Reactive oxygen species signaling in plants

The evolution of aerobic metabolism such as respiration and photosynthesis resulted in the generation of reactive oxygen species (ROS). A common property of all ROS types is that they can cause oxidative damage to proteins, DNA, and lipids. This toxicity of ROS explains the evolution of complex arrays of nonenzymatic and enzymatic detoxification mechanisms in plants. However, increasing evidence indicates that plants also make use of ROS as signaling molecules for regulating development and various physiological responses. In this review, novel insights into the mechanisms of how plants sense and respond to ROS are discussed in the context of the biological effects and functions of ROS in plants.     

Reactive oxygen species regulate activation-induced T cell apoptosis.

Reactive oxygen species (ROS) mediate apoptosis in a number of cell types. We studied the role that ROS play in activated T cell apoptosis by activating T cells in vivo and then culturing them for a short time. Activated T cells died independently of Fas and TNF alpha. Their death was characterized by rapid loss of mitochondrial transmembrane potential (delta psi(m)), caspase-dependent DNA fragmentation, and superoxide generation. A superoxide dismutase mimetic, Mn (III) tetrakis (5, 10, 15, 20-benzoic acid) porphyrin (MnTBAP), protected T cells from superoxide generation, caspase-dependent DNA loss, loss of delta psi(m), and cell death. These results indicate that ROS can regulate signals involved in caspase activation and apoptosis and may contribute to peripheral T cell deletion.     

Reactive oxygen species and oocyte fertilization

Sir, The oocyte resides in a metabolically active environment consistingof steroid hormones, growth factors, cytokines, granulosa cellsand leukocytes. Even though the impact of follicular fluid oxidativestress on oocyte maturation, fertilization and pregnancy isnot clear, in bovine oocytes, the formation of reactive oxygenspecies (ROS) is reported to increase the developmental potentialduring in vitro maturation to     

Reactive oxygen species mediate angiotensin II-induced leukocyte-endothelial cell interactions in vivo

Chronically elevated angiotensin II (Ang-II)-induced hypertension is partly mediated by superoxide production. In this study, we have investigated whether the leukocyte-endothelial cell interactions elicited by Ang-II involve reactive oxygen species (ROS) generation. Intravital microscopy within the rat mesenteric microvessels was used. Superfusion (60 min) with Ang-II (1 nM) induced significant increases in leukocyte rolling flux, adhesion, and emigration, which were inhibited by pretreatment with superoxide dismutase or catalase. Dihydrorhodamine-123 oxidation indicated that ROS are primarily produced by the vessel wall. Administration of dimethylthiourea, desferrioxamine, or N-acetylcysteine provoked significant reductions in Ang-II-induced leukocyte-endothelial cell interactions. In addition, a blockade of platelet-activating factor or leukotrienes also attenuated such responses significantly. The results presented indicate that in vivo Ang-II-induced leukocyte recruitment is dependent on the generation of intra- and extracellular ROS. Therefore, the use of anti-oxidants might constitute an alternative therapy for the control of the subendothelial leukocyte infiltration associated with hypertension and atherosclerosis.     

Reactive oxygen species-dependent cell signaling regulates the mosquito immune response to Plasmodium falciparum

Reactive oxygen species (ROS) have been implicated in direct killing of pathogens, increased tissue damage, and regulation of immune signaling pathways in mammalian cells. Available research suggests that analogous phenomena affect the establishment of Plasmodium infection in Anopheles mosquitoes. We have previously shown that provision of human insulin in a blood meal leads to increased ROS levels in Anopheles stephensi. Here, we demonstrate that provision of human insulin significantly increased parasite development in the same mosquito host in a manner that was not consistent with ROS-induced parasite killing or parasite escape through damaged tissue. Rather, our studies demonstrate that ROS are important mediators of both the mitogen-activated protein kinase and phosphatidylinositol 3-kinase/Akt signaling branches of the mosquito insulin signaling cascade. Further, ROS alone can directly activate these signaling pathways and this activation is growth factor specific. Our data, therefore, highlight a novel role for ROS as signaling mediators in the mosquito innate immune response to Plasmodium parasites.     

Reactive oxygen species as signaling molecules in cardiovascular differentiation of embryonic stem cells and tumor-induced angiogenesis

Besides the well known pathophysiological impact of oxidative stress in cardiovascular disease, reactive oxygen species (ROS) generated at low concentrations exert a role as signaling molecules that are involved in signal transduction cascades of numerous growth factor-, cytokine-, and hormone-mediated pathways, and regulate biological effects such as apoptosis, cell proliferation, and differentiation. Embryonic stem cells have the capacity to differentiate into the cardiovascular cell lineage. Furthermore, upon confrontation culture with tumor tissue, they form blood vessel-like structures that induce tumor-induced angiogenesis within tumor tissues. The role of ROS in cardiovascular differentiation of embryonic stem cells appears to be antagonistic. Whereas continuous exposure to ROS results in inhibition of cardiomyogenesis and vasculogenesis, pulse chase exposure to low-level ROS enhances differentiation toward the cardiomyogenic as well as vascular cell lineage. This review summarizes the current knowledge of ROS-induced cardiovascular differentiation of embryonic stem cells as well as the role of ROS in tumor-induced angiogenesis.     

Reactive oxygen species in renal vascular function

Reactive oxygen species (ROS) are produced by the aerobic metabolism. The imbalance between production of ROS and antioxidant defence in any cell compartment is associated with cell damage and may play an important role in the pathogenesis of renal disease. NADPH oxidase (NOX) family is the major ROS source in the vasculature and modulates renal perfusion. Upregulation of Ang II and adenosine activates NOX via AT1R and A1R in renal microvessels, leading to superoxide production. Oxidative stress in the kidney prompts renal vascular remodelling and increases preglomerular resistance. These are key elements in hypertension, acute and chronic kidney injury, as well as diabetic nephropathy. Renal afferent arterioles (Af), the primary resistance vessel in the kidney, fine tune renal hemodynamics and impact on blood pressure. Vice versa, ROS increase hypertension and diabetes, resulting in upregulation of Af vasoconstriction, enhancement of myogenic responses and change of tubuloglomerular feedback (TGF), which further promotes hypertension and diabetic nephropathy. In the following, we highlight oxidative stress in the function and dysfunction of renal hemodynamics. The renal microcirculatory alterations brought about by ROS importantly contribute to the pathophysiology of kidney injury, hypertension and diabetes.     

Reactive oxygen species and respiratory plasticity following intermittent hypoxia

The neural network controlling breathing exhibits plasticity in response to environmental or physiological challenges. For example, while hypoxia initiates rapid and robust increases in respiratory motor output to defend against hypoxemia, it also triggers persistent changes, or plasticity, in chemosensory neurons and integrative pathways that transmit brainstem respiratory activity to respiratory motor neurons. Frequently studied models of hypoxia-induced respiratory plasticity include: (1) carotid chemosensory plasticity and metaplasticity induced by chronic intermittent hypoxia (CIH), and (2) acute intermittent hypoxia (AIH) induced phrenic long-term facilitation (pLTF) in na?ve and CIH preconditioned rats. These forms of plasticity share some mechanistic elements, although they differ in anatomical location and the requirement for CIH preconditioning. Both forms of plasticity require serotonin receptor activation and formation of reactive oxygen species (ROS). While the cellular sources and targets of ROS are not well known, recent evidence suggests that ROS modify the balance of protein phosphatase and kinase activities, shifting the balance towards net phosphorylation and favoring cellular reactions that induce and/or maintain plasticity. Here, we review possible sources of ROS, and the impact of ROS on phosphorylation events relevant to respiratory plasticity.     

Reactive oxygen and nitrogen species in normal physiological processes

Reactive oxygen species (ROS) and reactive nitrogen species have generally been considered as being highly reactive and cytotoxic molecules. Besides their noxious effects, ROS participate in physiological processes in a carefully regulated manner. By way of example, microbicidal ROS are produced in professional phagocytes, ROS function as short-lived messengers having a role in signal transduction and, among other processes, participate in the synthesis of the iodothyronine hormones, reproduction, apoptosis and necrosis. Because of their ability to mediate a crosstalk between key molecules, their role might be dual (at least in some cases). The levels of ROS increase from a certain age, being associated with various diseases typical of senescence. The aim of this review is to summarize the recent findings on the physiological role of ROS. Other issues addressed are an increase in ROS levels during ageing, and the possibility of the physiological nature of this process.     

Reactive oxygen species mediate ERK activation through different Raf-1-dependent signaling pathways following cerebral ischemia

Production of reactive oxygen species (ROS) results in up-regulation of the extracellular signal-regulated kinase (ERK) cascade in response to numerous stimuli. Cerebral ischemia induces calcium-dependent kinase activation followed by ROS production. Here, we examined how ROS mediates the activation of ERK following cerebral ischemia in the rat hippocampus. We found that alpha-tocopherol, a free radical scavenger, attenuated the initial, robust activation of ERK by inhibiting Raf-1 dephosphorylation at Ser259. Alpha-tocopherol also down-regulated the second and mild activation of ERK through inhibition of Src-dependent phosphorylation of Raf-1 at Tyr340/341. Our results suggest that ROS production mediates the biphasic activation of ERK through different signaling cascades following post-ischemic reperfusion. Mediation of these signaling pathways involves changes in Raf-1 phosphorylation at different sites.     

Reactive oxygen species inhibited by titanium oxide coatings

Titanium is a successful biomaterial that possesses good biocompatibility. It is covered by a surface layer of titanium dioxide, and this oxide may play a critical role in inhibiting reactive oxygen species, such as peroxynitrite, produced during the inflammatory response. In the present study, titanium dioxide was coated onto silicone substrates by radio-frequency sputtering. Silicone coating with titanium dioxide enhanced the breakdown of peroxynitrite by 79%. At physiologic pH, the peroxynitrite donor 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1) was used to nitrate 4-hydroxyphenylacetic acid (4-HPA) to form 4-hydroxy-3-nitrophenyl acetic acid (NHPA). Titanium dioxide-coated silicone inhibited the nitration of 4-HPA by 61% compared to aluminum oxide-coated silicone and 55% compared to uncoated silicone. J774A.1 mouse macrophages were plated on oxide-coated silicone and polystyrene and stimulated to produce superoxide and interleukin-6. Superoxide production was measured by the chemiluminescent reaction with 2-methyl-6-[p-methoxyphenyl]-3,7-dihydroimidazo[1,2-a]pyrazin-3-one (MCLA). Titanium dioxide-coated silicone exhibited a 55% decrease in superoxide compared to uncoated silicone and a 165% decrease in superoxide compared to uncoated polystyrene. Titanium dioxide-coated silicone inhibited IL-6 production by 77% compared to uncoated silicone. These results show that the anti-inflammatory properties of titanium dioxide can be transferred to the surfaces of silicone substrates.     

Reactive oxygen species and synaptic plasticity in the aging hippocampus

Aging is associated with a general decline in physiological functions including cognitive functions. Given that the hippocampus is known to be critical for certain forms of learning and memory, it is not surprising that a number of neuronal processes in this brain area appear to be particularly vulnerable to the aging process. Long-term potentiation (LTP), a form of synaptic plasticity that has been proposed as a biological substrate for learning and memory, has been used to examine age-related changes in hippocampal synaptic plasticity. A current hypothesis states that oxidative stress contributes to age-related impairment in learning and memory. This is supported by a correlation between age, memory impairment, and the accumulation of oxidative damage to cellular macromolecules. However, it also has been demonstrated that ROS are necessary components of signal transduction cascades during normal physiological processes. This review discusses the evidence supporting the dual role of reactive oxygen species (ROS) as cellular messenger molecules in normal LTP, as well their role as damaging toxic molecules in the age-related impairment of LTP. In addition, we will discuss parallel analyses of LTP and behavioral tests in mice that overexpress antioxidant enzymes and how the role of antioxidant enzymes and ROS in modulating these processes may vary over the lifespan of an animal.