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**烏頭鹼**（）是一種生物鹼毒素。是常用中藥烏頭屬中所含有的一種化學物質，具強烈毒性,口服0.2mg左右即能使人中毒，3-5mg即可致死。民间常用草乌、川乌等植物来泡制药酒，但这种药酒可能是极端危险的，也经常因此出现中毒甚至死亡的情况。

用途
--

烏頭鹼以前被用作解熱藥和鎮痛藥，但在草藥中的應用仍然有限。狹窄的治療指數使計算合適的劑量很困難。

結構和反應性
------

附子屬和翠雀屬植物的生物活性分離物被歸類為去甲二萜生物碱。根據C18碳的存在與否進一步細分。烏頭鹼是一種C19去甲二萜生物碱，因為它含有C18。烏頭鹼幾乎不溶於水，但極易溶於有機溶劑，例如氯仿或乙醚。如果酒精濃度足夠高，烏頭鹼也可溶於乙醇和水的混合物中。

像許多其他生物鹼一樣，烏頭鹼六元環的鹼性氮很容易形成鹽和離子，使其對極性和親脂性結構過血腦屏障。

已隱藏部分未翻譯内容，歡迎參與翻譯。

已隱藏部分未翻譯内容，歡迎參與翻譯。
The acetoxyl group at the c8 position can readily be replaced by a methoxy group, by heating aconitine in methanol, to produce a 8-deacetyl-8-*O*-methyl derivatives. If aconitine is heated in its dry state, it undergoes a pyrolysis to form pyroaconitine ((1α,3α,6α,14α,16β)-20-ethyl-3,13-dihydroxy-1,6,16-trimethoxy-4-(methoxymethyl)-15-oxoaconitan-14-yl benzoate) with the chemical formula C32H43NO9.

作用
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已隱藏部分未翻譯内容，歡迎參與翻譯。
Aconitine can interact with the voltage-dependent sodium-ion channels, which are proteins in the cell membranes of excitable tissues, such as cardiac and skeletal muscles and neurons. These proteins are highly selective for sodium ions. They open very quickly to depolarize the cell membrane potential, causing the upstroke of an action potential. Normally, the sodium channels close very rapidly, but the depolarization of the membrane potential causes the opening (activation) of potassium channels and potassium efflux, which results in repolarization of the membrane potential.

Aconitine binds to the channel at the neurotoxin binding site 2 on the alpha subunit. This binding results in a sodium-ion channel that stays open longer. Aconitine suppresses the conformational change in the sodium-ion channel from the active state to the inactive state. The membrane stays depolarized due to the constant sodium influx (which is 10–1000-fold greater than the potassium efflux). As a result, the membrane cannot be repolarized. The binding of aconitine to the channel also leads to the channel to change conformation from the inactive state to the active state at a more negative voltage. In neurons, aconitine increases the permeability of the membrane for sodium ions, resulting in a huge sodium influx in the axon terminal. As a result, the membrane depolarizes rapidly. Due to the strong depolarization, the permeability of the membrane for potassium ions increases rapidly, resulting in a potassium reflux to release the positive charge out of the cell. Not only the permeability for potassium ions but also the permeability for calcium ions increases as a result of the depolarization of the membrane. A calcium influx takes place. The increase of the calcium concentration in the cell stimulates the release of the neurotransmitter acetylcholine into the synaptic cleft. Acetylcholine binds to acetylcholine receptors at the postsynaptic membrane to open the sodium-channels there, generating a new action potential.

Research with mouse nerve-hemidiaphragm muscle preparation indicate that at low concentrations (<0.1 μM) aconitine increases the electrically evoked acetylcholine release causing an induced muscle tension. Action potentials are generated more often at this concentration. At higher concentration (0.3–3 μM) aconitine decreases the electrically evoked acetylcholine release, resulting in a decrease in muscle tension. At high concentration (0.3–3 μM), the sodium-ion channels are constantly activated, transmission of action potentials is suppressed, leading to non-excitable target cells or paralysis.

合成
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已隱藏部分未翻譯内容，歡迎參與翻譯。
Aconitine is biosynthesized by the monkshood plant via the terpenoid biosynthesis pathway (MEP chloroplast pathway). Approximately 700 naturally occurring C19-diterpenoid alkaloids have been isolated and identified, but the biosynthesis of only a few of these alkaloids are well understood.

Likewise, only a few alkaloids of the aconitine family have been synthesized in the laboratory. In particular, despite over one hundred years having elapsed since its isolation, the prototypical member of its family of norditerpenoid alkaloids, aconitine itself, represents a rare example of a well-known natural product that has yet to succumb to efforts towards its total synthesis. The challenge that aconitine poses to synthetic organic chemists is due to both the intricate interlocking hexacyclic ring system that make up its core and the elaborate collection of oxygenated functional groups at its periphery. A handful of simpler members of the aconitine alkaloids, however, have been prepared synthetically. In 1971, the Weisner group discovered the total synthesis of talatisamine (a C19-norditerpenoid). In the subsequent years, they also discovered the total syntheses of other C19-norditerpenoids, such as chasmanine, and 13-deoxydelphonine.

Schematic for the syntheses of Napelline Deoxydelphonine, and Talatisamine Wiesner Syntheses of Napelline Deoxydelphonine, and Talatisamine
The total synthesis of napelline (**Scheme a**) begins with aldehyde **100**. In a 7 step process, the A-ring of napelline is formed (**104**). It takes another 10 steps to form the lactone ring in the pentacyclic structure of napelline (**106**). An additional 9 steps creates the enone-aldehyde **107**. Heating in methanol with potassium hydroxide causes an aldol condensation to close the sixth and final ring in napelline (**14**). Oxidation then gives rise to diketone **108** which was converted to (±)-napelline (**14**) in 10 steps.

A similar process is demonstrated in Wiesner's synthesis of 13-desoxydelphinone (**Scheme c**). The first step of this synthesis is the generation of a conjugated dienone **112** from **111** in 4 steps. This is followed by the addition of a benzyl vinyl ether to produce **113**. In 11 steps, this compound is converted to ketal 114. The addition of heat, DMSO and o-xylene rearranges this ketol (**115**), and after 5 more steps (±)-13-desoxydelphinone (**15**) is formed.

Lastly, talatisamine (**Scheme d**) is synthesized from diene **116** and nitrile **117**. The first step is to form tricycle **118** in 16 steps. After another 6 steps, this compound is converted to enone **120**. Subsequently, this allene is added to produce photoadduct **121**. This adduct group is cleaved and rearrangement gives rise to the compound **122**. In 7 steps, this compound forms **123**, which is then rearranged, in a similar manner to compound **114**, to form the aconitine-like skeleton in **124**. A racemic relay synthesis is completed to produce talatisamine (**13**).

More recently, the laboratory of the late David Y. Gin completed the total syntheses of the aconitine alkaloids nominine and neofinaconitine.

代謝
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已隱藏部分未翻譯内容，歡迎參與翻譯。
Aconine: an amorphous, bitter, non-poisonous alkaloid, derived from the decomposition of aconitine
Aconitine is metabolized by cytochrome P450 isozymes (CYPs). There has been research in 2011 in China to investigate in-depth the CYPs involved in aconitine metabolism in human liver microsomes. It has been estimated that more than 90 percent of currently available human drug metabolism can be attributed to eight main enzymes (CYP 1A2, 2C9, 2C8, 2C19, 2D6, 2E1, 3A4, 3A5). The researchers used recombinants of these eight different CYPs and incubated it with aconitine. To initiate the metabolism pathway the presence of NADPH was needed. Six CYP-mediated metabolites (M1–M6) were found by liquid chromatography, these six metabolites were characterized by mass-spectrometry. The six metabolites and the involved enzymes are summarized in the following table:

| Metabolite | Name | Involved CYPs |
| --- | --- | --- |
| M1 | O-Demethyl-aconitine | CYP3A4, CYP3A5, CYP2D6, CYP2C8 |
| M2 | 16-O-Demethyl-aconitine | CYP3A4, CYP3A5, CYP2D6, CYP2C9 |
| M3 | N-deethyl-aconitine | CYP3A4, CYP3A5, CYP2D6, CYP2C9 |
| M4 | O-didemethyl-aconitine | CYP3A5, CYP2D6 |
| M5 | 3-Dehydrogen-aconitine | CYP3A4, CYP3A5 |
| M6 | Hydroxyl-aconitine | CYP3A5, CYP2D6 |

Selective inhibitors were used to determine the involved CYPs in the aconitine metabolism. The results indicate that aconitine was mainly metabolized by CYP3A4, 3A5 and 2D6. CYP2C8 and 2C9 had a minor role to the aconitine metabolism, whereas CYP1A2, 2E1 and 2C19 did not produce any aconitine metabolites at all. The proposed metabolic pathways of aconitine in human liver microsomes and the CYPs involved to it are summarized in the table above.

診斷和治療
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已隱藏部分未翻譯内容，歡迎參與翻譯。
For the analysis of the *Aconitum* alkaloids in biological specimens such as blood, serum and urine, several GC-MS methods have been described. These employ a variety of extraction procedures followed by derivatisation to their trimethylsilyl derivatives. New sensitive HPLC-MS methods have been developed as well, usually preceded by SPE purification of the sample. The antiarrhythmic drug lidocaine has been reported to be an effective treatment of aconitine poisoning of a patient. Considering the fact that aconitine acts as an agonist of the sodium channel receptor, antiarrhythmic agents which block the sodium channel (Vaughan-Williams' classification I) might be the first choice for the therapy of aconitine induced arrhythmias. Animal experiments have shown that the mortality of aconitine is lowered by tetrodotoxin. The toxic effects of aconitine were attenuated by tetrodotoxin, probably due to their mutual antagonistic effect on excitable membranes. Also paeoniflorin seems to have a detoxifying effect on the acute toxicity of aconitine in test animals. This may result from alternations of pharmacokinetic behavior of aconitine in the animals due to the pharmacokinetic interaction between aconitine and paeoniflorin. In addition, in emergencies, one can wash the stomach using either tannic acid or powdered charcoal. Heart stimulants such as strong coffee or caffeine may also help until professional help is available.

著名中毒事件
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已隱藏部分未翻譯内容，歡迎參與翻譯。
During the Indian Rebellion of 1857, a British detachment was the target of attempted poisoning with aconitine by the Indian regimental cooks. The plot was thwarted by John Nicholson who, having detected the plot, interrupted the British officers just as they were about to consume the poisoned meal. The chefs refused to taste their own preparation, whereupon it was force-fed to a monkey who "expired on the spot". The cooks were hanged.

Aconitine was the poison used by George Henry Lamson in 1881 to murder his brother-in-law in order to secure an inheritance. Lamson had learned about aconitine as a medical student from professor Robert Christison, who had taught that it was undetectable—but forensic science had improved since Lamson's student days.

Rufus T. Bush, American industrialist and yachtsman, died on September 15, 1890, after accidentally taking a fatal dose of aconite.

In 1953 aconitine was used by a Soviet biochemist and poison developer, Grigory Mairanovsky, in experiments with prisoners in the secret NKVD laboratory in Moscow. He admitted killing around 10 people using the poison.

In 2004 Canadian actor Andre Noble died from aconitine poisoning. He accidentally ate some monkshood while he was on a hike with his aunt in Newfoundland.

In 2009 Lakhvir Singh of Feltham, west London, used aconitine to poison the food of her ex-lover Lakhvinder Cheema (who died as a result of the poisoning) and his current fiancée Aunkar Singh. Singh received a life sentence with a 23-year minimum for the murder on February 10, 2010.

流行文化
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已隱藏部分未翻譯内容，歡迎參與翻譯。
烏頭鹼是古代世界最受歡迎的毒藥。普布利烏斯·奧維修斯·納索提到了眾所周知的繼母不喜歡繼子的問題，他寫道：

> *Lurida terribiles miscent aconita novercae*.  
> 
>   
> 
> Fearsome stepmothers mix lurid aconites.
> 
>  

Aconitine was also made famous by its use in Oscar Wilde's 1891 story "Lord Arthur Savile's Crime". Aconite also plays a prominent role in James Joyce's *Ulysses*, in which the father to protagonist Leopold Bloom used pastilles of the chemical to commit suicide. Aconitine poisoning plays a key role in the murder mystery *Breakdown* by Jonathan Kellerman (2016). In Twin Peaks (season 3) Part 13, aconitine is suggested to poison the main character.

Monk's Hood is the name of the third Cadfael Novel written in 1980 by Ellis Peters. The novel was made into an episode of the well known television series Cadfael starring Derek Jacobi.

毒性
--

烏頭鹼的毒性作用已在多種動物身上進行了測試有效，包括哺乳動物（狗、貓、豚鼠、小鼠、大鼠和兔子）、鴿、青蛙。觀察到的毒性作用有：局部麻醉、腹瀉、抽搐、心律失常、死亡。

根據對人類附子中毒的不同報導的回顧，觀察到以下臨床特徵：

* 神經系統：感覺異常和臉、口周區域和四肢麻木、肌肉無力。
* 心血管：低血壓、心悸、胸痛、心動過緩、竇性心動過速、室性異位及其他心律失常、室性心律失常、交界性心律
* 胃腸道：噁心、嘔吐、腹痛、腹瀉
* 其他：頭暈、過度換氣、出汗、呼吸困難、意識模糊、頭痛、流淚

烏頭鹼中毒的最初症狀出現在口服後約20分鐘至2小時，包括感覺異常、出汗、噁心。這會導致嚴重的嘔吐、絞痛性腹瀉、劇烈疼痛，然後骨骼肌麻痺。威脅生命的心律失常，包括室性心動過速、心室顫動，會因呼吸麻痺或心臟驟停而死亡。

小鼠的LD50值為口服 1 mg/kg、靜脈 0.100 mg/kg、腹膜 0.270 mg/kg 和皮下 0.270 mg/kg。小鼠的最低致死量（LDLo）為口服 1 mg/kg 和腹腔 0.100 mg/kg。小鼠的最低中毒量（TDLo）為 0.0549 mg/kg 皮下注射。大鼠靜脈注射的LD50值為 0.064 mg/kg。大鼠的LDLo為靜脈注射 0.040 mg/kg和腹腔 0.250 mg/kg。大鼠的腸胃TDLo為 0.040 mg/kg。有關更多參見下表：LD50表示平均致死量；LDLo是指最低致死量；TDLo表示最低中毒量。

| 物種 | 測試 | 路線 | 劑量（mg/kg） | 毒性 |
| --- | --- | --- | --- | --- |
| 人類 | LDLo | 口服 | 0.028 | 行為：興奮
胃腸道：運動亢進、腹瀉、其他變化 |
| 人類 | LDLo | 口服 | 0.029 | 除致死劑量值外未報告詳情毒性作用 |
| 貓 | LD50 | 靜脈 | 0.080 | 行為：抽搐或對癲癇發作閾值的影響 |
| 貓 | LDLo | 皮下 | 0.100 | 除致死劑量值外未報告詳情毒性作用 |
| 豚鼠 | LD50 | 靜脈 | 0.060 | 行為：抽搐或對癲癇發作閾值的影響 |
| 豚鼠 | LDLo | 皮下 | 0.050 | 除致死劑量值外未報告詳情毒性作用 |
| 豚鼠 | LDLo | 靜脈 | 0.025 | 心臟：心律失常（包括傳導改變） |
| 小鼠 | LD50 | 腹腔 | 0.270 | 除致死劑量值外未報告詳情毒性作用 |
| 小鼠 | LD50 | 靜脈 | 0.100 | 感覺器官和特殊感覺（眼睛）：流淚
行為：抽搐或對癲癇發作閾值的影響
肺、胸：呼吸困難 |
| 小鼠 | LD50 | 口服 | 1 | 除致死劑量值外未報告詳情毒性作用 |
| 小鼠 | LD50 | 皮下 | 0.270 | 除致死劑量值外未報告詳情毒性作用 |
| 小鼠 | LDLo | 腹腔 | 0.100 | 除致死劑量值外未報告詳情毒性作用 |
| 小鼠 | LDLo | 口服 | 1 | 行為：抽搐或對癲癇發作閾值的影響
心臟：心律失常（包括傳導改變）
胃腸道：運動亢進、腹瀉 |
| 小鼠 | TDLo | 皮下 | 0.0549 | 周圍神經和感覺：局部麻醉
行為：鎮痛 |
| 兔子 | LDLo | 皮下 | 0.131 | 除致死劑量值外未報告詳情毒性作用 |
| 大鼠 | LD50 | 靜脈 | 0.080 | 行為：抽搐或對癲癇發作閾值的影響 |
| 大鼠 | LD50 | 靜脈 | 0.064 | 除致死劑量值外未報告詳情毒性作用 |
| 大鼠 | LDLo | 腹腔 | 0.250 | 心臟：其他變化
肺、胸：呼吸困難 |
| 大鼠 | LDLo | 靜脈 | 0.040 | 心臟：心律失常（包括傳導改變） |
| 大鼠 | TDLo | 腸外 | 0.040 | 心臟：心律失常（包括傳導改變） |
| 青蛙 | LDLo | 皮下 | 0.586 | 除致死劑量值外未報告詳情毒性作用 |
| 鴿子 | LDLo | 皮下 | 0.066 | 除致死劑量值外未報告詳情毒性作用 |

對於人類，1969 年報導的最低口服致死劑量為 28 μg/kg。

乌头碱（草乌、川乌）中毒在急诊及内科中常见，多因服用自制中药及自制药膳不当所致。

它主要使迷走神经兴奋，对周围神经损害临床主要表现为口舌及四肢麻木，全身紧束感等，通过兴奋迷走神经而降低窦房结的自律性，引起異位起搏点的自律性增高而引起各心律失常，损害心肌。

临床作用
----

本品具有镇痛作用，临床上用于缓解癌痛，尤其适用于消化系统癌痛；外用时能麻痹周围神经末梢，产生局部麻醉和镇痛作用；有消炎作用，本品毒性极大，能兴奋麻痹感觉神经和中枢神经，兴奋心脏迷走神经，直接毒害心肌细胞。还有发汗作用。[來源請求]

参考文献
----

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25. 1 2  Beike J, Frommherz L, Wood M, Brinkmann B, Köhler H.. International Journal of Legal Medicine. October 2004, **118** (5): 289–93. PMID 15674996. S2CID 2490984. doi:10.1007/s00414-004-0463-2.
26. ↑  Tsukada K, Akizuki S, Matsuoka Y, Irimajiri S.. Kokyu to Junkan. Respiration & Circulation. October 1992, **40** (10): 1003–6. PMID 1439251 （日语）.
27. ↑  Ohno Y, Chiba S, Uchigasaki S, Uchima E, Nagamori H, Mizugaki M, Ohyama Y, Kimura K, Suzuki Y.  (pdf). The Tohoku Journal of Experimental Medicine. June 1992, **167** (2): 155–8  [2022-07-26]. PMID 1475787. doi:10.1620/tjem.167.155 可免费查阅. （原始内容存档于2021-10-06）.
28. ↑  Fan YF, Xie Y, Liu L, Ho HM, Wong YF, Liu ZQ, Zhou H.. Journal of Ethnopharmacology. June 2012, **141** (2): 701–8. PMID 21930193. doi:10.1016/j.jep.2011.09.005.
29. ↑  Irving SN.  Fifth. New York: Van Nostrand Reinhold Company Inc. 1979. ISBN 978-0-442-27373-6. LCCN 78-20812.
30. ↑  Macinnis P.. Allen & Unwin. 2006: 80–81. ISBN 9781741146264.
31. ↑  Macinnis P.. Arcade Publishing. 2005: 25–26. ISBN 978-1-55970-761-9.
32. ↑  Parry LA, Wright WH.. Beard Books. 2000: 103. ISBN 978-1-58798-031-2.
33. ↑   [Laboratory X]. Novaya Gazeta. 2010-05-06  [2013-04-08]. （原始内容存档于2010-05-30） （俄语）.
34. ↑ . BBC TV News. 2010-02-10  [2022-07-26]. （原始内容存档于2020-05-27）.
35. ↑  Ovid, Metamorphoses, 1.147
36. ↑  Jensen, Jeff.. Entertainment Weekly (Meredith Corporation). 7 August 2017  [4 May 2020]. （原始内容存档于2022-04-19）. Clark offered to sell him Aconitine, a toxin with a rich literary history.
37. ↑ . Drugs.com. 9 August 2019  [23 June 2020]. （原始内容存档于2022-07-26）.
38. 1 2 . Oct 2011.
39. ↑  龙明洁.. 正义网.  [2011-12-05]. （原始内容存档于2017-05-06）.

外部連結
----

* 烏頭堿 Aconitine（页面存档备份，存于） 中草藥化學圖像數據庫 (香港浸會大學中醫藥學院) （中文）（英文）
* 乌头碱 aconitine（页面存档备份，存于） 化学空间 Chem-Station （中文）


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* 论
* 编
生物鹼类 |
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| 吲哚： | 5-甲氧基二甲基色胺 · 二甲基色胺 · 骆驼蓬生物碱 · 脱磷酸裸盖菇素 · 裸盖菇素 · 利血平 · 血清素 · 色胺 · 育亨宾 · 芦竹碱 · 田麦角碱 · 钩吻碱 |
|  |
| 苯乙胺： | 苯丙胺 · 卡西酮 · 多巴胺 · 麻黃素 · 麦司卡林 · 甲基苯丙胺 · 苯乙胺 · 酪胺 |
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| 嘌呤： | 咖啡因 · 可可碱 · 茶碱 |
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| 哌啶： | 毒芹碱 |
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| 吡咯： | 尼古丁 |
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| 喹啉： | 奎寧 |
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| 异喹啉： | 可待因 · 嗎啡 · 小檗鹼 |
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| 莨菪烷： | 阿托品 · 可卡因 · 天仙子胺 · 東莨菪鹼 |
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| 萜类： | 乌头碱 · 翠雀碱 · 茄碱 |
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| 甜菜碱： | 胆碱 · 毒蕈碱 |
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* 论
* 编
生物化學物質種類索引 |
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| 糖类 | 
* 醇類
* 糖醇
* 醣蛋白
* 苷

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| 酯質 | 
* 类花生酸类
* 脂肪酸
	+ 中間物
* 甘油酯
* 磷脂
* 鞘脂類
* 胆固醇与甾体中间产物

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| 核酸 | 
* 成分
	+ 中間物

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| 蛋白質 | 
* 胺基酸
	+ 中間物

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| 其他 | 
* 四吡咯
	+ 中間物

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