scholarly journals Keratinocytes-Derived Reactive Oxygen Species Play an Active Role to Induce Type 2 Inflammation of the Skin: A Pathogenic Role of Reactive Oxygen Species at the Early Phase of Atopic Dermatitis

2021 ◽  
Vol 33 (1) ◽  
pp. 26
Author(s):  
Da-In Choi ◽  
Jun-Hyeong Park ◽  
Jee-Young Choi ◽  
MeiShan Piao ◽  
Min-Song Suh ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Atopic Dermatitis ◽  
Early Phase ◽  
Reactive Oxygen ◽  
Active Role ◽  
Oxygen Species ◽  
Pathogenic Role ◽  
Type 2 Inflammation

Mo2060 Pathogenic Role of NADPH Oxidase 1 (NOX1)-Derived Reactive Oxygen Species in 5-Fluorouracil-Induced Intestinal Mucositis in Mice

2012 ◽  
Vol 142 (5) ◽  
pp. S-731
Author(s):  
Masashi Yasuda ◽  
Shinichi Kato ◽  
Naoki Yamanaka ◽  
Maho Iimori ◽  
Kazumi Iwata ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Pathogenic Role ◽  
Nadph Oxidase 1 ◽  
Intestinal Mucositis

scholarly journals Role of Perivascular Adipose Tissue on Vascular Reactive Oxygen Species in Type 2 Diabetes: A Give-and-Take Relationship: Figure 1

Diabetes ◽  
2015 ◽  
Vol 64 (6) ◽  
pp. 1904-1906 ◽  
Author(s):  
Jaume Padilla ◽  
Victoria J. Vieira-Potter ◽  
Guanghong Jia ◽  
James R. Sowers
Keyword(s):  
Reactive Oxygen Species ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Perivascular Adipose Tissue

scholarly journals The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

2016 ◽  
Vol 397 (8) ◽  
pp. 709-724 ◽  
Author(s):  
José Pedro Castro ◽  
Tilman Grune ◽  
Bodo Speckmann
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Animal Studies ◽  
Energy Homeostasis ◽  
Reactive Oxygen ◽  
Whole Body ◽  
Oxygen Species ◽  
Body Energy

Abstract White adipose tissue (WAT) is actively involved in the regulation of whole-body energy homeostasis via storage/release of lipids and adipokine secretion. Current research links WAT dysfunction to the development of metabolic syndrome (MetS) and type 2 diabetes (T2D). The expansion of WAT during oversupply of nutrients prevents ectopic fat accumulation and requires proper preadipocyte-to-adipocyte differentiation. An assumed link between excess levels of reactive oxygen species (ROS), WAT dysfunction and T2D has been discussed controversially. While oxidative stress conditions have conclusively been detected in WAT of T2D patients and related animal models, clinical trials with antioxidants failed to prevent T2D or to improve glucose homeostasis. Furthermore, animal studies yielded inconsistent results regarding the role of oxidative stress in the development of diabetes. Here, we discuss the contribution of ROS to the (patho)physiology of adipocyte function and differentiation, with particular emphasis on sources and nutritional modulators of adipocyte ROS and their functions in signaling mechanisms controlling adipogenesis and functions of mature fat cells. We propose a concept of ROS balance that is required for normal functioning of WAT. We explain how both excessive and diminished levels of ROS, e.g. resulting from over supplementation with antioxidants, contribute to WAT dysfunction and subsequently insulin resistance.

Alzheimer disease: Evidence for a central pathogenic role of iron-mediated reactive oxygen species

2004 ◽  
Vol 6 (2) ◽  
pp. 165-169 ◽  
Author(s):  
Gemma Casadesus ◽  
Mark A. Smith ◽  
Xiongwei Zhu ◽  
Gjumrakch Aliev ◽  
Adam D. Cash ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Alzheimer Disease ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Pathogenic Role

scholarly journals Increased monocyte-derived reactive oxygen species in type 2 diabetes: role of endoplasmic reticulum stress

2017 ◽  
Vol 102 (2) ◽  
pp. 139-153 ◽  
Author(s):  
Robert M. Restaino ◽  
Shekhar H. Deo ◽  
Alan R. Parrish ◽  
Paul J. Fadel ◽  
Jaume Padilla
Keyword(s):  
Reactive Oxygen Species ◽  
Type 2 Diabetes ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Reactive Oxygen ◽  
Oxygen Species

Accelerated endothelial dysfunction in mild prediabetic insulin resistance: the early role of reactive oxygen species

2007 ◽  
Vol 293 (5) ◽  
pp. E1311-E1319 ◽  
Author(s):  
Edward R. Duncan ◽  
Simon J. Walker ◽  
Vivienne A. Ezzat ◽  
Stephen B. Wheatcroft ◽  
Jian-Mei Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Type 2 Diabetes ◽  
Endothelial Dysfunction ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Wild Type

Insulin resistance is well established as an independent risk factor for the development of type 2 diabetes and cardiovascular atherosclerosis. Most studies have examined atherogenesis in models of severe insulin resistance or diabetes. However, by the time of diagnosis, individuals with type 2 diabetes already demonstrate a significant atheroma burden. Furthermore, recent studies suggest that, even in adolescence, insulin resistance is a progressive disorder that increases cardiovascular risk. In the present report, we studied early mechanisms of reduction in the bioavailability of the antiatheroscerotic molecule nitric oxide (NO) in very mild insulin resistance. Mice with haploinsufficiency for the insulin receptor (IRKO) are a model of mild insulin resistance with preserved glycemic control. We previously demonstrated that 2-mo-old (Young) IRKO mice have preserved vasorelaxation responses to ACh. This remained the case at 4 mo of age. However, by 6 mo, despite no significant deterioration in glucose homeostasis (Adult), IRKO mice had marked blunting of ACh-mediated vasorelaxation [IRKO maximum contraction response (Emax) 66 ± 5% vs. wild type 87 ± 4%, P < 0.01]. Despite the endothelial dysfunction demonstrated, aortic endothelial nitric oxide synthase (eNOS) mRNA levels were similar in Adult IRKO and wild-type mice, and, interestingly, aortic eNOS protein levels were increased, suggesting a compensatory upregulation in the IRKO. We then examined the potential role of reactive oxygen species in mediating early endothelial dysfunction. The superoxide dismutase mimetic Mn(III)tetrakis(1-methyl-4-pyridyl) porphyrin pentachloride (MnTMPyP) restored ACh relaxation responses in the Adult IRKO (Emax to ACh with MnTMPyP 85 ± 5%). Dihydroethidium fluorescence of aortas and isolated coronary microvascular endothelial cells confirmed a substantial increase in endothelium-derived reactive oxygen species in IRKO mice. These data demonstrate that mild insulin resistance is a potent substrate for accelerated endothelial dysfunction and support a role for endothelial cell superoxide production as a mechanism underlying the early reduction in NO bioavailability.

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