穀胱甘肽二硫化物

穀胱甘肽二硫化物
	系統名; (2S,2′S)-5,5′-(Disulfanediylbis{(2R)-3-[(carboxymethyl)amino]-3-oxopropane-1,2-diyl})bis(2-amino-5-oxopentanoic acid)
識別
縮寫	GSSG
CAS號	27025-41-8
PubChem	65359; 11215652
ChemSpider	58835
SMILES	C(CC(=O)N[C@@H](CSSC[C@@H](C(=O)NCC(=O)O)NC(=O)CC[C@@H](C(=O)O)N)C(=O)NCC(=O)O)[C@@H](C(=O)O)N;
InChI	1/C20H32N6O12S2/c21-9(19(35)36)1-3-13(27)25-11(17(33)23-5-15(29)30)7-39-40-8-12(18(34)24-6-16(31)32)26-14(28)4-2-10(22)20(37)38/h9-12H,1-8,21-22H2,(H,23,33)(H,24,34)(H,25,27)(H,26,28)(H,29,30)(H,31,32)(H,35,36)(H,37,38)/t9-,10-,11-,12-/m0/s1;
InChIKey	YPZRWBKMTBYPTK-BJDJZHNGBD
KEGG	C00127
IUPHAR配體	6835
性質
化學式	C20H32N6O12S2
摩爾質量	612.63 g·mol−1
	若非註明，所有數據均出自標準狀態（25 ℃，100 kPa）下。

穀胱甘肽二硫化物（英語：Glutathione disulfide）縮寫:（GSSG）是由兩個穀胱甘肽分子生成的二硫化物。^[1] 在活細胞中，穀胱甘肽二硫化物在輔酶的還原等價物作用下還原成兩分子穀胱甘肽。 NADPH的還原當量還原成兩分子穀胱甘肽。該反應由酶穀胱甘肽還原酶催化。^[2]

抗氧化酶，如穀胱甘肽過氧化物酶和過氧化物還原酶，在還原過氧化氫(H₂O₂)和有機過氧化氫(ROOH)等過氧化物時生成穀胱甘肽二硫化物^[3]

2 GSH + ROOH → GSSG + ROH + H₂O

其他酶，如穀胱甘肽，通過與蛋白質二硫鍵或其他低分子質量化合物（如輔酶A二硫化物或脫氫抗壞血酸）進行硫醇-二硫化物交換，生成穀胱甘肽二硫化物。^[4]

2 GSH + R-S-S-R → GSSG + 2 RSH

因此，GSH:GSSG 比率是細胞健康的一個重要生物指標，比率越高，表明生物體內的氧化壓力越小。較低的比率甚至可能預示着神經退行性疾病，如帕金森病和阿爾茨海默病。^[5]

神經調控[編輯]

研究發現，GSSG 與穀胱甘肽和S-亞硝基穀胱甘肽（GSNO）可與NMDA和AMPA 受體的穀氨酸識別位點結合（通過其γ-穀氨酰基），可能是內源性神經調控。^[6]^[7]在毫摩爾濃度下，它們還可能調節 NMDA 受體複合物的氧化還原狀態。^[7]

參見[編輯]

參考文獻[編輯]

^ Meister A, Anderson ME. Glutathione. Annual Review of Biochemistry. 1983, 52: 711–60. PMID 6137189. doi:10.1146/annurev.bi.52.070183.003431.
^ Deneke SM, Fanburg BL. Regulation of cellular glutathione. The American Journal of Physiology. 1989, 257 (4 Pt 1): L163–73 [2024-04-05]. PMID 2572174. doi:10.1152/ajplung.1989.257.4.L163. （原始內容存檔於2020-06-10）.
^ Meister A. Glutathione metabolism and its selective modification. The Journal of Biological Chemistry. 1988, 263 (33): 17205–8 [2024-04-05]. PMID 3053703. doi:10.1016/S0021-9258(19)77815-6 . （原始內容存檔於2020-06-10）.
^ Holmgren A, Johansson C, Berndt C, Lönn ME, Hudemann C, Lillig CH. Thiol redox control via thioredoxin and glutaredoxin systems. Biochem. Soc. Trans. December 2005, 33 (Pt 6): 1375–7. PMID 16246122. doi:10.1042/BST20051375.
^ Owen, Joshua B.; Butterfield, D. Allan. Measurement of oxidized/reduced glutathione ratio. Bross, Peter; Gregersen, Niels (編). Protein Misfolding and Cellular Stress in Disease and Aging. Methods in Molecular Biology 648. 2010: 269–77. ISBN 978-1-60761-755-6. PMID 20700719. doi:10.1007/978-1-60761-756-3_18.
^ Steullet P, Neijt HC, Cuénod M, Do KQ. Synaptic plasticity impairment and hypofunction of NMDA receptors induced by glutathione deficit: relevance to schizophrenia. Neuroscience. 2006, 137 (3): 807–19. PMID 16330153. S2CID 1417873. doi:10.1016/j.neuroscience.2005.10.014.
^ ^7.0 ^7.1 Varga V, Jenei Z, Janáky R, Saransaari P, Oja SS. Glutathione is an endogenous ligand of rat brain N-methyl-D-aspartate (NMDA) and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors. Neurochemical Research. 1997, 22 (9): 1165–71. PMID 9251108. S2CID 24024090. doi:10.1023/A:1027377605054.

[MeisterB-1] Meister A, Anderson ME. Glutathione. Annual Review of Biochemistry. 1983, 52: 711–60. PMID 6137189. doi:10.1146/annurev.bi.52.070183.003431.

[2] Deneke SM, Fanburg BL. Regulation of cellular glutathione. The American Journal of Physiology. 1989, 257 (4 Pt 1): L163–73 [2024-04-05]. PMID 2572174. doi:10.1152/ajplung.1989.257.4.L163. （原始內容存檔於2020-06-10）.

[3] Meister A. Glutathione metabolism and its selective modification. The Journal of Biological Chemistry. 1988, 263 (33): 17205–8 [2024-04-05]. PMID 3053703. doi:10.1016/S0021-9258(19)77815-6 . （原始內容存檔於2020-06-10）.

[4] Holmgren A, Johansson C, Berndt C, Lönn ME, Hudemann C, Lillig CH. Thiol redox control via thioredoxin and glutaredoxin systems. Biochem. Soc. Trans. December 2005, 33 (Pt 6): 1375–7. PMID 16246122. doi:10.1042/BST20051375.

[5] Owen, Joshua B.; Butterfield, D. Allan. Measurement of oxidized/reduced glutathione ratio. Bross, Peter; Gregersen, Niels (編). Protein Misfolding and Cellular Stress in Disease and Aging. Methods in Molecular Biology 648. 2010: 269–77. ISBN 978-1-60761-755-6. PMID 20700719. doi:10.1007/978-1-60761-756-3_18.

[SteulletNeijt2006-6] Steullet P, Neijt HC, Cuénod M, Do KQ. Synaptic plasticity impairment and hypofunction of NMDA receptors induced by glutathione deficit: relevance to schizophrenia. Neuroscience. 2006, 137 (3): 807–19. PMID 16330153. S2CID 1417873. doi:10.1016/j.neuroscience.2005.10.014.

[VargaJenei1997-7] 7.0 ^7.1 Varga V, Jenei Z, Janáky R, Saransaari P, Oja SS. Glutathione is an endogenous ligand of rat brain N-methyl-D-aspartate (NMDA) and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors. Neurochemical Research. 1997, 22 (9): 1165–71. PMID 9251108. S2CID 24024090. doi:10.1023/A:1027377605054.

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