2019
DOI: 10.3390/nu11030504
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Abstract: The reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) protects against redox stress by providing reducing equivalents to antioxidants such as glutathione and thioredoxin. NADPH levels decline with aging in several tissues, but whether this is a major driving force for the aging process has not been well established. Global or neural overexpression of several cytoplasmic enzymes that synthesize NADPH have been shown to extend lifespan in model organisms such as Drosophila suggesting a positive… Show more

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Cited by 112 publications
(83 citation statements)
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References 303 publications
(372 reference statements)
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“…proposed pathway, it is not yet clear how NADPH production corresponds to actual activity of 8 the cycle-given that metabolites can enter and exit the cycle at multiple points depending on 9 nutritional conditions-nor how the cellular compartmentalization of NADPH production 10 contributes to the transmission of the NADPH status to the ER. The NADPH/NADP+ ratio is 11 regulated by nutritional state, exercise, diet, and circadian rhythms (Bradshaw, 2019;Ying, 12 2008 thioredoxin reductase in the cytosol, and that cytosolic glutathione becomes more oxidized 26 because it must compensate in the reduction of reactive oxygen species for the shortage of 1 reduced thioredoxin. An alternate possibility is that cytosolic NADPH manipulation ultimately 2 affects matrix NADPH status through metabolite shuttles, which are used to convey reducing 3 equivalents across the mitochondrial membranes by coupling mitochondrial redox reactions with 4 their cytosolic counterparts (for example, using the transport of citrate to couple IDH2 and IDH1) 5 .…”
Section: Tca Cycle Activity Links Oxidative Metabolism To Er Homeostamentioning
confidence: 99%
“…proposed pathway, it is not yet clear how NADPH production corresponds to actual activity of 8 the cycle-given that metabolites can enter and exit the cycle at multiple points depending on 9 nutritional conditions-nor how the cellular compartmentalization of NADPH production 10 contributes to the transmission of the NADPH status to the ER. The NADPH/NADP+ ratio is 11 regulated by nutritional state, exercise, diet, and circadian rhythms (Bradshaw, 2019;Ying, 12 2008 thioredoxin reductase in the cytosol, and that cytosolic glutathione becomes more oxidized 26 because it must compensate in the reduction of reactive oxygen species for the shortage of 1 reduced thioredoxin. An alternate possibility is that cytosolic NADPH manipulation ultimately 2 affects matrix NADPH status through metabolite shuttles, which are used to convey reducing 3 equivalents across the mitochondrial membranes by coupling mitochondrial redox reactions with 4 their cytosolic counterparts (for example, using the transport of citrate to couple IDH2 and IDH1) 5 .…”
Section: Tca Cycle Activity Links Oxidative Metabolism To Er Homeostamentioning
confidence: 99%
“…Particularly important for mitochondrial fitness is the role of mGSH in the regulation of ATP production. Critical protein sulfhydryl redox states depend on mGSH levels, which in turn influence both NADH and FADH2 generation and the electron flow through the ETC [ 24 , 143 , 144 ]. mGSH decreases up to 50% with age [ 145 , 146 ], being more marked in male than female mice in many tissues.…”
Section: Mgsh In Pathological Settingsmentioning
confidence: 99%
“…Reductive stress is induced by excessive levels of reductive stressors that results from an elevation in GSH/GSSG ratio, NAD + /NADH, NADP + /NADPH and/or or overexpression of antioxidative enzymatic systems such as the GSH system, catalase, thioredoxin-peroxiredoxin (TRX-PRDX) system, α-ketoglutarate dehydrogenase (GPDH), and glycerol phosphate dehydrogenase [ 166 , 167 ]. The reductive stressors deplete reactive oxidative species and are harmful as oxidative stressors and implicated in pathological processes in AD, PD, and sporadic motor neuron disease, among others [ 168 ].…”
Section: Reductive Stressmentioning
confidence: 99%