NADH Dehydrogenase

A flavoprotein and iron sulfur-containing oxidoreductase that catalyzes the oxidation of NADH to NAD. In eukaryotes the enzyme can be found as a component of mitochondrial electron transport complex I. Under experimental conditions the enzyme can use CYTOCHROME C GROUP as the reducing cofactor. The enzyme was formerly listed as EC 1.6.2.1.

Also Known As:

Networked: 237 relevant articles (2 outcomes, 18 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Matsuno-Yagi, Akemi: 6 articles (03/2013 - 01/2006)
2.	Yagi, Takao: 6 articles (03/2013 - 01/2006)
3.	Seo, Byoung Boo: 5 articles (12/2009 - 01/2006)
4.	Yoshida, Masao: 4 articles (01/2014 - 03/2005)
5.	Matsunaga, Naomi: 4 articles (01/2014 - 03/2005)
6.	Kokaze, Akatsuki: 4 articles (01/2014 - 03/2005)
7.	Takashima, Yutaka: 4 articles (01/2014 - 03/2005)
8.	Ishikawa, Mamoru: 4 articles (01/2014 - 03/2005)
9.	Marella, Mathieu: 4 articles (12/2009 - 01/2006)
10.	Bai, Yidong: 3 articles (04/2011 - 05/2007)

Related Diseases

1.	Ischemia 08/01/2006 - "Prolonged ischemia-reperfusion produced a selective defect in complex I function distal to the NADH dehydrogenase component. " 01/01/1993 - "Furthermore, there is considerable evidence that the exogenous NADH-dehydrogenase of heart mitochondria is mainly responsible for functional changes of these organelles during ischemia/reperfusion." 12/01/1990 - "The results suggest that ischemia decreases the NADH-dehydrogenase activity of cardiac mitochondria." 01/01/1986 - "Our results, using autolysis in the rat heart as experimental model, indicate that the NADH dehydrogenase system was impaired relatively early during ischemia while transhydrogenation and NADPH dehydrogenation appeared to be relatively resistant." 04/13/1995 - "Our results show a redistribution of the electron flux with an increased rate of superoxide anion/hydrogen peroxide production at NADH dehydrogenase in mitochondria subjected to ischemia only. "
2.	Experimental Autoimmune Encephalomyelitis (Encephalomyelitis, Autoimmune Experimental) 10/01/2013 - "To address mitochondrial dysfunction that mediates irreversible visual loss and neurodegeneration of the optic nerve in the experimental autoimmune encephalomyelitis (EAE) animal model of multiple sclerosis (MS), mice sensitized for EAE were vitreally injected with self-complementary adenoassociated virus (scAAV) containing the NADH-dehydrogenase type-2 (NDI1) complex I gene that quickly expressed in mitochondria of almost all retinal ganglion cells (RGCs). " 01/23/1995 - "We measured the activities of five respiratory chain enzymes in brain macrophages/microglial cells from Lewis rats with experimental autoimmune encephalomyelitis (EAE) and found a significant reduction of the activity of nicotinamide adenine dinucleotide-dehydrogenase (NADH-DH), succinate cytochrome c reductase (SCCR) and succinate dehydrogenase (SDH) when compared with age-matched healthy control animals. "
3.	Neoplasms (Cancer) 09/01/2003 - "Here we investigated mitochondrial complex I and found that its NADH dehydrogenase activity and protein content were specifically decreased in oncocytomas, in stark contrast with the parallel decrease of all respiratory chain complexes in other, malignant, renal tumors. " 05/01/1980 - "In addition, we found that the mitochondria from the cancer cells exhibited reduced NADH-cytochrome c reductase activity. " 01/01/2015 - "In this study, we used quantitative proteomic analyses to compare a highly metastatic cancer cell line and a parental breast cancer cell line; and observed that NDUFB9, an accessory subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (complex I), was down-regulated in highly metastatic breast cancer cells. " 01/01/2015 - "Previous study showed that mitochondrial ND6 (mitND6) gene missense mutation resulted in NADH dehydrogenase deficiency and was associated with tumor metastasis in several mouse tumor cell lines. " 02/01/2010 - "To investigate the possible role of mitochondrial inherited polymorphisms in breast cancer development we analyzed the sequence of NADH-dehydrogenase genes in cancer samples and their corresponding normal tissues. "
4.	Anoxia (Hypoxia) 10/25/2005 - "In vitro, NO treatment and hypoxia caused a switch from transcription of type I to type II NADH dehydrogenase. " 06/01/2005 - "Left ventricle NADH-cytochrome-c reductase and cytochrome oxidase activities decreased by 36 and 12%, respectively, from 2 to 18 mo of age, but they were not affected by hypoxia. " 02/01/2004 - "In contrast, NADH-cytochrome c reductase and cytochrome oxidase activities were not affected by hypoxia. " 02/15/2013 - "Treatment with hypoxia mimetics CoCl(2) or incubation with 2% O(2) impaired mitochondria function as demonstrated by decreases in ATP production, NADH dehydrogenase activity, mitochondrial membrane potential, and reduced expression of mitochondria-related genes including NRF-1, PGC-1α, COX1 and SOD in 3T3-L1 adipocyte cells. " 02/01/2006 - "In this organism, nitrate respiration is performed by a mobilizable respiratory island that encodes a new type of respiratory NADH dehydrogenase as electron donor, a tetrameric membrane nitrate reductase as final electron acceptor, two nitrate/nitrite transporters and the transcription factors required for their expression in response to nitrate and anoxia."
5.	Leber Hereditary Optic Atrophy (Leber's Hereditary Optic Neuropathy) 11/01/1991 - "This study showed that there is decreased activity of complex I of the respiratory chain in muscle and that cerebral striatal lesions occur in Leber's hereditary optic neuropathy with the NADH-dehydrogenase 4 gene point mutation." 12/01/2013 - "Fifteen novel mutations in the mitochondrial NADH dehydrogenase subunit 1, 2, 3, 4, 4L, 5 and 6 genes from Iranian patients with Leber's hereditary optic neuropathy (LHON)." 05/01/2007 - "G11778A in the subunit ND4 gene of NADH dehydrogenase complex is the most common primary mutation found in Leber's hereditary optic neuropathy (LHON) patients. " 06/01/1991 - "Allelic mutations of the fourth subunit of NADH dehydrogenase are not pathogenetically important in 11778-negative Leber hereditary optic neuropathy." 06/01/1989 - "These mutations have occurred in genes coding for subunits of NADH dehydrogenase, suggesting that a defect of the respiratory chain complex I may cause Leber's disease."

Related Drugs and Biologics

1.	NAD (NADH)
2.	Electron Transport Complex IV (Cytochrome c Oxidase)
3.	Succinate Dehydrogenase (Fumarate Reductase)
4.	Enzymes
5.	Succinic Acid (Succinate)
6.	Succinate Cytochrome c Oxidoreductase
7.	Mitochondrial DNA (mtDNA)
8.	Adenosine Triphosphate (ATP)
9.	Cytochromes b (Cytochrome b)
10.	DNA (Deoxyribonucleic Acid)

Related Therapies and Procedures

1.	Transplantation (Transplant Recipients)
2.	Ovariectomy (Oophorectomy)
3.	Subcutaneous Injections