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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2021/03/09 09:37:20」(JST)
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| ユビキノン | |
|---|---|
| 識別情報 | |
| CAS登録番号 | 1339-63-5, 303-98-0 (CoQ10) |
| 日化辞番号 | J2.969.265C J11.405G (CoQ10) |
| KEGG | C00399 C11378 (CoQ10) |
| ChEBI |
|
| 特記なき場合、データは常温 (25 °C)・常圧 (100 kPa) におけるものである。 | |
ユビキノン（英: ubiquinone, 略号：UQ）とは、ミトコンドリア内膜や原核生物の細胞膜に存在する電子伝達体の1つであり、電子伝達系において呼吸鎖複合体IとIIIの電子の仲介を果たしている。ベンゾキノン（単にキノンでも良い）の誘導体であり、比較的長いイソプレン側鎖を持つので、その疎水性がゆえに膜中に保持されることとなる。酸化還元電位 (Eo') は+0.10V。ウシ心筋ミトコンドリア電子伝達系の構成成分として1957年に発見された[1]。
広義には電子伝達体としての意味合いを持つが、狭義には酸化型のユビキノンのことをさす。還元型のユビキノンはユビキノールと呼称していることが多い。別名、補酵素Q、コエンザイムQ10（キューテン）、CoQ10、ユビデカレノンなど。かつてビタミンQと呼ばれたこともあるが、動物体内で合成することができるためビタミンではない。
目次
- 1 ユビキノンの構造と酸化還元様式
- 2 ユビキノンの生理的意義
- 3 紅色光合成細菌の光合成反応中心における電子移動反応
- 4 プロトンキノンサイクル機構
- 5 ユビキノンの生合成
- 5.1 4-ヒドロキシ安息香酸
- 5.2 イソプレン側鎖
- 5.3 ベンゼン環修飾
- 6 医薬品としての効能
- 6.1 有効性評価
- 6.2 基礎研究
- 6.3 相互作用
- 7 原料製造メーカー
- 8 存在
- 9 関連項目
- 10 出典
- 11 外部リンク
ユビキノンの構造と酸化還元様式
ユビキノンは炭素と水素と酸素のみから成る有機化合物である。ユビキノンの酸化と還元に関わるベンゾキノン誘導体部位はパラ型に酸素原子が結合しており、C2にはメチル基、C5、C6にはメトキシ基が結合している。C3にはイソプレン側鎖が結合しており、生体膜中に保持されるべく長い炭素鎖を形成している。構造は以下の図の通りである。
イソプレン側鎖の数(n=)は高等動物では10、下等動物では6～9であり、イソプレン側鎖が長くなればなるほど黄橙色を呈するようになる。なおn=10のユビキノンは『UQ10』と、イソプレン側鎖の数字を筆記する。
ユビキノンは2電子還元を受け（ユビキノールとなる）、1電子還元を受けて中間型（ユビセミキノン）も形成する。中間型はプロトンキノンサイクル機構でその意義があるとされている。ユビキノンの酸化還元様式は以下の図を参照。
酸化型のユビキノンは275nmの波長の電磁波を吸収する。したがって、ユビキノンに電子伝達を行う酵素群の活性測定はこの波長に類する吸収帯を使用する。
ユビキノンの生理的意義
ユビキノンはミトコンドリア内膜や原核生物の細胞膜から単離され、膜内の電子伝達に関与することが古くから知られている。特に電子伝達系、呼吸鎖複合体I（NADH脱水素酵素複合体）から呼吸鎖複合体III（シトクロムbc1複合体）への電子伝達に寄与している。
- 呼吸鎖複合体Iにおける反応
- NADH + ユビキノン(UQox) → NAD+ + ユビキノール (UQred)
- 呼吸鎖複合体IIIにおける反応
- ユビキノール + シトクロムc (Cytox, Fe3+) → ユビキノン + Cytred(Fe2+)
紅色光合成細菌の光合成反応中心における電子移動反応
ユビキノンは蛋白質内部に配位され、タンパク質内部における電子伝達にも機能している。もっとも有名な例としては紅色光合成細菌の光合成反応中心蛋白質における電子移動経路の一端として2つのユビキノンQAとQB間のプロトン移動とカップリングした電子移動反応QA→QBがあげられる。この反応は、植物の酸素発生を行う蛋白質光化学系II （photosystem II あるいはPSII）のプラストキノンQA→QBとの反応と実質的に同じであるため、近年の光化学系IIのX線構造解析結果によりその立体構造が次第に明らかにされつつあることと相まって、植物をはじめとする光合成系の酸素発生機構を解明する上で重要な反応である。
他の興味深い例として、呼吸鎖複合体III内のプロトンキノンサイクル機構（スカラー反応）に関与していることがあげられる。キノンサイクル機構には1電子還元を受けた中間型が重要な役割を果たしており、可動性リスケ鉄硫黄タンパク質と共同的な興味深いシステムが提案されている。
プロトンキノンサイクル機構
呼吸鎖複合体III（シトクロムbc1複合体）においては、複合体Iや複合体IVとは異なる機構でプロトンが膜外に輸送される。複合体I、IVにおいてはプロトンポンプ機構と言う、輸送を受けるプロトンが膜内から膜外に輸送されるのみである。しかしながら複合体IIIにおいてはプロトンキノンサイクル機構という独自の輸送機構を用いている。
プロトンキノンサイクル機構とは、膜内部においてプロトンが消費され、その還元力を使用して膜外側でのプロトンの放出が見られる現象である（この反応をスカラー反応と言う）。実際輸送を受けるプロトンは膜内から放出されるわけではなく、見かけ上そのように見えるだけなのでプロトンポンプ機構とはことなる機構であることが理解できる。その素反応の詳細は、以下の反応ステップからなる。
- 複合体IIIのシトクロムbに存在する、膜外側に存在するユビキノール酸化部位 （QP部位あるいはQO）にてユビキノールが酸化される。
- ユビキノールから2電子が抜き取られ、同時に膜外側へプロトンが2分子放出される。
- その2電子は異なる方向にそれぞれ伝達される。その内約は以下の通りである。
- 1個目の電子は、可動性リスケ鉄硫黄タンパク質を経て、シトクロムc1、シトクロムcの順番に電子伝達される。
- 2個目の電子は、シトクロムbに存在する2つのヘム（ヘムbL, bH）を経て膜内側に存在するユビキノン還元部位（QN部位あるいはQI部位）に電子伝達される。
- QN部位に電子が2電子伝達されることにより、ユビキノンは2電子還元を受けてユビキノールとなり、再びプロトンキノンサイクル機構に組み込まれる。
- その2電子は異なる方向にそれぞれ伝達される。その内約は以下の通りである。
以上が、プロトンキノンサイクル機構の反応であるが、この中でも特に優れた機構なのが可動性リスケ鉄硫黄タンパク質の関与する、電子伝達の方向性を変化させる過程である。それらの過程については構造生物学的研究より、以下のモデルが提唱されている。
- 可動性リスケ鉄硫黄タンパク質はc1側、中間型、b側の3つのコンフォメーションを持っており、酸化還元を受けない状態では、中間型を呈する。
- ユビキノールがQN部位に結合し、酸化を受けてプロトンを放出する。
- その時の、余剰の電子がリスケ鉄硫黄タンパク質にb側の状態を取らせ、1電子を鉄硫黄クラスターに受け取らせる。
- 可動性リスケ鉄硫黄タンパク質は酸化還元電位の高いシトクロムc1側の状態を取りヘムc1に電子伝達が行われ、シトクロムcにそのまま電子伝達される。
- 1電子酸化を受けたセミキノン型のキノンはヘムbLによって酸化を受け、プロトンを1つ膜外へ放出する。
- そしてヘムbLに電子伝達が行われ、ヘムbHを経てQN部位にてユビキノン還元反応を起こす。
- リスケ鉄硫黄タンパク質は酸化還元反応を終了し中間型に戻る。
以上が、プロトンキノンサイクル機構の主格を担うスイッチング反応である。極めて複雑な反応であるが、収支式が理解への一助となる。
- 2UQred + 4Cytcox → 2セミキノン(SQ) + 4Cytcred + 2H+out
- 2SQ + UQox) → 2UQox + UQred + 2H+out
ユビキノンの生合成
ユビキノンを呼吸鎖電子伝達体として利用する生物（たとえばヒト）は、自身でユビキノンを合成することができる。ユビキノンの合成は、4-ヒドロキシ安息香酸とイソプレン側鎖をそれぞれ合成した後に、この2つを4-ヒドロキシ安息香酸ポリプレニルトランスフェラーゼで結合し、さらにベンゼン環を修飾するという段階を踏む。それぞれの段階で、生物種によって合成経路に差がある。
4-ヒドロキシ安息香酸
4-ヒドロキシ安息香酸は、シキミ酸経路によって合成されるコリスミ酸から、真正細菌では直接、真核生物ではチロシンを経由し合成される。
なお例外的に出芽酵母では、葉酸の合成前駆体である4-アミノ安息香酸を、4-ヒドロキシ安息香酸の代わりに利用できることが示されている[2]。
イソプレン側鎖
イソプレン側鎖はメバロン酸経路または非メバロン酸経路によって合成されるイソペンテニル二リン酸を繰り返し重合して用意する。
ベンゼン環修飾
イソプレン側鎖が結合した後は、脱炭酸1回と、水酸化とメチル基転移を3回ずつ行うことでユビキノンが合成される。真正細菌と真核生物では修飾の順番が一部異なっていると考えられており、真正細菌では最初に脱炭酸された後に5位のメトキシ化が起きるのに対し、真核生物では先に5位のメトキシ化が起きてから脱炭酸される[3]。
医薬品としての効能
ユビキノンは、日本でかつて医療用医薬品として「軽度及び中等度のうっ血性心不全症状」などに期待されて1日30mgの投与量で用いられていた。人での効果を明確に実証した研究はなかった。小規模な無作為化試験では運動耐容能や左室駆出率に関してプラセボと有意差を示せず、心臓に関しては薬剤としての効能はほぼ否定され、『心不全治療ガイドライン2005』で米国心臓学会/米国心臓協会はユビキノン(コエンザイムQ10)の治療目的での摂取について「心不全の治療法に対しては、さらに多くの科学的根拠が蓄積されるまで推奨できない」と位置づけている。一般臨床の場では処方されなくなり、一般消費者をターゲットとして日本の複数の製薬メーカーが、一般用医薬品（OTC医薬品）・医薬部外品として発売するようになった。その薬剤としての実証性のなさから、米国FDAは薬剤として認めておらずあくまで食品との位置づけであり、従って規制の対象外であり、医師の処方箋なしに消費者が直接店頭などで購入できるようになった。
日本でも2001年に医薬品の範囲に関する基準（いわゆる「食薬区分」）が改正され、さらに2004年化粧品基準が改正されて、健康食品や化粧品への利用に道が開かれた。体内で合成されるものを摂取すること、消化器で分解されることを考慮すると、その効能は未知数ではある。ただ、加齢とともに減少することは確認されており、最近のサプリメントでは、消化されないよう加工されたものも作られている。摂取量については、どの程度までなら摂取しても安全なのか、などといった推奨量や上限量はわかっていない。また「多量に摂取した場合に軽度の胃腸症状（悪心、下痢、上腹部痛）」[1]があらわれるという報告があり、1日に数十mg以上の過剰摂取は避けた方が望ましい。厚生労働省からは医薬品として用いられる量（1日30mg）を超えないようにとの通知が出されている。
ユビキノンの誘導体であるイデベノン（商品アバン）は、脳循環・代謝改善剤として使用されていたが、日本では1998年に医薬品の承認を取り消されている。
有効性評価
2014年の調査時点で、心不全に対してのランダム化比較試験が7つあったがデータの測定基準が異なるため解析できなかった[4]。2017年では14つであり、心不全の死亡率を下げ運動能力を向上させていることが判明した[5]。433名の高齢者に4年間セレンとユビキノンをサプリメントで補給した試験のその後12年後の調査が2018年に論文となり、その時点でなお偽薬と比較して心血管疾患の死亡率の低下が認められた[6]。
2016年の研究は2試験から血圧に影響なし[7]、2018年の研究は17のランダム化比較試験から収縮期血圧のみ低下させるとし、拡張期血圧も低下したが統計的に有意だとはされていない[8]。
2016年の研究では14のランダム化比較試験から空腹時血糖を低下させたが、減少の度合いは少ないとされた[9]。
基礎研究
小児性線維筋痛症の発症の原因がユビキノンの欠乏にあると、東京工科大学応用生物学部の山本順寛らと、横浜市立大学医学部小児科との研究チームにより発見されたと、2013年7月16日に報じられた[10]。
2009年11月に、ユビキノンの抗酸化作用がマウスの老人性難聴の予防に効果があることを、東京大学が実験で明らかにした。これは動物実験のレベルであり、実臨床では証明されていない。それによると、人間にとっては1日20ミリグラムにあたる量のユビキノンを生後4ヶ月から与えられ続けてきたマウスは、人間の50歳に相当する生後15ヶ月の時点で、同じ月齢のマウスが45デシベル以上の音しか聞き取れないのに対し、12デシベルの小さい音を聞き取れるようになった。[11]
相互作用
薬剤（医薬品）の作用に悪影響を与える相互作用として、ワーファリンの作用を減弱させる可能性がある[12]。
原料製造メーカー
2007年現在コエンザイムQ10の原料製造を行っているのは世界でも日本企業5社（日清ファルマ（日清製粉グループ本社子会社）、カネカ、旭化成ファーマ（旭化成子会社）、三菱ガス化学、協和醗酵工業）のみであり、世界シェア100%を握っている。中でもカネカは最大のシェア（約65%）を持っている。各社とも、発酵法によって製造を行っている。
存在
動物の心臓や赤身肉に比較的多く含まれる傾向がある。
| 食品名 | CoQ10 (mg/Kg) |
備考 |
|---|---|---|
| 大豆油 | 221-279 | 伊の研究 |
| 大豆油 | 53.8-92.3 | 日本の研究 |
| 菜種油 | 63.5-73.4 | |
| ごま油 | 32.0 | |
| オリーブ油 | 109 | 伊の研究 |
| オリーブ油 | 4.1 | 日本の研究 |
| 牛肉(肩) | 40.1 | |
| 牛肉 | 16.1-36.5 | |
| 豚(肩) | 45.0 | |
| 豚 | 24.3-41.1 | |
| 鶏肉 | 14-21 | |
| ピーナツ(煎) | 26.7 | |
| 大豆(乾) | 6.8-19.0 | |
| 鮭 | 4.3-7.6 |
関連項目
- 電子伝達体
- 電子伝達系
- 補酵素
- 山本順寛 - 日本コエンザイムQ協会理事長、東京工科大学応用生物学部教授
- 川向 誠 - 日本コエンザイムQ協会理事、国際コエンザイムQ10協会理事、島根大学生物資源科学部教授
出典
| [脚注の使い方] |
- ^ 藤井健志、「食事から摂りたい還元型コエンザイムQ10」 『日本家政学会誌』 2012年 63巻 4号 p.205-207, doi:10.11428/jhej.63.205, 日本家政学会
- ^ Marbois et al. (2010). “para-Aminobenzoic Acid Is a Precursor in Coenzyme Q6 Biosynthesis in Saccharomyces cerevisiae”. J Biol. Chem. 285 (36): 27827-27838. doi:10.1074/jbc.M110.151894.
- ^ Kawamukai, Makoto (2016). “Biosynthesis of coenzyme Q in eukaryotes”. Biosci. Biotech. Biochem. 80 (1): 23-33. doi:10.1080/09168451.2015.1065172.
- ^ Madmani ME, Yusuf Solaiman A, Tamr Agha K, Madmani Y, Shahrour Y, Essali A, Kadro W (June 2014). “Coenzyme Q10 for heart failure”. Cochrane Database Syst Rev (6): CD008684. doi:10.1002/14651858.CD008684.pub2. PMID 24049047.
- ^ Lei L, Liu Y (July 2017). “Efficacy of coenzyme Q10 in patients with cardiac failure: a meta-analysis of clinical trials”. BMC Cardiovasc Disord 17 (1): 196. doi:10.1186/s12872-017-0628-9. PMC: 5525208. PMID 28738783. https://doi.org/10.1186/s12872-017-0628-9.
- ^ Alehagen U, Aaseth J, Alexander J, Johansson P (2018). “Still reduced cardiovascular mortality 12 years after supplementation with selenium and coenzyme Q10 for four years: A validation of previous 10-year follow-up results of a prospective randomized double-blind placebo-controlled trial in elderly”. PLoS ONE 13 (4): e0193120. doi:10.1371/journal.pone.0193120. PMC: 5894963. PMID 29641571. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5894963/.
- ^ Ho MJ, Li EC, Wright JM (March 2016). “Blood pressure lowering efficacy of coenzyme Q10 for primary hypertension”. Cochrane Database Syst Rev 3: CD007435. doi:10.1002/14651858.CD007435.pub3. PMID 26935713.
- ^ Tabrizi R, Akbari M, Sharifi N, Lankarani KB, Moosazadeh M, Kolahdooz F, Taghizadeh M, Asemi Z (March 2018). “The Effects of Coenzyme Q10 Supplementation on Blood Pressures Among Patients with Metabolic Diseases: A Systematic Review and Meta-analysis of Randomized Controlled Trials”. High Blood Press Cardiovasc Prev 25 (1): 41–50. doi:10.1007/s40292-018-0247-2. PMID 29330704.
- ^ Moradi M, Haghighatdoost F, Feizi A, Larijani B, Azadbakht L (August 2016). “Effect of Coenzyme Q10 Supplementation on Diabetes Biomarkers: a Systematic Review and Meta-analysis of Randomized Controlled Clinical Trials”. Arch Iran Med 19 (8): 588–96. PMID 27544369.
- ^ “東京工科大学 「小児線維筋痛症」が、コエンザイムQ10の欠乏で起こることを発見”. 大学プレスセンター. 2013年7月16日閲覧。
- ^ 「コエンザイムQ10で老人性難聴予防？東大などメカ解明」『読売新聞』2009年11月14日
- ^ コエンザイムQ10、ユビキノン、ビタミンQ - 「健康食品」の安全性・有効性情報（国立健康・栄養研究所）
- ^ “Coenzyme Q10 Contents in Foods and Fortification Strategies”. Critical Reviews in Food Science and Nutrition 50 (4). (2010). doi:10.1080/10408390902773037.
外部リンク
- コエンザイムQ10 - （オレゴン州大学・ライナス・ポーリング研究所）
- コエンザイムQ10、ユビキノン、ビタミンQ - 「健康食品」の安全性・有効性情報（国立健康・栄養研究所）
- コエンザイムQ10について - 同
- 日本コエンザイムQ協会
- 国際コエンザイムQ10協会
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| IUPAC name
2-[(2E,6E,10E,14E,18E,22E,26E,30E,34E)-3,7,11,15,19,23,27,31,35,39-Decamethyltetraconta-2,6,10,14,18,22,26,30,34,38-decaenyl]-5,6-dimethoxy-3-methylcyclohexa-2,5-diene-1,4-dione
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| Other names
Ubiquinone, ubidecarenone, coenzyme Q, CoQ10 /ˌkoʊˌkjuːˈtɛn/, CoQ, Q10
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CAS Number
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3D model (JSmol)
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| ChEBI |
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| ChEMBL |
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| ChemSpider |
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| ECHA InfoCard | 100.005.590 |
PubChem CID
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CompTox Dashboard (EPA)
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InChI
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SMILES
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| Properties | |
Chemical formula
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C59H90O4 |
| Molar mass | 863.365 g·mol−1 |
| Appearance | yellow or orange solid |
| Melting point | 48–52 °C (118–126 °F; 321–325 K) |
Solubility in water
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insoluble |
| Pharmacology | |
ATC code
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C01EB09 (WHO) |
| Related compounds | |
Related quinones
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1,4-Benzoquinone Plastoquinone Ubiquinol |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). | |
| Y verify (what is YN ?) | |
| Infobox references | |
Coenzyme Q, also known as ubiquinone, is a coenzyme family that is ubiquitous in animals and most bacteria (hence the name ubiquinone). In humans, the most common form is Coenzyme Q10 or ubiquinone-10. CoQ10 is not approved by the U.S. Food and Drug Administration (FDA) for the treatment of any medical condition;[1] however, it is sold as a dietary supplement and is an ingredient in some cosmetics.[2][3]
It is a 1,4-benzoquinone, where Q refers to the quinone chemical group and 10 refers to the number of isoprenyl chemical subunits in its tail. In natural ubiquinones, the number can be anywhere from 6 to 10. This family of fat-soluble substances, which resemble vitamins, is present in all respiring eukaryotic cells, primarily in the mitochondria. It is a component of the electron transport chain and participates in aerobic cellular respiration, which generates energy in the form of ATP. Ninety-five percent of the human body's energy is generated this way.[4][5] Organs with the highest energy requirements—such as the heart, liver, and kidney—have the highest CoQ10 concentrations.[6][7][8]
There are three redox states of CoQ: fully oxidized (ubiquinone), semiquinone (ubisemiquinone), and fully reduced (ubiquinol). The capacity of this molecule to act as a two-electron carrier (moving between the quinone and quinol form) and a one-electron carrier (moving between the semiquinone and one of these other forms) is central to its role in the electron transport chain due to the iron–sulfur clusters that can only accept one electron at a time, and as a free-radical–scavenging antioxidant.
Contents
- 1 Deficiency and toxicity
- 1.1 Assessment
- 1.2 Statins
- 2 Dietary supplement
- 2.1 Regulation and composition
- 2.2 Heart disease
- 2.3 Migraine headaches
- 2.4 Statin myopathy
- 2.5 Cancer
- 2.6 Dental disease
- 2.7 Chronic kidney disease
- 2.8 Additional uses
- 3 Interactions
- 4 Chemical properties
- 5 Biosynthesis
- 6 Absorption and metabolism
- 6.1 Absorption
- 6.2 Metabolism
- 7 Pharmacokinetics
- 7.1 Improving the bioavailability of CoQ10
- 7.1.1 Reduction of particle size
- 7.1.2 Soft-gel capsules with CoQ10 in oil suspension
- 7.1.3 Novel forms of CoQ10 with increased water-solubility
- 7.1 Improving the bioavailability of CoQ10
- 8 History
- 9 Dietary concentrations
- 9.1 Intake
- 9.2 Effect of heat and processing
- 10 See also
- 11 References
- 12 External links
Deficiency and toxicity
There are two major factors that lead to deficiency of CoQ10 in humans: reduced biosynthesis, and increased use by the body. Biosynthesis is the major source of CoQ10. Biosynthesis requires at least 12 genes, and mutations in many of them cause CoQ deficiency. CoQ10 levels also may be affected by other genetic defects (such as mutations of mitochondrial DNA, ETFDH, APTX, FXN, and BRAF, genes that are not directly related to the CoQ10 biosynthetic process). Some of these, such as mutations in COQ6, can lead to serious diseases such as steroid-resistant nephrotic syndrome with sensorineural deafness.
Some adverse effects, largely gastrointestinal, are reported with very high intakes. The observed safe level (OSL) risk assessment method indicated that the evidence of safety is strong at intakes up to 1200 mg/day, and this level is identified as the OSL.[9]
Assessment
Although CoQ10 may be measured in blood plasma, these measurements reflect dietary intake rather than tissue status. Currently, most clinical centers measure CoQ10 levels in cultured skin fibroblasts, muscle biopsies, and blood mononuclear cells.[10] Culture fibroblasts can be used also to evaluate the rate of endogenous CoQ10 biosynthesis, by measuring the uptake of 14C-labelled p-hydroxybenzoate.[11]
Statins
It has been suggested that the myotoxicity of statins is due to impairment of CoQ biosynthesis, but the evidence supporting this was deemed controversial in 2011.[10][needs update]
While statins may reduce coenzyme Q10 in the blood it is unclear if they reduce coenzyme Q10 in muscle.[12] Evidence does not support that supplementation improves side effects from statins.[12]
Dietary supplement
Regulation and composition
CoQ10 is sold in many jurisdictions as a dietary supplement in the name of UbiQ 300 & UbiQ 100, not subject to the same regulations as medicinal drugs, but not approved for the treatment of any medical condition.[1][13] The manufacture of CoQ10 is not regulated, and different batches and brands may vary significantly:[1] a 2004 laboratory analysis by ConsumerLab.com of CoQ10 supplements on sale in the US found that some did not contain the quantity identified on the product label. Amounts ranged from "no detectable CoQ10", through 75% of stated dose, up to a 75% excess.[14]
Generally, CoQ10 is well tolerated. The most common side effects are gastrointestinal symptoms (nausea, vomiting, appetite suppression, and abdominal pain), rashes, and headaches.[15]
While there is no established ideal dosage of CoQ10, a typical daily dose is 100–200 milligrams. Different formulations have varying declared amounts of CoQ10 and other ingredients.
Heart disease
A 2014 Cochrane review found "no convincing evidence to support or refute" the use of CoQ10 for the treatment of heart failure.[16] Another 2014 Cochrane review found insufficient evidence to make a conclusion about its use for the prevention of heart disease.[17] A 2016 Cochrane review concluded that CoQ10 had no effect on blood pressure.[18] In a 2017 meta-analysis of people with heart failure 30–100 mg/d of CoQ10 resulted in 31% lower mortality. Exercise capacity was also increased. No significant difference was found in the endpoints of left heart ejection fraction and New York Heart Association (NYHA) classification.[19]
Migraine headaches
The Canadian Headache Society guideline for migraine prophylaxis recommends, based on low-quality evidence, that 300 mg of CoQ10 be offered as a choice for prophylaxis.[20]
Statin myopathy
CoQ10 has been routinely used to treat muscle breakdown associated as a side effect of use of statin medications. A 2015 meta-analysis of randomized controlled trials found that CoQ10 had no effect on statin myopathy.[21] A 2018 meta-analysis concluded that there was preliminary evidence for oral CoQ10 reducing statin-associated muscle symptoms, including muscle pain, muscle weakness, muscle cramps and muscle tiredness.[22]
Cancer
As of 2014[update] no large clinical trials of CoQ10 in cancer treatment had been conducted.[1] The US' National Cancer Institute identified issues with the few, small studies that had been carried out, stating, "the way the studies were done and the amount of information reported made it unclear if benefits were caused by the CoQ10 or by something else".[1] The American Cancer Society concluded, "CoQ10 may reduce the effectiveness of chemo and radiation therapy, so most oncologists would recommend avoiding it during cancer treatment."[23]
Dental disease
A 1995 review study found that there is no clinical benefit to the use of CoQ10 in the treatment of periodontal disease.[24] Most of the studies suggesting otherwise were outdated, focused on in vitro tests,[25][26][27] had too few test subjects and/or erroneous statistical methodology and trial setup,[28][29] or were sponsored by a manufacturer of the product.[30]
Chronic kidney disease
A review of the effects of CoQ10 supplementation in people with CKD was proposed in 2019.[31]
Additional uses
Coenzyme Q10 has also been used to treat Alzheimer's disease, high cholesterol, or amyotrophic lateral sclerosis (Lou Gehrig's disease). However, research has shown that this medicine may not be effective in treating these conditions[32]
Interactions
Coenzyme Q10 has potential to inhibit the effects of theophylline as well as the anticoagulant warfarin; coenzyme Q10 may interfere with warfarin's actions by interacting with cytochrome p450 enzymes thereby reducing the INR, a measure of blood clotting.[33] The structure of coenzyme Q10 is very similar to that of vitamin K, which competes with and counteracts warfarin's anticoagulation effects. Coenzyme Q10 should be avoided in patients currently taking warfarin due to the increased risk of clotting.[15]
Chemical properties
The oxidized structure of CoQ10 is shown on the top-right. The various kinds of Coenzyme Q may be distinguished by the number of isoprenoid subunits in their side-chains. The most common Coenzyme Q in human mitochondria is CoQ10. Q refers to the quinone head and 10 refers to the number of isoprene repeats in the tail. The molecule below has three isoprenoid units and would be called Q3.
In its pure state, it is an orange-coloured lipophile powder, and has no taste nor odour.[34]:230
Biosynthesis
Biosynthesis occurs in most human tissue. There are three major steps:
- Creation of the benzoquinone structure (using phenylalanine or tyrosine, via 4-hydroxybenzoate)
- Creation of the isoprene side chain (using acetyl-CoA)
- The joining or condensation of the above two structures
The initial two reactions occur in mitochondria, the endoplasmic reticulum, and peroxisomes, indicating multiple sites of synthesis in animal cells.[35]
An important enzyme in this pathway is HMG-CoA reductase, usually a target for intervention in cardiovascular complications. The "statin" family of cholesterol-reducing medications inhibits HMG-CoA reductase. One possible side effect of statins is decreased production of CoQ10, which may be connected to the development of myopathy and rhabdomyolysis. However, the role statin plays in CoQ deficiency is controversial. Although these drug reduce blood levels of CoQ, studies on the effects of muscle levels of CoQ are yet to come. CoQ supplementation also does not reduce side effects of statin medications.[10][12]
Genes involved include PDSS1, PDSS2, COQ2, and ADCK3 (COQ8, CABC1).[36]
Organisms other than human use somewhat different source chemicals to produce the benzoquinone structure and the isoprene structure. For example, the bacteria E. coli produces the former from chorismate and the latter from a non-mevalonate source. The common yeast S. cerevisiae, however, derives the former from either chorismate or tyrosine and the latter from mevalonate. Most organisms share the common 4-hydroxybenzoate intermediate, yet again uses different steps to arrive at the "Q" structure.[37]
Absorption and metabolism
Absorption
CoQ10 is a crystalline powder insoluble in water. Absorption follows the same process as that of lipids; the uptake mechanism appears to be similar to that of vitamin E, another lipid-soluble nutrient. This process in the human body involves secretion into the small intestine of pancreatic enzymes and bile, which facilitates emulsification and micelle formation required for absorption of lipophilic substances.[38] Food intake (and the presence of lipids) stimulates bodily biliary excretion of bile acids and greatly enhances absorption of CoQ10. Exogenous CoQ10 is absorbed from the small intestine and is best absorbed if taken with a meal. Serum concentration of CoQ10 in fed condition is higher than in fasting conditions.[39][40]
Metabolism
Data on the metabolism of CoQ10 in animals and humans are limited.[41] A study with 14C-labeled CoQ10 in rats showed most of the radioactivity in the liver two hours after oral administration when the peak plasma radioactivity was observed, but CoQ9 (with only 9 isoprenyl units) is the predominant form of coenzyme Q in rats.[42] It appears that CoQ10 is metabolised in all tissues, while a major route for its elimination is biliary and fecal excretion. After the withdrawal of CoQ10 supplementation, the levels return to normal within a few days, irrespective of the type of formulation used.[43]
Pharmacokinetics
Some reports have been published on the pharmacokinetics of CoQ10. The plasma peak can be observed 2–6 hours after oral administration, depending mainly on the design of the study. In some studies, a second plasma peak also was observed at approximately 24 hours after administration, probably due to both enterohepatic recycling and redistribution from the liver to circulation.[38] Tomono et al. used deuterium-labeled crystalline CoQ10 to investigate pharmacokinetics in humans and determined an elimination half-time of 33 hours.[44]
Improving the bioavailability of CoQ10
The importance of how drugs are formulated for bioavailability is well known. In order to find a principle to boost the bioavailability of CoQ10 after oral administration, several new approaches have been taken; different formulations and forms have been developed and tested on animals and humans.[41]
Reduction of particle size
Nanoparticles have been explored as a delivery system for various drugs, such as improving the oral bioavailability of drugs with poor absorption characteristics.[45] However, this has not proved successful with CoQ10, although reports have differed widely.[46][47] The use of aqueous suspension of finely powdered CoQ10 in pure water also reveals only a minor effect.[43]
Soft-gel capsules with CoQ10 in oil suspension
A successful approach was to use the emulsion system to facilitate absorption from the gastrointestinal tract and to improve bioavailability. Emulsions of soybean oil (lipid microspheres) could be stabilised very effectively by lecithin and were used in the preparation of soft gelatin capsules. In one of the first such attempts, Ozawa et al. performed a pharmacokinetic study on beagles in which the emulsion of CoQ10 in soybean oil was investigated; about twice the plasma CoQ10 level than that of the control tablet preparation was determined during administration of a lipid microsphere.[43] Although an almost negligible improvement of bioavailability was observed by Kommuru et al. with oil-based softgel ucapsules in a later study on dogs,[48] the significantly increased bioavailability of CoQ10 was confirmed for several oil-based formulations in most other studies.[49]
Novel forms of CoQ10 with increased water-solubility
Facilitating drug absorption by increasing its solubility in water is a common pharmaceutical strategy and also has been shown to be successful for CoQ10. Various approaches have been developed to achieve this goal, with many of them producing significantly better results over oil-based softgel capsules in spite of the many attempts to optimize their composition.[41] Examples of such approaches are use of the aqueous dispersion of solid CoQ10 with the polymer tyloxapol,[50] formulations based on various solubilising agents, such as hydrogenated lecithin,[51] and complexation with cyclodextrins; among the latter, the complex with β-cyclodextrin has been found to have highly increased bioavailability[52][53] and also is used in pharmaceutical and food industries for CoQ10-fortification.[41]
History
In 1950, G. N. Festenstein was the first to isolate a small amount of CoQ10 from the lining of a horse's gut at Liverpool, England. In subsequent studies the compound was briefly called substance SA, it was deemed to be quinone and it was noted that it could be found from many tissues of a number of animals.[54]
In 1957, Frederick L. Crane and colleagues at the University of Wisconsin–Madison Enzyme Institute isolated the same compound from mitochondrial membranes of beef heart and noted that it transported electrons within mitochondria. They called it Q-275 for short as it was a quinone.[55][54] Soon they noted that Q-275 and substance SA studied in England may be the same compound. This was confirmed later that year and Q-275/substance SA was renamed ubiquinone as it was a ubiquitous quinone that could be found from all animal tissues.[54][34]
In 1958, its full chemical structure was reported by D. E. Wolf and colleagues working under Karl Folkers at Merck in Rahway.[56][54][34] Later that year D. E. Green and colleagues belonging to the Wisconsin research group suggested that ubiquinone should be called either mitoquinone or coenzyme Q due to its participation to the mitochondrial electron transport chain.[54][34]
In 1966, A. Mellors and A. L. Tappel at the University of California were to first to show that reduced CoQ6 was an effective antioxidant in cells.[57][34]
In 1960s Peter D. Mitchell enlarged upon the understanding of mitochondrial function via his theory of electrochemical gradient, which involves CoQ10, and in late 1970s studies of Lars Ernster enlargened upon the importance of CoQ10 as an antioxidant. The 1980s witnessed a steep rise in the number of clinical trials involving CoQ10.[34]
Dietary concentrations
Detailed reviews on occurrence of CoQ10 and dietary intake were published in 2010.[58] Besides the endogenous synthesis within organisms, CoQ10 also is supplied to the organism by various foods. Despite the scientific community's great interest in this compound, however, a very limited number of studies have been performed to determine the contents of CoQ10 in dietary components. The first reports on this aspect were published in 1959, but the sensitivity and selectivity of the analytical methods at that time did not allow reliable analyses, especially for products with low concentrations.[58] Since then, developments in analytical chemistry have enabled a more reliable determination of CoQ10 concentrations in various foods:
| Food | CoQ10 concentration (mg/kg) | |
|---|---|---|
| Beef | heart | 113 |
| liver | 39–50 | |
| muscle | 26–40 | |
| Pork | heart | 12–128 |
| liver | 23–54 | |
| muscle | 14–45 | |
| Chicken | breast | 8–17 |
| thigh | 24–25 | |
| wing | 11 | |
| Fish | sardine | 5–64 |
| mackerel: | ||
| – red flesh | 43–67 | |
| – white flesh | 11–16 | |
| salmon | 4–8 | |
| tuna | 5 | |
| Oils | soybean | 54–280 |
| olive | 4–160 | |
| grapeseed | 64–73 | |
| sunflower | 4–15 | |
| canola | 64–73 | |
| Nuts | peanut | 27 |
| walnut | 19 | |
| sesame seed | 18–23 | |
| pistachio | 20 | |
| hazelnut | 17 | |
| almond | 5–14 | |
| Vegetables | parsley | 8–26 |
| broccoli | 6–9 | |
| cauliflower | 2–7 | |
| spinach | up to 10 | |
| Chinese cabbage | 2–5 | |
| Fruit | avocado | 10 |
| blackcurrant | 3 | |
| grape | 6–7 | |
| strawberry | 1 | |
| orange | 1–2 | |
| grapefruit | 1 | |
| apple | 1 | |
| banana | 1 | |
Meat and fish are the richest sources of dietary CoQ10; levels over 50 mg/kg may be found in beef, pork, and chicken heart and liver. Dairy products are much poorer sources of CoQ10 than animal tissues. Vegetable oils also are quite rich in CoQ10. Within vegetables, parsley and perilla are the richest CoQ10 sources, but significant differences in their CoQ10 levels may be found in the literature. Broccoli, grapes, and cauliflower are modest sources of CoQ10. Most fruit and berries represent a poor to very poor source of CoQ10, with the exception of avocados, which have a relatively high CoQ10 content.[58]
Intake
In the developed world, the estimated daily intake of CoQ10 has been determined at 3–6 mg per day, derived primarily from meat.[58]
Effect of heat and processing
Cooking by frying reduces CoQ10 content by 14–32%.[59]
See also
- Idebenone – synthetic analog with reduced oxidant generating properties
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- ^ Ochiai A, Itagaki S, Kurokawa T, Kobayashi M, Hirano T, Iseki K (August 2007). "Improvement in intestinal coenzyme q10 absorption by food intake". Yakugaku Zasshi. 127 (8): 1251–4. doi:10.1248/yakushi.127.1251. PMID 17666877.[verification needed]
- ^ a b c d Žmitek; et al. (2008). "Improving the bioavailability of CoQ10". Agro Food Industry Hi Tech. 19 (4): 9. Archived from the original on 5 October 2011. Retrieved 21 October 2008.
- ^ Kishi, H.; Kanamori, N.; Nisii, S.; Hiraoka, E.; Okamoto, T.; Kishi, T. (1964). "Metabolism and Exogenous Coenzyme Q10 in vivo and Bioavailability of Coenzyme Q10 Preparations in Japan". Biomedical and Clinical Aspects of Coenzyme Q. Amsterdam: Elsevier. pp. 131–142.
- ^ a b c Ozawa Y, Mizushima Y, Koyama I, Akimoto M, Yamagata Y, Hayashi H, Murayama H (April 1986). "Intestinal absorption enhancement of coenzyme Q10 with a lipid microsphere". Arzneimittel-Forschung. 36 (4): 689–90. PMID 3718593.
- ^ Tomono Y, Hasegawa J, Seki T, Motegi K, Morishita N (October 1986). "Pharmacokinetic study of deuterium-labelled coenzyme Q10 in man". International Journal of Clinical Pharmacology, Therapy, and Toxicology. 24 (10): 536–41. PMID 3781673.
- ^ Mathiowitz E, Jacob JS, Jong YS, Carino GP, Chickering DE, Chaturvedi P, et al. (March 1997). "Biologically erodable microspheres as potential oral drug delivery systems". Nature. 386 (6623): 410–4. Bibcode:1997Natur.386..410M. doi:10.1038/386410a0. PMID 9121559. S2CID 4324209.
- ^ Hsu CH, Cui Z, Mumper RJ, Jay M (2003). "Preparation and characterization of novel coenzyme Q10 nanoparticles engineered from microemulsion precursors". AAPS PharmSciTech. 4 (3): E32. doi:10.1208/pt040332. PMC 2750625. PMID 14621964.[verification needed]
- ^ Joshi SS, Sawant SV, Shedge A, Halpner AD (January 2003). "Comparative bioavailability of two novel coenzyme Q10 preparations in humans". International Journal of Clinical Pharmacology and Therapeutics. 41 (1): 42–8. doi:10.5414/CPP41042. PMID 12564745.[verification needed]
- ^ Kommuru TR, Ashraf M, Khan MA, Reddy IK (July 1999). "Stability and bioequivalence studies of two marketed formulations of coenzyme Q10 in beagle dogs". Chemical & Pharmaceutical Bulletin. 47 (7): 1024–8. doi:10.1248/cpb.47.1024. PMID 10434405.
- ^ Bhagavan HN, Chopra RK (June 2007). "Plasma coenzyme Q10 response to oral ingestion of coenzyme Q10 formulations". Mitochondrion. 7 Suppl (Suppl): S78-88. doi:10.1016/j.mito.2007.03.003. PMID 17482886.[verification needed]
- ^ US 6197349, Westesen, K. & B. Siekmann, "Particles with modified physicochemical properties, their preparation and uses", published 2001
- ^ US 4483873, Ohashi, H.; T. Takami & N. Koyama et al., "Aqueous solution containing ubidecarenone", published 1984
- ^ Zmitek J, Smidovnik A, Fir M, Prosek M, Zmitek K, Walczak J, Pravst I (2008). "Relative bioavailability of two forms of a novel water-soluble coenzyme Q10". Annals of Nutrition & Metabolism. 52 (4): 281–7. doi:10.1159/000129661. PMID 18645245. S2CID 825159.
- ^ Kagan, Daniel; Madhavi, Doddabele (2010). "A Study on the Bioavailability of a Novel Sustained-Release Coenzyme Q10-β-Cyclodextrin Complex". Integrative Medicine. 9 (1).
- ^ a b c d e Morton RA (December 1958). "Ubiquinone". Nature. 182 (4652): 1764–7. Bibcode:1958Natur.182.1764M. doi:10.1038/1821764a0. PMID 13622652.
- ^ Crane FL, Hatefi Y, Lester RL, Widmer C (July 1957). "Isolation of a quinone from beef heart mitochondria". Biochimica et Biophysica Acta. 25 (1): 220–1. doi:10.1016/0006-3002(57)90457-2. PMID 13445756.
- ^ Wolf DE, et al. (1958). "Coenzyme Q. I. structure studies on the coenzyme Q group". Journal of the American Chemical Society. 80 (17): 4752. doi:10.1021/ja01550a096. ISSN 0002-7863.
- ^ Mellors A, Tappel AL (July 1966). "Quinones and quinols as inhibitors of lipid peroxidation". Lipids. 1 (4): 282–4. doi:10.1007/BF02531617. PMID 17805631. S2CID 2129339.
- ^ a b c d e Pravst I, Zmitek K, Zmitek J (April 2010). "Coenzyme Q10 contents in foods and fortification strategies". Critical Reviews in Food Science and Nutrition. 50 (4): 269–80. doi:10.1080/10408390902773037. PMID 20301015. S2CID 38779392.
- ^ Weber C, Bysted A, Hłlmer G (1997). "The coenzyme Q10 content of the average Danish diet". International Journal for Vitamin and Nutrition Research. Internationale Zeitschrift für Vitamin- und Ernahrungsforschung. Journal International de Vitaminologie et de Nutrition. 67 (2): 123–9. PMID 9129255.
External links
- "List of USP Verified CoQ10 Ingredients". U.S. Pharmacopeial Convention. Archived from the original on 9 February 2009.
- "Coenzyme Q10". National Cancer Institute. 23 September 2005.
- Bonakdar, Robert Alan; Guarneri, Erminia (15 September 2005). "Coenzyme Q10". American Family Physician. 72 (6): 1065–1070. PMID 16190504.
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Japanese Journal
- パーキンソン病の進行抑制を目指した神経保護代替医療アプローチ
- 室山 明子
- YAKUGAKU ZASSHI 133(8), 849-856, 2013
- … Coenzyme Q10 (CoQ10) is a component of the electron transport chain as well as an important antioxidant in mitochondrial and lipid membranes. … The central role of CoQ10 in two areas implicated in the pathogenesis of PD, mitochondrial dysfunction and oxidative damages, suggest that it may be useful for treatment to slow the progression of PD. … The neuroprotective effect of CoQ10 has been reported in several in vivo and in vitro models of neurodegenerative disorders. …
- NAID 130003361978
- Dietary Coenzyme Q10 Suppressed Hepatic Hydroxymethylglutaryl-CoA Reductase Activity in Laying Hens
- HONDA Kazuhisa,SANEYASU Takaoki,MOTOKI Tohru,PARK Yuriko,KAMISOYAMA Hiroshi
- Bioscience, Biotechnology, and Biochemistry, 2013
- … The effects of dietary coenzyme Q10 (CoQ10) on cholesterol metabolism in laying hens were investigated. … Dietary CoQ10 significantly reduced egg yolk cholesterol content and suppressed hepatic hydroxymethylglutaryl-CoA reductase (HMGR) activity. … It is therefore likely that CoQ10 acts as an HMGR inhibitor in the livers of laying hens, which in turn results in a reduction in egg-yolk cholesterol. …
- NAID 130003361133
- コエンザイムQ10を高蓄積するイネの開発
- 高橋 咲子
- 農業生物資源研究所研究資料 (9), 1-46, 2012-06-00
- NAID 40019388704
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