Linsidomine: Difference between revisions
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==Overview== | ==Overview== | ||
'''Linsidomine''' ('''3-morpholinosydnonimine''' or '''SIN-1'''<ref name="Wen-2005">{{Cite journal | last1 = Wen | first1 = TC. | last2 = Rogido | first2 = MR. | last3 = Moore | first3 = JE. | last4 = Genetta | first4 = T. | last5 = Peng | first5 = H. | last6 = Sola | first6 = A. | title = Cardiotrophin-1 protects cortical neuronal cells against free radical-induced injuries in vitro. | journal = Neurosci Lett | volume = 387 | issue = 1 | pages = 38–42 |date=Oct 2005 | doi = 10.1016/j.neulet.2005.07.018 | PMID = 16084018 }}</ref>) is a [[vasodilator]]. It is a metabolite of the antianginal drug [[molsidomine]] and acts by releasing [[Nitric oxide|NO]] from the endothelial cells nonenzymatically. It also hyperpolarizes the cell membrane through influencing the sodium-potassium pump and thereby rendering it less responsive to adrenergic stimulation. Linsidomine injection at a dose of 1 mg produces usable erection | '''Linsidomine''' ('''3-morpholinosydnonimine''' or '''SIN-1'''<ref name="Wen-2005">{{Cite journal | last1 = Wen | first1 = TC. | last2 = Rogido | first2 = MR. | last3 = Moore | first3 = JE. | last4 = Genetta | first4 = T. | last5 = Peng | first5 = H. | last6 = Sola | first6 = A. | title = Cardiotrophin-1 protects cortical neuronal cells against free radical-induced injuries in vitro. | journal = Neurosci Lett | volume = 387 | issue = 1 | pages = 38–42 |date=Oct 2005 | doi = 10.1016/j.neulet.2005.07.018 | PMID = 16084018 }}</ref>) is a [[vasodilator]]. It is a metabolite of the antianginal drug [[molsidomine]] and acts by releasing [[Nitric oxide|NO]] from the endothelial cells nonenzymatically. It also hyperpolarizes the cell membrane through influencing the sodium-potassium pump and thereby rendering it less responsive to adrenergic stimulation. Linsidomine injection at a dose of 1 mg produces usable erection in about 70% of patients and full erection in up to 50% of patients. Linsidomine does not appear to be associated with priapism. | ||
Linsidomine is neurotoxic and promotes [[oxidative stress]] on neurons.<ref name="Wallace-2006">{{Cite journal | last1 = Wallace | first1 = DR. | last2 = Dodson | first2 = S. | last3 = Nath | first3 = A. | last4 = Booze | first4 = RM. | title = Estrogen attenuates gp120- and tat1-72-induced oxidative stress and prevents loss of dopamine transporter function. | journal = Synapse | volume = 59 | issue = 1 | pages = 51–60 |date=Jan 2006 | doi = 10.1002/syn.20214 | PMID = 16237680 }}</ref> Linsidomine is a [[peroxynitrite]]-generating compound involved in the pathogenesis of [[neurodegenerative diseases]].<ref name="Jang-2004">{{Cite journal | last1 = Jang | first1 = JH. | last2 = Aruoma | first2 = OI. | last3 = Jen | first3 = LS. | last4 = Chung | first4 = HY. | last5 = Surh | first5 = YJ. | title = Ergothioneine rescues PC12 cells from beta-amyloid-induced apoptotic death. | journal = Free Radic Biol Med | volume = 36 | issue = 3 | pages = 288–99 |date=Feb 2004 | doi = 10.1016/j.freeradbiomed.2003.11.005 | PMID = 15036348 }}</ref> | Linsidomine is neurotoxic and promotes [[oxidative stress]] on neurons.<ref name="Wallace-2006">{{Cite journal | last1 = Wallace | first1 = DR. | last2 = Dodson | first2 = S. | last3 = Nath | first3 = A. | last4 = Booze | first4 = RM. | title = Estrogen attenuates gp120- and tat1-72-induced oxidative stress and prevents loss of dopamine transporter function. | journal = Synapse | volume = 59 | issue = 1 | pages = 51–60 |date=Jan 2006 | doi = 10.1002/syn.20214 | PMID = 16237680 }}</ref> Linsidomine is a [[peroxynitrite]]-generating compound involved in the pathogenesis of [[neurodegenerative diseases]].<ref name="Jang-2004">{{Cite journal | last1 = Jang | first1 = JH. | last2 = Aruoma | first2 = OI. | last3 = Jen | first3 = LS. | last4 = Chung | first4 = HY. | last5 = Surh | first5 = YJ. | title = Ergothioneine rescues PC12 cells from beta-amyloid-induced apoptotic death. | journal = Free Radic Biol Med | volume = 36 | issue = 3 | pages = 288–99 |date=Feb 2004 | doi = 10.1016/j.freeradbiomed.2003.11.005 | PMID = 15036348 }}</ref> | ||
Revision as of 21:40, 24 July 2014
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| E number | {{#property:P628}} |
| ECHA InfoCard | {{#property:P2566}}Lua error in Module:EditAtWikidata at line 36: attempt to index field 'wikibase' (a nil value). |
| Chemical and physical data | |
| Formula | C6H10N4O2 |
| Molar mass | 170.17 g/mol |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Linsidomine (3-morpholinosydnonimine or SIN-1[1]) is a vasodilator. It is a metabolite of the antianginal drug molsidomine and acts by releasing NO from the endothelial cells nonenzymatically. It also hyperpolarizes the cell membrane through influencing the sodium-potassium pump and thereby rendering it less responsive to adrenergic stimulation. Linsidomine injection at a dose of 1 mg produces usable erection in about 70% of patients and full erection in up to 50% of patients. Linsidomine does not appear to be associated with priapism.
Linsidomine is neurotoxic and promotes oxidative stress on neurons.[2] Linsidomine is a peroxynitrite-generating compound involved in the pathogenesis of neurodegenerative diseases.[3]
References
- ↑ Wen, TC.; Rogido, MR.; Moore, JE.; Genetta, T.; Peng, H.; Sola, A. (Oct 2005). "Cardiotrophin-1 protects cortical neuronal cells against free radical-induced injuries in vitro". Neurosci Lett. 387 (1): 38–42. doi:10.1016/j.neulet.2005.07.018. PMID 16084018.
- ↑ Wallace, DR.; Dodson, S.; Nath, A.; Booze, RM. (Jan 2006). "Estrogen attenuates gp120- and tat1-72-induced oxidative stress and prevents loss of dopamine transporter function". Synapse. 59 (1): 51–60. doi:10.1002/syn.20214. PMID 16237680.
- ↑ Jang, JH.; Aruoma, OI.; Jen, LS.; Chung, HY.; Surh, YJ. (Feb 2004). "Ergothioneine rescues PC12 cells from beta-amyloid-induced apoptotic death". Free Radic Biol Med. 36 (3): 288–99. doi:10.1016/j.freeradbiomed.2003.11.005. PMID 15036348.
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