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Nicotinamide adenine dinucleotide phosphate

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Nicotinamide adenine dinucleotide phosphate
Nicotinamide adenine dinucleotide phosphate
General
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Except where noted otherwise, data are given for
materials in their standard state (at 25 °C, 100 kPa)
Infobox disclaimer and references


Nicotinamide adenine dinucleotide phosphate, abbreviated NADPTemplate:+ or, in older notation, TPN (triphosphopyridine nucleotide), is a coenzyme used in anabolic reactions, such as lipid and nucleic acid synthesis, which require NADPH as a reducing agent.

NADPH is the reduced form of NADPTemplate:+. NADPTemplate:+ differs from [[NAD+|NADTemplate:+]] in the presence of an additional phosphate group on the 2' position of the ribose ring that carries the adenine moiety.

In plantsEdit

In photosynthetic organisms, NADPH is produced by [[ferredoxin-NADP+ reductase|ferredoxin-NADPTemplate:+ reductase]] in the last step of the electron chain of the light reactions of photosynthesis. It is used as reducing power for the biosynthetic reactions in the Calvin cycle to assimilate carbon dioxide.

In animalsEdit

SynthesisEdit

The oxidative phase of the pentose phosphate pathway is a major source of NADPH in cells,[1] and in cells without mitochondria (such as red blood cells), it is the only source.[2]

However there are several other lesser-known mechanisms of generating NADPH, all of which depend on the presence of mitochondria. The key enzymes in these processes are: NADP-linked malic enzyme, NADP-linked isocitrate dehydrogenase, and nicotinamide nucleotide transhydrogenase.[3] The isocitrate dehydrogenase mechanism appears to be the major source of NADPH in fat and possibly also liver cells.[1] Also in mitochondria, NADH kinase produces NADPH and ADP using NADH and ATP as substrate.

Biological functionsEdit

NADPH provides the reducing equivalents for biosynthetic reactions and the oxidation-reduction involved in protecting against the toxicity of ROS (reactive oxygen species), allowing the regeneration of GSH (reduced glutathione).[4] NADPH is also used for anabolic pathways, such as lipid synthesis, cholesterol synthesis, and fatty acid chain elongation.

The NADPH system is also responsible for generating free radicals in immune cells. These radicals are used to destroy pathogens in a process termed the respiratory burst.[5] It is the source of reducing equivalents for cytochrome P450 hydroxylation of aromatic compounds, steroids, alcohols, and drugs.

Ball-and-stick models of NADP+ and NADPH
NADP+  
NADPH 

See alsoEdit

Template:Enzyme cofactors

ReferencesEdit

  1. 1.0 1.1 Palmer, Michael 10.4.3 Supply of NADPH for fatty acid synthesis. Metabolism Course Notes. URL accessed on 6 April 2012.
  2. Clarke, Jeremy M. Berg, John L. Tymoczko, Lubert Stryer ; web content by Neil D. (2002). Biochemistry, 5th, New York: W. H. Freeman and Co..
  3. Hanukoglu, I, Rapoport, R (1995 Feb-May). Routes and regulation of NADPH production in steroidogenic mitochondria. Endocrine research 21 (1–2): 231–41.
  4. Rush, Glenn F., Gorski, Joel R.; Ripple, Mary G.; Sowinski, Janice; Bugelski, Peter; Hewitt, William R. (NaN undefined NaN). Organic hydroperoxide-induced lipid peroxidation and cell death in isolated hepatocytes. Toxicology and Applied Pharmacology 78 (3): 473–483.
  5. (2008). The association of elevated reactive oxygen species levels from neutrophils with low-grade inflammation in the elderly. Immun Ageing 5: 13.
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