The Unified Theory of Aging-Nitric Oxide
ATP Energy Production is Linked to Nitric Oxide- The Importance for Sexual and Exercise
Nathan Bryan, MD
The reproduction and survival of the cell is dependent on efficient mitochondrial production of ATP energy. The efficiency of the mitochondria equates to the state of health and rate of aging. In fact, it has been asserted that all existing theories of aging are really secondary to one primary unifying explanation: a decrease in cellular ATP energy production in the mitochondria. Currently, increasing environmental pollution and disconcerting dietary / lifestyle influences are negatively impacting the mitochondria. But how can physicians positively and immediately influence these vital organelles that control their patients’ well-being? One primary way is to restore optimal levels of nitric oxide (N- 0). Nitric oxide is a critical cell signaling molecule that regulates mitochondrial biogenesis as well as mitochondrial energy production.
Inducible nitric oxide synthase-derived nitric oxide in gene regulation, cell death and cell survival
Author links open overlay panelKlaus-DietrichKrönckeKarinFehselChristophSuschekVictoriaKolb-Bachofen
https://doi.org/10.1016/S1567-5769(01)00087-XGet rights and content
Studies from many laboratories have demonstrated the complex role of NO in inflammatory processes. Prolonged exposure to NO shifts the cellular redox potential to a more oxidized state and this is critically regulated by intracellular levels of reduced glutathione. NO-mediated stress will alter gene expression patterns, and the number of genes known to be involved is steadily increasing. Indeed, due to its S-nitrosating activity in the presence of oxygen, NO can modify the activity of transcription factors containing zinc finger motifs or cysteines within the DNA-binding domain. In addition, we are faced with not only NO acting as a powerful inducer of apoptosis or of necrosis in some cells, but also representing an equally powerful protection from cell death in many instances. Some of these apparent discrepancies may be explained by different capacities of cells to cope with the stress of NO exposure. Here, we review our findings on the complex impact of NO on transcriptional regulation of genes, cell death and cell survival. These NO-mediated actions will contribute to a better understanding of the impact of inducible nitric oxide synthase (iNOS) enzyme activity during inflammatory reactions.
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BSO, l-buthionine-[S,R]-sulfoximBCNU, 1,3-bis(2-chloroethyl)-1-nitrosoureaDETA/NO, ((Z-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolateEC, endothelial cellsGR, glutathione reductaseGSH, reduced glutathioneGSNO, S-nitrosoglutathioneGSSG, oxidized glutathioneγGCS, γ-glutamylcysteine synthetaseHUDEC, human dermal endothelial cellsiNOS, inducible nitric oxide synthasePARP, poly(ADP-ribose) polymeraseROI, reactive oxygen intermediatesRXR, retinoic X receptorSNOC, S-nitrosocysteineSNAP, S-nitroso-N-acetyl-penicillamineVDR, vitamin D3 receptorVDRE, vitamin D3 responsive element
Inducible nitric oxide synthase-derived nitric oxide in gene regulation, cell death and cell survival - ScienceDirect https://www.sciencedirect.com/science/article/pii/S156757690100087X