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Micronutrients in Prevention and Improvement of the Standard Therapy in Arthritis
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
A clinical study involving 30 patients with RA, 15 patients with OA, and 15 patients with systemic lupus erythematosus (SLE) showed that the levels of 3-nitrotyrosine in synovial fluid and sera of patients with RA and OA were elevated compared to SLE.15 The levels of 3-nitrotyrosine also correlated with the disease activity. High levels of nitrated type III collagen was found in synovial tissues of the patients with RA and knee OA compared to healthy controls. In addition, the serum levels of nitrated type III collagen was elevated in patients with OA 1.5-fold more than in healthy control subjects.16 In patients with OA, the erythrocyte levels of MDA and activities of SOD, glutathione peroxidase, and plasma glutathione-s-transferase increased, whereas the erythrocyte levels of glutathione and ascorbic acid and plasma vitamin E decreased compared to those in healthy control subjects.17 Macrophages and T-cells from RA patients produced more NO than that produced by these cells obtained from healthy subjects. TNF-α also increased production of NO in T cells obtained from RA patients. Overproduction NO may contribute to the T-cell dysfunction that is commonly found in the inflamed joint.18 The synovial fluid neutrophils from RA patients are activated to produce increased amounts of ROS within the cells.19 It has been reported that aldehydic products, primarily the 4-hydroxy-2-alkenals, form adducts with proteins that make them highly immunogenic, which can induce pathogenic antibodies in RA.20
General Nutritional Considerations for Chronic Hyperglycemia—Type 2 Diabetes
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
Note: Nitrotyrosine is a product of reactive nitrogen species and indicates cell damage, inflammation, and NO production. The prostaglandin 8-iso-PGF(2alpha) in urine is a reliable, noninvasive index of lipid peroxidation (Tacconelli, Capone, and Patrignani. 2010). IL-6 is an interleukin that acts as both a pro-inflammatory cytokine and an anti-inflammatory myokine. ICAM-1 plays an important role in adhesion phenomena involved in the immune response (Roy, Audette, and Tremblay. 2001).
Nitric Oxide as a Mediator of Intestinal Mucosal Function
Published in T. S. Gaginella, Regulatory Mechanisms — in — Gastrointestinal Function, 2017
Mark J. S. Miller, Timothy S. Gaginella
What is the relationship between the iNOS-generated inflammation and gut injury? Figure 1 offers some of the possible mechanisms that may lead to cell injury/death and secondary consequences of IBD, viz., carcinoma. Nitric oxide can interact with superoxide, also present in excess amounts in IBD,66 to form peroxynitrite (ONOO-). Peroxynitrite formation in vivo can be traced by its ability to nitrate tyrosine residues to yield nitrotyrosine.9, 49Nitric oxide itself cannot form nitrotyrosine, so this test is more specific for ONOO-. iNOS expression and nitrotyrosine colocalize in models of gut inflammation (TNBS and FCA).67 Furthermore, inhibition of NOS activity prevents nitrotyrosine formation, confirming that nitrotyrosine is dependent on NO formation.68 Peroxynitrite is injurious through a multitude of mechanisms including peroxidation and nitration reactions, and the protonated form (ONOOH) can act like an OH and NO2 donor. Whether the effects of peroxynitrite explain the beneficial action of superoxide dismutase in gut inflammation remains to be defined.
Long-term consumption of Western diet contributes to endothelial dysfunction and aortic remodeling in rats: Implication of Rho-kinase signaling
Published in Clinical and Experimental Hypertension, 2019
Rania A. Elrashidy, Jing Zhang, Guiming Liu
Oxidative stress can modulate vascular function via several mechanisms including direct oxidative damage, altered NO bioavailability, ROS-induced inflammation, and remodeling of the vasculature, contributing to endothelial dysfunction (31). In the present study, nitrotyrosine was assessed as a marker of oxidative stress. The reaction between superoxide anion and NO produces peroxynitrite which induces uncoupling of eNOS yielding a dysfunctional superoxide-generating enzyme or causes nitration of tyrosine residue of target proteins resulting in nitrotyrosine formation (29). Thus, the increased nitrotyrosine levels in thoracic aortic tissue reflected a reduced NO bioavailability, which further impaired the endothelial function in WD-fed rats. Interestingly, the relationship between ROCK pathway and ROS is unique with each one can activate the other. ROS can serve as second messengers to activate multiple intracellular signal cascades, including RhoA/ROCK pathway (32). Meanwhile, ROCK activation can promote ROS generation through upregulation of NADPH oxidase (33). This was further supported by the positive correlations between ROCK isoforms and nitrotyrosine levels in aortic tissue.
Phosphatidylcholine attenuated docetaxel-induced peripheral neurotoxicity in rats
Published in Drug and Chemical Toxicology, 2018
Sung Tae Kim, Eun Jung Kyung, Jung Sook Suh, Ho Sung Lee, Jun Ho Lee, Soo In Chae, Eon Sub Park, Yoon Hee Chung, Jinhyung Bae, Tae Jin Lee, Won Mo Lee, Uy Dong Sohn, Ji Hoon Jeong
In histopathology, docetaxel-induced peripheral neuropathy is characterized by decrease in density of myelinated fibers, axonal degeneration, and demyelination of nerve fibers. In this study, these docetaxel-induced neuronal damages were observed in sciatic nerve and lumbar spinal cord of docetaxel-treated rat by H&E staining. Sciatic nerve of docetaxel group section showed demyelination and degeneration of nerve fibers compared with control group. PC administration attenuated these docetaxel-induced damages; sciatic nerve of docetaxel + PC group section showed morphologic appearance similar to the sciatic nerve section of control group. Similar results were observed in rat lumbar spinal cord. Docetaxel-treated lumbar spinal cord showed decrease in neuronal cell bodies compared with control group, which was ameliorated by PC. As nitrotyrosine is considered to be a marker of oxidative stress in many experiments (Lyall et al. 1998, Azevedo et al. 2013, Tanabe et al. 2014), nitrotyrosine immunostaining was also conducted to evaluate the level of protein oxidative modification. The sciatic nerve and lumbar spinal cord section of docetaxel treated group showed increase in nitrotyrosine compared with control group, and these docetaxel-induced increase of nitrotyrosine was attenuated by PC administration. These results confirmed that PC attenuated docetaxel-induced oxidative damage on sciatic nerve and lumbar spinal cord.
Polyphenol-Rich Fraction of Parquetina nigrescens Mitigates Dichlorvos-Induced Cardiorenal Dysfunction Through Reduction in Cardiac Nitrotyrosine and Renal p38 Expressions in Wistar Rats
Published in Journal of Dietary Supplements, 2018
Ademola A. Oyagbemi, Temidayo O. Omobowale, Grace O. Ochigbo, Ebunoluwa R. Asenuga, Olufunke Eunice Ola-Davies, Temitayo O. Ajibade, Adebowale B. Saba, Adeolu A. Adedapo
The higher expression of nitrotyrosine observed in the heart of rats exposed to dichlorvos alone compared to control is an indication of cell damage and inflammation. Nitrotyrosine is the product of oxidative nitration of tyrosine in proteins by peroxynitrite. However, quantification of nitrotyrosine might serve as an indirect measure of peroxynitrite in tissues. From this study, increased expression of nitrotyrosine is indicative of an increased cardiovascular disorder in rats exposed to dichlorvos alone. The heart of rats treated with the prf of P. nigrescens showed lesser expressions of nitrotyrosine, attributable to lesser amounts of peroxynitrite; thus, it can be inferred that there was less oxidative stress and inflammation in treated rats. Immunohistochemistry of the kidney of rats administered dichlorvos alone revealed a higher p38 (MAPK) expression compared to both control and prf of P. nigrescens–treated rats. The p38 is a class of mitogen-activated protein kinases that respond to stress stimuli such as apoptosis, environmental stresses, and inflammatory cytokines. An increase in its expression is indicative of stress and inflammation and suggestive of increased apoptosis in untreated rats. We report for the first time the chemoprotective effect of polyphenol fraction of Parquetina nigrescens on dichlorvos-induced cardiorenal dysfunction.