NADH Dehydrogenase

NADH Dehydrogenase is a class of enzymes that play a key role in the process of cellular respiration and belongs to the oxidoreductase family. NADH Dehydrogenase can catalyze the oxidation of NADH and transfer electrons to other molecules. There are two main subtypes of this enzyme, namely proton transporting NADH-quinone oxidoreductase (such as complex I in mitochondria and NDH-1 in bacteria) and non-proton transporting NADH-quinone oxidoreductase (such as NDI, NDE in mitochondria and NDH-2 in bacteria). NADH dehydrogenase is in an upstream position in the electron transport chain, accepts electrons provided by NADH, and interacts with a variety of proteins. For example, in mammalian cells, AIFM1, as a type of NADH dehydrogenase, interacts with MIA40 and participates in the assembly and maintenance of mitochondrial respiratory chain complexes. Its main function is to participate in mitochondrial respiration. During the electron transfer process, it generates energy for cells by oxidizing NADH. It also plays an important role in regulating cell apoptosis. For example, some NADH dehydrogenases can produce pro-apoptotic fragments and trigger cell death. Mitochondrial NADH dehydrogenase deficiency is associated with a variety of mitochondrial diseases, such as mitochondrial encephalomyopathy, Parkinson's disease, and Huntington's disease. In cystic fibrosis, the activity and properties of NADH Dehydrogenase are altered, affecting the course of the disease. Type I NADH Dehydrogenase (NDH-1) is involved in inhibiting host macrophage apoptosis in Mycobacterium tuberculosis infection, affecting the virulence of the pathogen and the course of infection^[1]^[2]^[3]^[4]^[5]^[6].

References:

[1]. Heikal A, et al. Activation of type II NADH dehydrogenase by quinolinequinones mediates antitubercular cell death. J Antimicrob Chemother. 2016 Oct;71(10):2840-7. [Content Brief]

[2]. Herrmann JM, et al. Apoptosis inducing factor and mitochondrial NADH dehydrogenases: redox-controlled gear boxes to switch between mitochondrial biogenesis and cell death. Biol Chem. 2020 Aug 25;402(3):289-297. [Content Brief]

[3]. Weiss H, et al. The respiratory-chain NADH dehydrogenase (complex I) of mitochondria. Eur J Biochem. 1991 May 8;197(3):563-76. [Content Brief]

[4]. Shapiro B L, et al. Mitrochondrial NADH dehydrogenase in cystic fibrosis. Proceedings of the National Academy of Sciences, 1979, 76(6): 2979-2983.

[5]. Yagi T, et al. NADH dehydrogenases: from basic science to biomedicine. J Bioenerg Biomembr. 2001 Jun;33(3):233-42. [Content Brief]

[6]. Miller JL, et al. The type I NADH dehydrogenase of Mycobacterium tuberculosis counters phagosomal NOX2 activity to inhibit TNF-alpha-mediated host cell apoptosis. PLoS Pathog. 2010 Apr 22;6(4):e1000864. [Content Brief]

NADH Dehydrogenase Inhibitor (1)

NADH Dehydrogenase Related Products (1):

Cat. No.	Product Name	Effect	Purity	Chemical Structure

HY-W722277A

LCC-12 formate	Inhibitor
LCC-12 (formate) is a copper (II) chelator and a derivative of the biguanide metformin (HY-B0627). LCC-12 (formate) reduces its hydrogen peroxide-dependent oxidation of NADH to NAD+. LCC-12 (formate) reduces IL-1β, IL-2, IL-6, IL-8, and TNF-α levels, as well as JAK2, STAT2, and IL-1 receptor-associated kinase 4 (IRAK4) levels in primary human cytokine-activated monocyte-derived macrophages (MDMs). LCC-12 (formate) reduces the number of CD80+ and CD86+ cytokine-activated MDMs. LCC-12 LCC-12 (formate) improves survival in a mouse model of sepsis induced by LPS or cecal ligation and puncture.

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