TCAサイクル、TCA回路、トリカルボン酸回路、クエン酸回路

関: citric acid cycle、tricarboxylic acid cycle

WordNet

pass through a cycle; "This machine automatically cycles"
an interval during which a recurring sequence of events occurs; "the never-ending cycle of the seasons" (同)rhythm, round
recur in repeating sequences
a single complete execution of a periodically repeated phenomenon; "a year constitutes a cycle of the seasons" (同)oscillation
a periodically repeated sequence of events; "a cycle of reprisal and retaliation"
a series of poems or songs on the same theme; "Schuberts song cycles"
cause to go through a recurring sequence; "cycle the laundry in this washing program"
the 20th letter of the Roman alphabet (同)t
the sport of traveling on a bicycle or motorcycle

PrepTutorEJDIC

『周期』,循環期;一巡り / 周波,サイクル / (英雄・伝説などを扱った)一連の詩(物語) / 『自転車』;三輪車;オートバイ / 自転車に乗る / 循環する,反復する
tritiumの化学記号
Teachers College 教員養成大学
自転車に乗ること,サイクリング

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/04/23 10:00:15」(JST)

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Overview of the citric acid cycle (click to enlarge)

The citric acid cycle — also known as the tricarboxylic acid cycle (TCA cycle), or the Krebs cycle,^[1]^[2]^[3] — is a series of chemical reactions used by all aerobic organisms to generate energy through the oxidation of acetate derived from carbohydrates, fats and proteins into carbon dioxide and chemical energy in the form of adenosine triphosphate (ATP). In addition, the cycle provides precursors of certain amino acids as well as the reducing agent NADH that is used in numerous other biochemical reactions. Its central importance to many biochemical pathways suggests that it was one of the earliest established components of cellular metabolism and may have originated abiogenically.^[4]

The name of this metabolic pathway is derived from citric acid (a type of tricarboxylic acid) that is consumed and then regenerated by this sequence of reactions to complete the cycle. In addition, the cycle consumes acetate (in the form of acetyl-CoA) and water, reduces NAD⁺ to NADH, and produces carbon dioxide as a waste byproduct. The NADH generated by the TCA cycle is fed into the oxidative phosphorylation (electron transport) pathway. The net result of these two closely linked pathways is the oxidation of nutrients to produce usable chemical energy in the form of ATP.

In eukaryotic cells, the citric acid cycle occurs in the matrix of the mitochondrion. In prokaryotic cells, such as bacteria which lack mitochondria, the TCA reaction sequence is performed in the cytosol with the proton gradient for ATP production being across the cell's surface (plasma membrane) rather than the inner membrane of the mitochondrion.

Several of the components and reactions of the citric acid cycle were established in the 1930s by the research of the Nobel laureate Albert Szent-Györgyi, for which he received the Nobel Prize in 1937 for his discoveries pertaining to fumaric acid, a key component of the cycle.^[5]

The citric acid cycle itself was finally identified in 1937 by Hans Adolf Krebs while at the University of Sheffield, for which he received the Nobel Prize for Physiology or Medicine in 1953.^[6]

Evolution

Components of the TCA cycle were derived from anaerobic bacteria, and the TCA cycle itself may have evolved more than once.^[7] Theoretically there are several alternatives to the TCA cycle; however, the TCA cycle appears to be the most efficient. If several TCA alternatives had evolved independently, they all appear to have converged to the TCA cycle.^[8]^[9]

Overview

The citric acid cycle is a key component of the metabolic pathway by which all aerobic organisms generate energy. Through catabolism of sugars, fats, and proteins, a two-carbon organic product acetate in the form of acetyl-CoA is produced. Acetyl-CoA along with two equivalents of water (H₂O) is consumed by the citric acid cycle producing two equivalents of carbon dioxide (CO₂) and one equivalent of HS-CoA. In addition, one complete turn of the cycle converts three equivalents of nicotinamide adenine dinucleotide (NAD⁺) into three equivalents of reduced NAD⁺ (NADH), one equivalent of ubiquinone (Q) into one equivalent of reduced ubiquinone (QH₂), and one equivalent each of guanosine diphosphate (GDP) and inorganic phosphate (P_i) into one equivalent of guanosine triphosphate (GTP). The NADH and QH₂ generated by the citric acid cycle are in turn used by the oxidative phosphorylation pathway to generate energy-rich adenosine triphosphate (ATP).

One of the primary sources of acetyl-CoA is sugars that are broken down by glycolysis to produce pyruvate that in turn is decarboxylated by the enzyme pyruvate dehydrogenase generating acetyl-CoA according to the following reaction scheme:^[1]

CH₃C(=O)C(=O)O^– (pyruvate) + HSCoA + NAD⁺ → CH₃C(=O)SCoA (acetyl-CoA) + NADH + CO₂

The product of this reaction, acetyl-CoA, is the starting point for the citric acid cycle. Below is a schematic outline of the cycle:^[1]

The citric acid cycle begins with the transfer of a two-carbon acetyl group from acetyl-CoA to the four-carbon acceptor compound (oxaloacetate) to form a six-carbon compound (citrate).
The citrate then goes through a series of chemical transformations, losing two carboxyl groups as CO₂. The carbons lost as CO₂ originate from what was oxaloacetate, not directly from acetyl-CoA. The carbons donated by acetyl-CoA become part of the oxaloacetate carbon backbone after the first turn of the citric acid cycle. Loss of the acetyl-CoA-donated carbons as CO₂ requires several turns of the citric acid cycle. However, because of the role of the citric acid cycle in anabolism, they might not be lost, since many TCA cycle intermediates are also used as precursors for the biosynthesis of other molecules.^[10]
Most of the energy made available by the oxidative steps of the cycle is transferred as energy-rich electrons to NAD⁺, forming NADH. For each acetyl group that enters the citric acid cycle, three molecules of NADH are produced.
Electrons are also transferred to the electron acceptor Q, forming QH₂.
At the end of each cycle, the four-carbon oxaloacetate has been regenerated, and the cycle continues.

Steps

Two carbon atoms are oxidized to CO₂, the energy from these reactions being transferred to other metabolic processes by GTP (or ATP), and as electrons in NADH and QH₂. The NADH generated in the TCA cycle may later donate its electrons in oxidative phosphorylation to drive ATP synthesis; FADH₂ is covalently attached to succinate dehydrogenase, an enzyme functioning both in the TCA cycle and the mitochondrial electron transport chain in oxidative phosphorylation. FADH₂, therefore, facilitates transfer of electrons to coenzyme Q, which is the final electron acceptor of the reaction catalyzed by the Succinate:ubiquinone oxidoreductase complex, also acting as an intermediate in the electron transport chain.^[11]

The citric acid cycle is continuously supplied with new carbon in the form of acetyl-CoA, entering at step 1 below.^[1]^[12]

	Substrates	Products	Enzyme	Reaction type	Comment
1	Oxaloacetate + Acetyl CoA + H₂O	Citrate + CoA-SH	Citrate synthase	Aldol condensation	irreversible, extends the 4C oxaloacetate to a 6C molecule
2	Citrate	cis-Aconitate + H₂O	Aconitase	Dehydration	reversible isomerisation
3	cis-Aconitate + H₂O	Isocitrate	Aconitase	Hydration	reversible isomerisation
4	Isocitrate + NAD⁺	Oxalosuccinate + NADH + H ⁺	Isocitrate dehydrogenase	Oxidation	generates NADH (equivalent of 2.5 ATP)
5	Oxalosuccinate	α-Ketoglutarate + CO₂	Isocitrate dehydrogenase	Decarboxylation	rate-limiting, irreversible stage, generates a 5C molecule
6	α-Ketoglutarate + NAD⁺ + CoA-SH	Succinyl-CoA + NADH + H⁺ + CO₂	α-Ketoglutarate dehydrogenase	Oxidative decarboxylation	irreversible stage, generates NADH (equivalent of 2.5 ATP), regenerates the 4C chain (CoA excluded)
7	Succinyl-CoA + GDP + P_i	Succinate + CoA-SH + GTP	Succinyl-CoA synthetase	substrate-level phosphorylation	or ADP→ATP instead of GDP→GTP,^[11] generates 1 ATP or equivalent Condensation reaction of GDP + P_i and hydrolysis of Succinyl-CoA involve the H₂O needed for balanced equation.
8	Succinate + ubiquinone (Q)	Fumarate + ubiquinol (QH₂)	Succinate dehydrogenase	Oxidation	uses FAD as a prosthetic group (FAD→FADH₂ in the first step of the reaction) in the enzyme,^[11] generates the equivalent of 1.5 ATP
9	Fumarate + H₂O	L-Malate	Fumarase	Hydration
10	L-Malate + NAD⁺	Oxaloacetate + NADH + H⁺	Malate dehydrogenase	Oxidation	reversible (in fact, equilibrium favors malate), generates NADH (equivalent of 2.5 ATP)

Mitochondria in animals, including humans, possess two succinyl-CoA synthetases: one that produces GTP from GDP, and another that produces ATP from ADP.^[13] Plants have the type that produces ATP (ADP-forming succinyl-CoA synthetase).^[12] Several of the enzymes in the cycle may be loosely associated in a multienzyme protein complex within the mitochondrial matrix.^[14]

The GTP that is formed by GDP-forming succinyl-CoA synthetase may be utilized by nucleoside-diphosphate kinase to form ATP (the catalyzed reaction is GTP + ADP → GDP + ATP).^[11]

Products

Products of the first turn of the cycle are: one GTP (or ATP), three NADH, one QH₂, two CO₂.

Because two acetyl-CoA molecules are produced from each glucose molecule, two cycles are required per glucose molecule. Therefore, at the end of two cycles, the products are: two GTP, six NADH, two QH₂, and four CO₂

Description	Reactants	Products
The sum of all reactions in the citric acid cycle is:	Acetyl-CoA + 3 NAD⁺ + Q + GDP + P_i + 2 H₂O	→ CoA-SH + 3 NADH + 3 H⁺ + QH₂ + GTP + 2 CO₂
Combining the reactions occurring during the pyruvate oxidation with those occurring during the citric acid cycle, the following overall pyruvate oxidation reaction is obtained:	Pyruvate ion + 4 NAD⁺ + Q + GDP + P_i + 2 H₂O	→ 4 NADH + 4 H⁺ + QH₂ + GTP + 3 CO₂
Combining the above reaction with the ones occurring in the course of glycolysis, the following overall glucose oxidation reaction (excluding reactions in the respiratory chain) is obtained:	Glucose + 10 NAD⁺ + 2 Q + 2 ADP + 2 GDP + 4 P_i + 2 H₂O	→ 10 NADH + 10 H⁺ + 2 QH₂ + 2 ATP + 2 GTP + 6 CO₂

The above reactions are balanced if P_i represents the H₂PO₄^- ion, ADP and GDP the ADP^2- and GDP^2- ions, respectively, and ATP and GTP the ATP^3- and GTP^3- ions, respectively.

The total number of ATP obtained after complete oxidation of one glucose in glycolysis, citric acid cycle, and oxidative phosphorylation is estimated to be between 30 and 38.^[15]

Efficiency

The theoretical maximum yield of ATP through oxidation of one molecule of glucose in glycolysis, citric acid cycle, and oxidative phosphorylation is 38 (assuming 3 molar equivalents of ATP per equivalent NADH and 2 ATP per FADH₂). In eukaryotes, two equivalents of NADH are generated in glycolysis, which takes place in the cytoplasm. Transport of these two equivalents into the mitochondria consumes two equivalents of ATP, thus reducing the net production of ATP to 36. Furthermore, inefficiencies in oxidative phosphorylation due to leakage of protons across of the mitochondrial membrane and slippage of the ATP synthase/proton pump commonly reduces the ATP yield from NADH and FADH₂ to less than the theoretical maximum yield.^[15] The observed yields are, therefore, closer to ~2.5 ATP per NADH and ~1.5 ATP per FADH₂, further reducing the total net production of ATP to approximately 30.^[16] An assessment of the total ATP yield with newly revised proton-to-ATP ratios provides an estimate of 29.85 ATP per glucose molecule.^[17] However, the total amount of ATP generated from just the Krebs Cycle for one molecule of glucose is around 25.^[1]

Regulation

The regulation of the TCA cycle is largely determined by product inhibition and substrate availability.If the cycle were permitted to run unchecked, large amounts of metabolic energy could be wasted in overproduction of reduced coenzyme such as NADH and ATP. The major eventual substrate of the cycle is ADP which gets converted to ATP. A reduced amount of ADP causes accumulation of precursor NADH which in turn can inhibit a number of enzymes.^[1] NADH, a product of all dehydrogenases in the TCA cycle with the exception of succinate dehydrogenase, inhibits pyruvate dehydrogenase, isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, and also citrate synthase. Acetyl-coA inhibits pyruvate dehydrogenase, while succinyl-CoA inhibits alpha-ketoglutarate dehydrogenase and citrate synthase. When tested in vitro with TCA enzymes, ATP inhibits citrate synthase and α-ketoglutarate dehydrogenase; however, ATP levels do not change more than 10% in vivo between rest and vigorous exercise. There is no known allosteric mechanism that can account for large changes in reaction rate from an allosteric effector whose concentration changes less than 10%.^[18]

Calcium is used as a regulator. Mitochondrial matrix calcium levels can reach the tens of micromolar levels during cellular activation.^[19] It activates pyruvate dehydrogenase phosphatase which in turn activates the pyruvate dehydrogenase complex. Calcium also activates isocitrate dehydrogenase and α-ketoglutarate dehydrogenase.^[20] This increases the reaction rate of many of the steps in the cycle, and therefore increases flux throughout the pathway.

Citrate is used for feedback inhibition, as it inhibits phosphofructokinase, an enzyme involved in glycolysis that catalyses formation of fructose 1,6-bisphosphate,a precursor of pyruvate. This prevents a constant high rate of flux when there is an accumulation of citrate and a decrease in substrate for the enzyme.

Recent work has demonstrated an important link between intermediates of the citric acid cycle and the regulation of hypoxia-inducible factors (HIF). HIF plays a role in the regulation of oxygen homeostasis, and is a transcription factor that targets angiogenesis, vascular remodeling, glucose utilization, iron transport and apoptosis. HIF is synthesized consititutively, and hydroxylation of at least one of two critical proline residues mediates their interaction with the von Hippel Lindau E3 ubiquitin ligase complex, which targets them for rapid degradation. This reaction is catalysed by prolyl 4-hydroxylases. Fumarate and succinate have been identified as potent inhibitors of prolyl hydroxylases, thus leading to the stabilisation of HIF.^[21]

Major metabolic pathways converging on the TCA cycle

Several catabolic pathways converge on the TCA cycle. Reactions that form intermediates of the TCA cycle in order to replenish them (especially during the scarcity of the intermediates) are called anaplerotic reactions.

The citric acid cycle is the third step in carbohydrate catabolism (the breakdown of sugars). Glycolysis breaks glucose (a six-carbon-molecule) down into pyruvate (a three-carbon molecule). In eukaryotes, pyruvate moves into the mitochondria. It is converted into acetyl-CoA by decarboxylation and enters the citric acid cycle.

In protein catabolism, proteins are broken down by proteases into their constituent amino acids. The carbon backbone of these amino acids can become a source of energy by being converted to acetyl-CoA and entering into the citric acid cycle.

In fat catabolism, triglycerides are hydrolyzed to break them into fatty acids and glycerol. In the liver the glycerol can be converted into glucose via dihydroxyacetone phosphate and glyceraldehyde-3-phosphate by way of gluconeogenesis. In many tissues, especially heart tissue, fatty acids are broken down through a process known as beta oxidation, which results in acetyl-CoA, which can be used in the citric acid cycle. Beta oxidation of fatty acids with an odd number of methylene bridges produces propionyl CoA, which is then converted into succinyl-CoA and fed into the citric acid cycle.^[22]

The total energy gained from the complete breakdown of one molecule of glucose by glycolysis, the citric acid cycle, and oxidative phosphorylation equals about 30 ATP molecules, in eukaryotes. The citric acid cycle is called an amphibolic pathway because it participates in both catabolism and anabolism.

Interactive pathway map

Click on genes, proteins and metabolites below to link to respective articles. ^{[§ 1]}

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TCA Cycle edit

^ The interactive pathway map can be edited at WikiPathways: "TCACycle_WP78".

References

^ ^a ^b ^c ^d ^e ^f The Kreb's Cycle or Citric Acid Cycle or Tricarboxylic Cycle- explained with animation
^ Lowenstein JM (1969). Methods in Enzymology, Volume 13: Citric Acid Cycle. Boston: Academic Press. ISBN 0-12-181870-5.
^ Krebs HA, Weitzman PDJ (1987). Krebs' citric acid cycle: half a century and still turning. London: Biochemical Society. ISBN 0-904498-22-0.
^ Lane, Nick (2009). Life Ascending: The Ten Great Inventions of Evolution. New York: W.W. Norton & Co. ISBN 0-393-06596-0.
^ "The Nobel Prize in Physiology or Medicine 1937". The Nobel Foundation. Retrieved 2011-10-26.
^ "The Nobel Prize in Physiology or Medicine 1953". The Nobel Foundation. Retrieved 2011-10-26.
^ Gest H (1987). "Evolutionary roots of the citric acid cycle in prokaryotes". Biochem. Soc. Symp. 54: 3–16. PMID 3332996.
^ Meléndez-Hevia E, Waddell TG, Cascante M (September 1996). "The puzzle of the Krebs citric acid cycle: assembling the pieces of chemically feasible reactions, and opportunism in the design of metabolic pathways during evolution". J. Mol. Evol. 43 (3): 293–303. doi:10.1007/BF02338838. PMID 8703096.
^ Ebenhöh O, Heinrich R (January 2001). "Evolutionary optimization of metabolic pathways. Theoretical reconstruction of the stoichiometry of ATP and NADH producing systems". Bull. Math. Biol. 63 (1): 21–55. doi:10.1006/bulm.2000.0197. PMID 11146883.
^ Wolfe RR, Jahoor F (February 1990). "Recovery of labeled CO2 during the infusion of C-1- vs C-2-labeled acetate: implications for tracer studies of substrate oxidation". Am. J. Clin. Nutr. 51 (2): 248–52. PMID 2106256.
^ ^a ^b ^c ^d Stryer L, Berg J, Tymoczko JL (2002). Biochemistry. San Francisco: W.H. Freeman. ISBN 0-7167-4684-0.
^ ^a ^b Jones RC, Buchanan BB, Gruissem W (2000). Biochemistry & molecular biology of plants (1st ed.). Rockville, Md: American Society of Plant Physiologists. ISBN 0-943088-39-9.
^ Johnson JD, Mehus JG, Tews K, Milavetz BI, Lambeth DO (October 1998). "Genetic evidence for the expression of ATP- and GTP-specific succinyl-CoA synthetases in multicellular eucaryotes". J. Biol. Chem. 273 (42): 27580–6. doi:10.1074/jbc.273.42.27580. PMID 9765291.
^ Barnes SJ, Weitzman PD (June 1986). "Organization of citric acid cycle enzymes into a multienzyme cluster". FEBS Lett. 201 (2): 267–70. doi:10.1016/0014-5793(86)80621-4. PMID 3086126.
^ ^a ^b Porter RK, Brand MD (September 1995). "Mitochondrial proton conductance and H+/O ratio are independent of electron transport rate in isolated hepatocytes". Biochem. J. 310 (2): 379–82. PMC 1135905. PMID 7654171.
^ Stryer L, Berg JM, Tymoczko JL (2002). "Section 18.6: The Regulation of Cellular Respiration Is Governed Primarily by the Need for ATP". Biochemistry. San Francisco: W.H. Freeman. ISBN 0-7167-4684-0.
^ Rich PR (December 2003). "The molecular machinery of Keilin's respiratory chain". Biochem. Soc. Trans. 31 (Pt 6): 1095–105. doi:10.1042/BST0311095. PMID 14641005.
^ Voet D, Voet JG (2004). Biochemistry (3rd ed.). New York: John Wiley & Sons, Inc. p. 615.
^ Ivannikov, M. et al. (2013). "Mitochondrial Free Ca²⁺ Levels and Their Effects on Energy Metabolism in Drosophila Motor Nerve Terminals". Biophys. J. 104 (11): 2353–2361. doi:10.1016/j.bpj.2013.03.064. PMC 3672877. PMID 23746507.
^ Denton RM, Randle PJ, Bridges BJ, Cooper RH, Kerbey AL, Pask HT, Severson DL, Stansbie D, Whitehouse S (October 1975). "Regulation of mammalian pyruvate dehydrogenase". Mol. Cell. Biochem. 9 (1): 27–53. doi:10.1007/BF01731731. PMID 171557.
^ Koivunen P, Hirsilä M, Remes AM, Hassinen IE, Kivirikko KI, Myllyharju J (February 2007). "Inhibition of hypoxia-inducible factor (HIF) hydroxylases by citric acid cycle intermediates: possible links between cell metabolism and stabilization of HIF". J. Biol. Chem. 282 (7): 4524–32. doi:10.1074/jbc.M610415200. PMID 17182618.
^ Halarnkar PP, Blomquist GJ (1989). "Comparative aspects of propionate metabolism". Comp. Biochem. Physiol., B 92 (2): 227–31. doi:10.1016/0305-0491(89)90270-8. PMID 2647392.

External links

An animation of the citric acid cycle at Smith College
Citric acid cycle variants at MetaCyc
Pathways connected to the citric acid cycle at Kyoto Encyclopedia of Genes and Genomes
Introduction at Khan Academy

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Related Pictures

★リンクテーブル★

リンク元	「クエン酸回路」「トリカルボン酸回路」
関連記事	「TCA」「TC」「T」「cycle」「cycling」

「クエン酸回路」

　　[★]

英: citric acid cycle
同: トリカルボン酸回路 tricarboxylic acid cycle TCAサイクル TCA cycle、クレブス回路 Krebs cycle

FB.317

ピルビン酸
↓　←　CoASH　＋　NAD+
↓　ピルビン酸デヒドロゲナーゼ
↓　→　CO2　＋　NADH
アセチルCoA　
↓　←　オキサロ酢酸　＋　H2O
↓　クエン酸シンターゼ
↓　→　CoASH
クエン酸　
↓　
↓　
↓　



CH3-CO-COOH ピルビン酸(3C)
CH3-CO-CoA アセチル-CoA(2C,０番目)
COOH-CH2-CO-COOH オキサロ酢酸(4C,８番目)
COOH-CH2-C(COOH)(OH)-CH2-COOH クエン酸(6C,１番目)
COOH-CH2-CH(COOH)-CH(OH)-COOH イソクエン酸(6C,２番目)
COOH-CH2-CH2-CO-COOH α-ケトグルタル酸(5C,３番目)

「オクイ アサコ 不倫」
オ・・・オキザロ酢酸 
ク・・・クエン酸
イ・・・イソクエン酸 
ア・・・α-ケトグルタル酸 （2-オキソグルタル酸）
サ・・・サクシニルCoA　(スクシニルCoA)
コ・・・コハク酸
不・・・フマル酸
倫・・・リンゴ酸

■物質の特徴
・コハク酸（succinic acid）
IUPAC　ブタン二酸 (butanedioic acid)
ジカルボン酸の一種。コハクの乾留により見つかる。
化学式: C4H6O4
示性式はHOOC-(CH2)2-COOH
分子量は118。融点185℃、沸点235℃、CAS登録番号は110-15-6。

クエン酸回路を構成する化合物のひとつで、コハク酸デヒドロゲナーゼによって酸化され、フマル酸となる。このときに使われる補酵素はFAD。

貝類に含まれるうま味物質でもある。うま味を感じさせる作用は、コハク酸ナトリウムの方が高い。pH調整剤や調味料として食品に用いられる他、メッキなどの工業用にも用いられる。また炭酸ガスを発泡する入浴剤の成分でもある。

・フマル酸
IUPAC命名法　(E)-2-ブテン二酸((E)-2-butenedioic acid)
ジカルボン酸。
示性式：HOOC-CH=HC-COOH(トランス型)、分子量116.07。幾何異性体にはマレイン酸がある。クエン酸回路を構成する物質の一つで、コハク酸とリンゴ酸の中間体にあたる。常温常圧で固体であり、水によく溶ける。CAS登録番号は110-17-8。

・リンゴ酸
IUPAC置換命名法：2-Hydroxybutanedioic acid
ヒドロキシ酸に分類されるカルボン酸。
リンゴから見つかった
化学式：C4H6O5、示性式：HOOC-CH(OH)-CH2-COOH
分子量は134。CAS登録番号は6915-15-7。
クエン酸回路を構成しており、リンゴ酸デヒドロゲナーゼによって酸化され、オキサロ酢酸となる。CAS登録番号はそれぞれL-リンゴ酸97-67-6 D-リンゴ酸636-61-3 DL-リンゴ酸617-48-1


・マロン酸
IUPAC プロパン二酸 (propandioic acid)
構造式HOOC-CH2-COOH　
ジカルボン酸の一種。常温常圧で無色の固体。分子量は104.1。
マロンの名称はギリシア語のりんごに由来する。酢酸マロン酸経路を構成する物質のひとつ。水などの極性溶媒によく溶ける。

マロン酸は構造がコハク酸 HOOC-(CH2)2-COOHによく似ているため、生物体内のクエン酸回路においてコハク酸デヒドロゲナーゼの活性部位に（誤って）結合してしまう。そのため本来の基質であるコハク酸の代謝を阻害し（競争阻害）、細胞呼吸を妨害する

・マレイン酸
のひとつ。
cis-butenedioic acid (cis-ブテン二酸)
鎖状不飽和ジカルボン酸
化学式：C4H4O4
示性式：C2H2(COOH)2(シス型)
分子量は116.1。室温で固体、融点は133℃。CAS登録番号は110-16-7
幾何異性体にはフマル酸(トランス型)IUPAC名はtrans-butenedioic acid (trans-ブテン二酸)がある。世界で初めて幾何異性体が発見された組。

加熱すると環状の酸無水物(無水マレイン酸)となる。これは、マレイン酸の2つのカルボキシル基が接近しているためである。このためフマル酸は一般には酸無水物を作らない。