Post-Translational Oxidative Modifications of Mitochondrial Complex I (NADH: Ubiquinone Oxidoreductase): Implications for Pathogenesis and Therapeutics in Human Diseases

2017 ◽  
Vol 60 (s1) ◽  
pp. S69-S86 ◽  
Author(s):  
M.M. Srinivas Bharath
Keyword(s):  
Complex I ◽  
Human Diseases ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Ubiquinone Oxidoreductase ◽  
Nadh Ubiquinone Oxidoreductase ◽  
Oxidative Modifications

Dynamic Function of the Alkyl Spacer of Acetogenins in Their Inhibitory Action with Mitochondrial Complex I (NADH-Ubiquinone Oxidoreductase)†

Biochemistry ◽  
2005 ◽  
Vol 44 (45) ◽  
pp. 14898-14906 ◽  
Author(s):  
Masato Abe ◽  
Masatoshi Murai ◽  
Naoya Ichimaru ◽  
Atsushi Kenmochi ◽  
Takehiko Yoshida ◽  
...  
Keyword(s):  
Complex I ◽  
Inhibitory Action ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Ubiquinone Oxidoreductase ◽  
Nadh Ubiquinone Oxidoreductase ◽  
Dynamic Function

Incorporation of NADH-ubiquinone Oxidoreductase (Mitochondrial Complex I) into Lipid Nanodiscs

2012 ◽  
Vol 18 (S2) ◽  
pp. 88-89
Author(s):  
D.J. Fowler ◽  
T. Ruiz ◽  
M. Radermacher ◽  
S.G. Sligar ◽  
V. Zickermann ◽  
...  
Keyword(s):  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Ubiquinone Oxidoreductase ◽  
Nadh Ubiquinone Oxidoreductase ◽  
Lipid Nanodiscs

Extended abstract of a paper presented at Microscopy and Microanalysis 2012 in Phoenix, Arizona, USA, July 29 – August 2, 2012.

scholarly journals Roles of Pyruvate, NADH, and Mitochondrial Complex I in Redox Balance and Imbalance inβCell Function and Dysfunction

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Xiaoting Luo ◽  
Rongrong Li ◽  
Liang-Jun Yan
Keyword(s):  
Insulin Secretion ◽  
Metabolic Pathways ◽  
Complex I ◽  
Redox Balance ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Glucose Levels ◽  
Cell Dysfunction ◽  
Chronic Hyperglycemia ◽  
Nadh Ubiquinone Oxidoreductase

Pancreaticβcells not only use glucose as an energy source, but also sense blood glucose levels for insulin secretion. While pyruvate and NADH metabolic pathways are known to be involved in regulating insulin secretion in response to glucose stimulation, the roles of many other components along the metabolic pathways remain poorly understood. Such is the case for mitochondrial complex I (NADH/ubiquinone oxidoreductase). It is known that normal complex I function is absolutely required for episodic insulin secretion after a meal, but the role of complex I inβcells in the diabetic pancreas remains to be investigated. In this paper, we review the roles of pyruvate, NADH, and complex I in insulin secretion and hypothesize that complex I plays a crucial role in the pathogenesis ofβcell dysfunction in the diabetic pancreas. This hypothesis is based on the establishment that chronic hyperglycemia overloads complex I with NADH leading to enhanced complex I production of reactive oxygen species. As nearly all metabolic pathways are impaired in diabetes, understanding how complex I in theβcells copes with elevated levels of NADH in the diabetic pancreas may provide potential therapeutic strategies for diabetes.

scholarly journals Shared evolutionary footprints suggest mitochondrial oxidative damage underlies multiple complex I losses in fungi

Open Biology ◽  
2021 ◽  
Vol 11 (4) ◽  
Author(s):  
Miquel Àngel Schikora-Tamarit ◽  
Marina Marcet-Houben ◽  
Jozef Nosek ◽  
Toni Gabaldón
Keyword(s):  
Complex I ◽  
Fungal Species ◽  
Mitochondrial Complex ◽  
Compensatory Mechanisms ◽  
Genomic Changes ◽  
Ubiquinone Oxidoreductase ◽  
Independent Events ◽  
Nadh Ubiquinone Oxidoreductase ◽  
Mitochondrial Oxidative Damage ◽  
Evolutionary Paths

Oxidative phosphorylation is among the most conserved mitochondrial pathways. However, one of the cornerstones of this pathway, the multi-protein complex NADH : ubiquinone oxidoreductase (complex I) has been lost multiple independent times in diverse eukaryotic lineages. The causes and consequences of these convergent losses remain poorly understood. Here, we used a comparative genomics approach to reconstruct evolutionary paths leading to complex I loss and infer possible evolutionary scenarios. By mining available mitochondrial and nuclear genomes, we identified eight independent events of mitochondrial complex I loss across eukaryotes, of which six occurred in fungal lineages. We focused on three recent loss events that affect closely related fungal species, and inferred genomic changes convergently associated with complex I loss. Based on these results, we predict novel complex I functional partners and relate the loss of complex I with the presence of increased mitochondrial antioxidants, higher fermentative capabilities, duplications of alternative dehydrogenases, loss of alternative oxidases and adaptation to antifungal compounds. To explain these findings, we hypothesize that a combination of previously acquired compensatory mechanisms and exposure to environmental triggers of oxidative stress (such as hypoxia and/or toxic chemicals) induced complex I loss in fungi.

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