Gıda Mühendisliği Dergisi

Dokularda meydana gelen reaktif oksijen türleri (ROS) ve serbest radikaller DNA, protein, karbonhidrat ve lipidler gibi biyolojik açıdan önemli materyallere zarar verebilmektedir. Serbest radikaller vücut dışından gelebileceği gibi insan metabolizmasının doğal bir sonucu olarak da oluşabilmektedir. Serbest radikallerin endojen olarak üretimi farklı yollarla gerçekleşmektedir. Buna karşılık, canlı organizmalar serbest radikallerin potansiyel yıkıcı etkilerine karşı kendilerini korumak için çeşitli mekanizmalara sahiptir. Bu makale, reaktif oksijen türlerinin oluşum mekanizmalarını ve vücuttaki antioksidan savunma sistemlerini kapsamaktadır.

Free Radical Biology & Medicine, Vol. 31, No. 11, pp. 1287–1312, 2001

Abstract
Reactive oxygen species (ROS) are known mediators of intracellular signaling cascades. Excessive production of ROS may, however, lead to oxidative stress, loss of cell function, and ultimately apoptosis or necrosis. A balance between oxidant and antioxidant intracellular systems is hence vital for cell function, regulation, and adaptation to diverse growth conditions. Thioredoxin reductase (TrxR) in conjunction with thioredoxin (Trx) is a ubiquitous oxidoreductase system with antioxidant and redox regulatory roles. In mammals, extracellular forms of Trx also have cytokine-like effects. Mammalian TrxR has a highly reactive active site selenocysteine residue resulting in a profound reductive capacity, reducing several substrates in addition to Trx. Due to the reactivity of TrxR, the enzyme is inhibited by many clinically used electrophilic compounds including nitrosoureas, aurothioglucose, platinum compounds, and retinoic acid derivatives. The properties of TrxR in combination with the functions of Trx position this system at the core of cellular thiol redox control and antioxidant defense. In this review, we focus on the reactions of the Trx system with ROS molecules and different cellular antioxidant enzymes. We summarize the TrxR-catalyzed regeneration of several antioxidant compounds, including ascorbic acid (vitamin C), selenium-containing substances, lipoic acid, and ubiquinone (Q10). We also discuss the general cellular effects of TrxR inhibition. Dinitrohalobenzenes constitute a unique class of immunostimulatory TrxR inhibitors and we consider the immunomodulatory effects of dinitrohalobenzene compounds in view of their reactions with the Trx system.

Keywords: Thioredoxin; Thioredoxin reductase; Redox regulation; Inflammation; Oxidative stress; Antioxidant; Dinitrohalobenzene; Reactive oxygen species; Free radicals

Diabetes Care February 2008 vol. 31 no. Supplement 2 S170-S180

Reactive oxygen species (ROS) influence many physiological processes including host defense, hormone biosynthesis, fertilization, and cellular signaling. Increased ROS production (termed “oxidative stress”) has been implicated in various pathologies, including hypertension, atherosclerosis, diabetes, and chronic kidney disease. A major source for vascular and renal ROS is a family of nonphagocytic NAD(P)H oxidases, including the prototypic Nox2 homolog-based NAD(P)H oxidase, as well as other NAD(P)H oxidases, such as Nox1 and Nox4. Other possible sources include mitochondrial electron transport enzymes, xanthine oxidase, cyclooxygenase, lipoxygenase, and uncoupled nitric oxide synthase. NAD(P)H oxidase-derived ROS plays a physiological role in the regulation of endothelial function and vascular tone and a pathophysiological role in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis, and rarefaction, important processes underlying cardiovascular and renal remodeling in hypertension and diabetes. These findings have evoked considerable interest because of the possibilities that therapies against nonphagocytic NAD(P)H oxidase to decrease ROS generation and/or strategies to increase nitric oxide (NO) availability and antioxidants may be useful in minimizing vascular injury and renal dysfunction and thereby prevent or regress target organ damage associated with hypertension and diabetes. Here we highlight current developments in the field of reactive oxygen species and cardiovascular disease, focusing specifically on the recently identified novel Nox family of NAD(P)H oxidases in hypertension. We also discuss the potential role of targeting ROS as a therapeutic possibility in the management of hypertension and cardiovascular disease.

Clinica Chimica Acta 390 (2008) 1–11

As the red cell emerges from the bone marrow, it loses its nucleus, ribosomes, and mitochondria and therefore all capacity for protein synthesis. However, because of the high O2 tension in arterial blood and heme Fe content, reactive oxygen species (ROS) are continuously produced within red cells. Erythrocytes transport large amount of oxygen over their lifespan resulting in oxidative stress. Various factors can lead to the generation of oxidizing radicals such as O2•−, H2O2, HO• in erythrocytes. Evidence indicates that many physiological and pathological conditions such as aging, inflammation, eryptosis develop through ROS action. As such, red cells have potent antioxidant protection consisting of enzymatic and nonenzymatic pathways that modify highly ROS into substantially less reactive intermediates.

The object of this review is to shed light on the role of ROS both at physiological and pathological levels and the structural requirements of antioxidants for appreciable radical-scavenging activity. Obviously, much is still to be discovered before we clearly understand mechanisms of free radical systems in erythrocytes. Ongoing trends in the field are recognition of undetermined oxidant/antioxidant interactions and elucidation of important signaling networks in radical metabolism.