）的生产方法主要有两种：发酵法和合成法。此外还有一些后续处理步骤用于进一步纯化乙醇。

发酵法制备乙醇

1. 原料准备：选择富含淀粉或糖类的原材料，如谷物、薯类、玉米等。
2. 预处理：将原料进行水洗并粉碎。
3. 糊化反应：在高压下对原料进行蒸煮，使其中的淀粉转化成易于发酵的形式（通常是糊化）。
4. 糖化与发酵：
   • 冷却至适合酶活性的温度（约60℃），加入淀粉酶将淀粉进一步转化为可发酵的糖类（如麦芽糖和葡萄糖）。
   • 加入酵母菌，通过生物化学过程将这些糖转化成乙醇。

合成法制备乙醇

1. 原料准备：使用乙烯作为基本原料，需要纯度较高的乙烯气。
2. 水合法制备乙醇：
   • 间接法（硫酸酯化-水解）：先用浓硫酸将乙烯转化为乙烯硫酸酯，然后在高温条件下水解生成乙醇和少量副产品如乙醚。
   • 直接法（一步反应）：在磷酸催化剂存在下，在较高温度和压力条件下直接使乙烯与水反应生成乙醇。这种方法流程更简单，但对设备要求较高且能耗较大。

后续处理

为了得到纯净的乙醇或不同浓度范围的产品，可以采用以下几种方式：

• 共沸精馏：利用95%（v/v）乙醇和水的共沸点进行多次精馏提纯。
• 分子筛或离子交换剂脱水：通过物理吸附或化学反应去除微量水分。

这些过程完成后即可得到不同用途所需的乙醇产品。需要注意的是，无论采用哪种方法生产，都需要严格遵守安全操作规程以防止火灾、爆炸等事故的发生。

希望上述信息能够帮助您了解乙醇的生产工艺流程。如果有任何疑问或者需要进一步的信息，请随时告知！

反应信息

• 作为反应物：
  描述：

  乙醇 在 ammonium acetate 作用下， 以 aq. phosphate buffer 为溶剂， 反应 10.0h， 以36%的产率得到三乙胺
  参考文献：
  名称：

  通过直接和间接借位氢机理将胺与醇进行电活化烷基化

  摘要：

  在水溶液中，通过简单的醇可实现胺的绿色高效N-烷基化所谓的“借用氢方法”的电化学形式。在活性炭布（Ru / ACC）上，通过Ru催化，该反应在甲醇，伯醇和仲醇中均能很好地进行。烷基化可以通过两种不同的电催化方法之一完成：（1）在未分隔的电池中，醇（过量存在）在Ru / ACC阳极被氧化；醛或酮产物与胺缩合；并在ACC阴极还原生成的亚胺，并与氧化释放的质子结合。该过程消耗化学计量的电流。（2）在膜分裂的电池中，电流激活的Ru / ACC阴极直接影响乙醇的C–H激活；所得的游离或仍表面吸附的羰基物质与胺缩合形成亚胺，并按（1）所述还原。

  DOI：

  10.1039/c9gc03747k
• 作为产物：
  描述：

  苄基乙基醚 在 Mortierella isabellina NRRL 1757 作用下， 以60%的产率得到乙醇
  参考文献：
  名称：

  Removal of O-and N-benzyl groups by fungal biotransformation

  摘要：

  DOI：

  10.1016/s0040-4039(00)82354-0
• 作为试剂：
  描述：

  3-甲巯基-2-丁酮 在 氯化亚砜 、 乙醇 、 sodium cyanoborohydride 、 一水合肼 、 potassium hydroxide 、 sodium hydroxide 作用下， 以 四氢呋喃 、 乙醇 、 1,2-二氯乙烷 为溶剂， 生成 N-ethyl-N-(pyridazin-4-yl)-1-(3-(methylthio)butan-2-yl)-5-methyl-1H-pyrazole-4-carboxamide
  参考文献：
  名称：

  N-哒嗪吡唑酰胺类化合物

  摘要：

  本发明公开了式(I)所示的N‑哒嗪吡唑酰胺类化合物及其制备方法与应用，本发明式(I)化合物具有优异的杀虫生物活性，尤其是对刺吸式口器害虫如蚜虫等具有很高的杀虫活性，可用于防治各类虫害。本发明的技术方案还包括一种制备式(I)化合物的中间体，该中间体的结构如通式(IV)所示。式(I)和式式(IV)中各取代基具有说明书中所给定义#imgabs0#

  公开号：

  CN118206533A

文献信息

• Properties and Reactions of Substituted 1,2-Thiazetidine 1,1-Dioxides: Chiral Mono- and Bicyclic 1,2-Thiazetidine 1,1-Dioxides fromα-Amino Acids
  作者：Alexandra Meinzer、Andrea Breckel、Bassam Abu Thaher、Nico Manicone、Hans-Hartwig Otto

  DOI：10.1002/hlca.200490021

  日期：2004.1

  New chiral mono- and bicyclic β-sultams, valuable building blocks for drug synthesis, have been prepared from L-Ala, L-Val, L-Leu, L-Ile, L-Phe, L-Cys, L-Ser, L-Thr, and D-penicillamine by transformation of the COOH group into a methylsulfonyl chloride function, followed by cyclization under basic conditions. Selected properties, derivatives, and reactions of the β-sultams are described.

  新的手性单环和双环β -sultams，为药物合成有价值积木，已经从L-丙氨酸，L-缬氨酸，L-亮氨酸，L-异亮氨酸，L-PHE，L-的Cys，L-丝氨酸，L制备-Thr和D-青霉胺，方法是将COOH基团转化为甲磺酰氯官能团，然后在碱性条件下环化。描述了β-合乎目的选择的性质，衍生物和反应。
• [EN] BENZAMIDE OR BENZAMINE COMPOUNDS USEFUL AS ANTICANCER AGENTS FOR THE TREATMENT OF HUMAN CANCERS<br/>[FR] COMPOSÉS BENZAMIDE OU BENZAMINE À UTILISER EN TANT QU'ANTICANCÉREUX POUR LE TRAITEMENT DE CANCERS HUMAINS
  申请人：UNIV TEXAS

  公开号：WO2017007634A1

  公开（公告）日：2017-01-12

  The described invention provides small molecule anti-cancer compounds for treating tumors that respond to cholesterol biosynthesis inhibition. The compounds selectively inhibit the cholesterol biosynthetic pathway in tumor-derived cancer cells, but do not affect normally dividing cells.

  所描述的发明提供了用于治疗对胆固醇生物合成抑制作出反应的肿瘤的小分子抗癌化合物。这些化合物选择性地抑制肿瘤来源的癌细胞中的胆固醇生物合成途径，但不影响正常分裂的细胞。
• A convergent approach to polycyclic aromatic hydrocarbons
  作者：Raphaël F. Guignard、Samir Z. Zard

  DOI：10.1039/c1cc15095b

  日期：——

  A new concise route to Polycyclic Aromatic Hydrocarbons (PAHs) through radical addition and cyclisation of xanthates is described.

  描述了一种通过黄原酸酯的自由基加成和环化反应合成多环芳烃（PAHs）的新简明路线。
• Alkyl 1-Chloroalkyl Carbonates: Reagents for the Synthesis of Carbamates and Protection of Amino Groups
  作者：Gérard Barcelo、Jean-Pierre Senet、Gérard Sennyey、Jean Bensoam、Albert Loffet

  DOI：10.1055/s-1986-31724

  日期：——

  The synthesis of 1-chloroalkyl carbonates and their reaction with various type of amines are described. This reaction is useful for the synthesis of carbamate pesticides and for the protection of various amino groups, including amino acids.

  描述了1-氯代烷基碳酸酯的合成及其与各种类型胺的反应。这一反应对于合成氨基甲酸酯类农药和保护包括氨基酸在内的各种氨基团具有重要作用。
• MgI₂-Mediated Chemoselective Cleavage of Protecting Groups: An Alternative to Conventional Deprotection Methodologies
  作者：Mathéo Berthet、Florian Davanier、Gilles Dujardin、Jean Martinez、Isabelle Parrot

  DOI：10.1002/chem.201501799

  日期：2015.7.27

  The scope of MgI2 as a valuable tool for quantitative and mild chemoselective cleavage of protecting groups is described here. This novel synthetic approach expands the use of protecting groups, widens the concept of orthogonality in synthetic processes, and offers a facile opportunity to release compounds from solid supports.

  在此描述了MgI 2作为定量和轻度化学选择性切割保护基的有价值工具的范围。这种新颖的合成方法扩大了保护基的使用范围，拓宽了合成过程中正交性的概念，并提供了从固体载体上释放化合物的简便机会。

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