| Name | SOD1 |
|---|---|
| Synonyms | ALS; ALS 1; ALS1; IPOA; Indophenoloxidase A; SOD; SOD 1; SOD1… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 15850589 | Rizzardini M, Mangolini A, Lupi M, Ubezio P, Bendotti C, Cantoni L: Low levels of ALS-linked Cu/Zn superoxide dismutase increase the production of reactive species and cause mitochondrial damage and death in motor neuron-like cells. J Neurol Sci. 2005 May 15;232(1-2):95-103. Mutations of Cu/Zn superoxide dismutase (SOD1) are found in patients with familial amyotrophic lateral sclerosis (FALS). The mutant protein rendered G93ASOD1 cells more sensitive to mitochondrial dysfunction induced by stimuli that alter cellular free radical homeostasis, like serum withdrawal, depletion of by ethacrynic acid or rotenone-mediated inhibition of complex I of the mitochondrial electron transport chain. |
4(0,0,0,4) | Details |
| 16790527 | Aquilano K, Vigilanza P, Rotilio G, Ciriolo MR: Mitochondrial damage due to SOD1 deficiency in SH-SY5Y neuroblastoma cells: a rationale for the redundancy of SOD1. FASEB J. 2006 Aug;20(10):1683-5. Epub 2006 Jun 21. These conditions induced a high susceptibility of SOD1-depleted cells to treatment with the mitochondrial reactive species producing agent rotenone. |
13(0,0,1,8) | Details |
| 16624679 | Rizzardini M, Lupi M, Mangolini A, Babetto E, Ubezio P, Cantoni L: Neurodegeneration induced by complex I inhibition in a cellular model of familial amyotrophic lateral sclerosis. Brain Res Bull. 2006 Apr 28;69(4):465-74. Epub 2006 Mar 10. G93A Cu/Zn superoxide dismutase (SOD1), a human mutant SOD1 associated with familial amyotrophic lateral sclerosis, increased the toxicity of the mitochondrial toxin rotenone in the NSC-34 motoneuronal cell line. |
13(0,0,2,3) | Details |
| 16337891 | Li Q, Sato EF, Kira Y, Nishikawa M, Utsumi K, Inoue M: A possible cooperation of SOD1 and cytochrome c in mitochondria-dependent apoptosis. Free Radic Biol Med. 2006 Jan 1;40(1):173-81. Epub 2005 Oct 21. Although inhibitors of electron transport, such as rotenone, antimycin A, and KCN, also increased ROS generation, they failed to (i) oxidize the critical thiol groups in ANT, (ii) induce swelling, and (iii) release SOD1 and cytochrome c. |
10(0,0,0,10) | Details |
| 19174508 | Nguyen KT, Garcia-Chacon LE, Barrett JN, Barrett EF, David G: The Psi (m) depolarization that accompanies mitochondrial Ca2+ uptake is greater in mutant SOD1 than in wild-type mouse motor terminals. Proc Natl Acad Sci U S A. 2009 Feb 10;106(6):2007-11. Epub 2009 Jan 27. Stimulation-induced Psi (m) depolarization and elevation of cytosolic [Ca (2+)] both increased when complex I of the ETC was partially inhibited by low concentrations of rotenone (25-50 nmol/l). |
3(0,0,0,3) | Details |
| 10641721 | Sauer H, Dagdanova A, Hescheler J, Wartenberg M: Redox-regulation of intrinsic prion expression in multicellular prostate tumor spheroids. Free Radic Biol Med. 1999 Dec;27(11-12):1276-83. ROS generation was mediated by the mitochondrial respiratory chain and a oxidaselike enzyme, because carbonylcyanide-m-chlorophenylhydrazone (CCCP), rotenone, and diphenylene iodonium (DPI) significantly reduced ROS levels. The elevated ROS were correlated to an increased expression of PrPc, Cu/Zn superoxide dismutase (SOD-1), and catalase in small as compared with large spheroids. |
1(0,0,0,1) | Details |
| 16584562 | Zhao Z, Lange DJ, Voustianiouk A, MacGrogan D, Ho L, Suh J, Humala N, Thiyagarajan M, Wang J, Pasinetti GM: A ketogenic diet as a potential novel therapeutic intervention in amyotrophic lateral sclerosis. BMC Neurosci. 2006 Apr 3;7:29. DBH prevented rotenone mediated inhibition of mitochondrial complex I but not inhibition of complex II. RESULTS: SOD1-G93A transgenic ALS mice were fed a ketogenic diet (KD) based on known formulations for humans. |
1(0,0,0,1) | Details |
| 17663266 | Sharma CS, Sarkar S, Periyakaruppan A, Barr J, Wise K, Thomas R, Wilson BL, Ramesh GT: Single-walled carbon nanotubes induces oxidative stress in rat lung epithelial cells. J Nanosci Nanotechnol. 2007 Jul;7(7):2466-72. Use of rotenone, the inhibitor of mitochondrial function have no effect on ROS levels suggested that mitochondria is not involved in SWCNT induced ROS production. Studies carried out on the effect of SWCNT on superoxide dismutase (SOD-1 and SOD-2) levels in LE cells, indicates that these enzyme levels decreased by 24 hours. |
1(0,0,0,1) | Details |
| 19670830 | Mali Y, Zisapel N: A novel decoy that interrupts G93A-superoxide dismutase gain of interaction with malate dehydrogenase improves survival in an amyotrophic lateral sclerosis cell model. J Med Chem. 2009 Sep 10;52(17):5442-8. Human G93A-superoxide dismutase-1 (G93AhSOD1) mutation causes amyotrophic lateral sclerosis (ALS) in rodents and humans. A cell permeable 5-carboxytetramethylrhodamine derivative of the decoy peptide improved ATP content of motor neuron derived NSC-34 cells expressing G93AhSOD1 and enhanced cell survival under rotenone and low challenges. |
1(0,0,0,1) | Details |