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The Beneficial Effect of Omega-3 PUFA and L-Arginine on Endothelial Nitric Oxide (NO) Bioavailability
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
NO has a key role in kidney function. It regulates renal haemodynamics, maintains perfusion of the middle (medullary) part of the kidney, mediates pressure-natriuresis (i.e., excretion of salt), inhibits tubular sodium reabsorption and modulates renal sympathetic neural activity. Its principal effect is to promote natriuresis and diuresis. Deficient renal NO synthesis is implicated in the pathogenesis of hypertension. All three isoforms of nitric oxide synthase (NOS)—namely, neuronal NOS (nNOS or NOS1), inducible NOS (iNOS or NOS2) and endothelial NOS (eNOS or NOS3)—are reported to contribute to NO synthesis in the kidney. (44)
Free Radicals and Antioxidants
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
L-arginine (L-arg), is the main precursor of nitric oxide (NO), an endogenous messenger molecule involved in a variety of endothelium-mediated physiological effects in the nervous, immune, and cardiovascular systems (88–89). L-arginine is metabolized by two major pathways under the action of two specific enzymes: nitric oxide synthase and arginase. The nitric oxide synthase (NOS) pathway converts L-arg to NO and L-citrulline by three distinct isoforms of this enzyme: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS) (26–29, 88–89). The arginase pathway catalyzes the hydrolysis of L-arg to urea and ornithine in the liver through the urea cycle with the genesis of different polyamines (putrescine, spermidine and spermine). Briefly, L-arg plays a central role in the biosynthesis of nitric oxide, creatinine, agmatine, polyamines, proline, glutamate, and so on (26–27, 88–89). Most tissues in the body must be supplied with adequate intracellular levels of L-arg from circulation for their good function. All animal and vegetable proteins from the diet can be catabolized by the body into L-amino acids, of which L-arg. L-arginine is found abundantly in meat, milk, seafood, poultry, egg, soybeans, nuts, seeds, and more (88). In contrast, cereals are comparatively devoid of L-arginine, with only 3–4% of their low protein content being L-arginine (88). About 5 g of L-arginine is ingested each day in a normal Western diet (88).
Molecular Regulation of NO Synthase in the Heart
Published in Malcolm J. Lewis, Ajay M. Shah, Endothelial Modulation of Cardiac Function, 2020
Jean-Luc Balligand, Thomas W. Smith
NOS1 refers to the constitutive isoform originally described in rat neural cells. The human homologue spans 150 kb of DNA (Hall et al., 1994), and is located on human chromosome 12. The mRNA is encoded by 29 exons and translated into a protein of approximately 160 kDa. NOS1 protein is constitutively expressed in a variety of neurons and epithelial cells, as well as in human and rat skeletal muscle (Schmidt et al., 1992; Asano et al., 1994; Nakane et al., 1993; Kobzik et al., 1994).
Identification of reversible and druggable pathways to improve beta-cell function and survival in Type 2 diabetes
Published in Islets, 2023
Smithamol Sithara, Tamsyn Crowley, Ken Walder, Kathryn Aston-Mourney
Lastly, our study showed the NOS1 pathway was significantly upregulated with HG and successfully reversed with the drug treatment. NOS1 (also known as nNOS) has previously shown to have important role in normal β-cell function.70 Inhibition of NOS1 has shown to increase ER stress and activate JNK, therefore activation of NOS could protect β-cells from stress and apoptosis induced by glucolipotoxicity.65 Hence, upregulation of ‘NOS1 pathway’ with HG in our study could represent an adaptive response to glucotoxicity. This is supported by a previous study that demonstrated that NOS1 activation in glucolipotoxic condition is an adaptive response to protect β-cells from stress and apoptosis.65 Hence, modulation of the NOS1 pathway could possibly be beneficial for restoring β-cell viability/health.
Neuroprotective effects of natural compounds on neurotoxin-induced oxidative stress and cell apoptosis
Published in Nutritional Neuroscience, 2022
Bo Chen, Jingjing Zhao, Rui Zhang, Lingling Zhang, Qian Zhang, Hao Yang, Jing An
RNS refer to NO and molecules derived from NO, such as ONOO− and NO•. RNS are important factors for the generation of oxidative stress. In mitochondria, NO is produced from L-arginine in a catalytic reaction mediated by NOS, which has three isoforms: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). NO is implicated in many important processes in the CNS, including the regulation of synaptic plasticity, sleep-wake cycle, neurosecretion, and cerebral blood flow. In general, physiological amounts of NO are neuroprotective, while higher concentrations are obviously neurotoxic. The excessive release of NO impairs mitochondrial function and acts on neighboring cells, damaging lipids, proteins and nucleic acids, thus affecting cell metabolism and survival[14]. The reactive species can react with each other to produce more active forms, such as the free form of NO reacts with O2−• to produce ONOO− or peroxynitrite radical (ONOO•)[15]. ONOO− can be rapidly decomposed into HO•, nitrogen dioxide radical (NO2•), and nitryl cation (NO2+). All of them can damage nerve cells[16].
Analgesic and anti-inflammatory effects of modafinil in a mouse model of neuropathic pain: A role for nitrergic and serotonergic pathways
Published in Neurological Research, 2022
Hossein Ghorbanzadeh, Parastoo Mohebkhodaei, Mehran Nematizadeh, Nastaran Rahimi, Mahsa Rafeiean, Mehdi Ghasemi, Ahmad R. Dehpour
Modafinil, 7-nitroindazole (7-NI; a selective nNOS inhibitor), citalopram (a selective serotonin reuptake inhibitor; SSRI), aminoguanidine (a selective inducible NOS inhibitor), and L-NG-nitroarginine methyl ester (L-NAME; a nonspecific NOS inhibitor) were purchased from Sigma-Aldrich (Germany). Xylazine and ketamine were purchased from Alfasanco (Woerden, Holland) and dimethylsulfoxide (DMSO), Tween 80, and formalin solution were bought from Merck Company (UK). Modafinil suspension was made using tween 80 1%. 7-NI was dissolved in DMSO 10%. Other chemicals were dissolved in saline. All drugs were prepared freshly before the experiments and injected intraperitoneally (i.p.) in a volume of 10 ml/kg. Mouse-specific enzyme-linked immunosorbent assay (ELISA) kits for measuring IL-6 and TNF- α were bought from DuoSet (R&D systems, United States). Nitric Oxide assay kit was bought from ZellBio GmbH (Germany).