scholarly journals Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

2008 ◽  
Vol 88 (1) ◽  
pp. 211-247 ◽  
Author(s):  
Tihomir Paul Obrenovitch
Keyword(s):  
Defense Mechanisms ◽  
Biological Response ◽  
Tissue Level ◽  
Ischemic Tolerance ◽  
Antioxidant Systems ◽  
Molecular Physiology ◽  
Adaptive Changes ◽  
Functional Changes ◽  
Subsequent Test ◽  
Neuroprotective Strategies

Ischemic tolerance describes the adaptive biological response of cells and organs that is initiated by preconditioning (i.e., exposure to stressor of mild severity) and the associated period during which their resistance to ischemia is markedly increased. This topic is attracting much attention because preconditioning-induced ischemic tolerance is an effective experimental probe to understand how the brain protects itself. This review is focused on the molecular and related functional changes that are associated with, and may contribute to, brain ischemic tolerance. When the tolerant brain is subjected to ischemia, the resulting insult severity (i.e., residual blood flow, disruption of cellular transmembrane gradients) appears to be the same as in the naive brain, but the ensuing lesion is substantially reduced. This suggests that the adaptive changes in the tolerant brain may be primarily directed against postischemic and delayed processes that contribute to ischemic damage, but adaptive changes that are beneficial during the subsequent test insult cannot be ruled out. It has become clear that multiple effectors contribute to ischemic tolerance, including: 1) activation of fundamental cellular defense mechanisms such as antioxidant systems, heat shock proteins, and cell death/survival determinants; 2) responses at tissue level, especially reduced inflammatory responsiveness; and 3) a shift of the neuronal excitatory/inhibitory balance toward inhibition. Accordingly, an improved knowledge of preconditioning/ischemic tolerance should help us to identify neuroprotective strategies that are similar in nature to combination therapy, hence potentially capable of suppressing the multiple, parallel pathophysiological events that cause ischemic brain damage.

scholarly journals Developmental Origins of Kidney Disease: Why Oxidative Stress Matters?

Antioxidants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 33
Author(s):  
Chien-Ning Hsu ◽  
You-Lin Tain
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Current Knowledge ◽  
Future Research ◽  
Antioxidant Systems ◽  
Developmental Origins ◽  
Adult Onset ◽  
Functional Changes ◽  
Health And Disease ◽  
Developing Kidney

The “developmental origins of health and disease” theory indicates that many adult-onset diseases can originate in the earliest stages of life. The developing kidney has emerged as being particularly vulnerable to adverse in utero conditions leading to morphological and functional changes, namely renal programming. Emerging evidence indicates oxidative stress, an imbalance between reactive oxygen/nitrogen species (ROS/RNS) and antioxidant systems, plays a pathogenetic role in the developmental programming of kidney disease. Conversely, perinatal use of antioxidants has been implemented to reverse programming processes and prevent adult-onset diseases. We have termed this reprogramming. The focus of this review is twofold: (1) To summarize the current knowledge on oxidative stress implicated in renal programming and kidney disease of developmental origins; and (2) to provide an overview of reprogramming effects of perinatal antioxidant therapy on renal programming and how this may prevent adult-onset kidney disease. Although early-life oxidative stress is implicated in mediating renal programming and adverse offspring renal outcomes, and animal models provide promising results to allow perinatal antioxidants applied as potential reprogramming interventions, it is still awaiting clinical translation. This presents exciting new challenges and areas for future research.

Towards a Unified Multi-Scaled Theoretical-Experimental Paradigm for Characterizing Vascular Remodeling

2007 ◽  
Author(s):  
Rudolph L. Gleason
Keyword(s):  
Vascular Remodeling ◽  
Biological Response ◽  
Temporal Variations ◽  
Tissue Level ◽  
Aortic Aneurysms ◽  
Material Behavior ◽  
Scale Model ◽  
Mechanical Environment ◽  
Abdominal Aortic ◽  
Development And Aging

Vascular remodeling plays a key role in many physiological and pathophysiological processes, as well as the success or failure of many clinical interventions; examples include vascular development and aging, hypertension and atherosclerosis, and restenosis of vascular grafts. Despite the explosion of information on vascular remodeling, from the molecular level to the tissue level, attempts at integrating these data into a predictive multi-scale model are still in their infancy. Humphrey and Rajagopal said well that in order to capture the salient features of these remodeling processes ‘one must track local balances or imbalances in the continual production, removal, [and remodeling] of individual constituents, the mechanical state in which the constituents are formed, and how these constituents are organized’. Abdominal aortic aneurysms (AAA’s) provide a good illustration of the need for a multi-scaled microstructurally-motivated mathematical model. During progression of AAA’s, circumferential expansion, vessel wall thinning and axial lengthening are coincident with a progressive loss of elastin and smooth muscle and decrease in glycosaminoglycans, with mature aneurysms consisting primarily of collagen and fibroblasts; thus, AAA’s experience spatial and temporal variations in their geometry, microstructural content and organization, and applied loads. To develop a predictive model for vascular remodeling, the complex interplay between evolving material behavior (via changes in microstructural content and organization) and applied loads, which determine the local mechanical environment and the mechano-biological response to this changing mechanical environment, must be incorporated.

scholarly journals Crosstalk between Neuron and Glial Cells in Oxidative Injury and Neuroprotection

2021 ◽  
Vol 22 (24) ◽  
pp. 13315
Author(s):  
Kyung Hee Lee ◽  
Myeounghoon Cha ◽  
Bae Hwan Lee
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Oxidative Injury ◽  
Redox Balance ◽  
Brain Diseases ◽  
Antioxidant Systems ◽  
Antioxidant Mechanisms ◽  
Brain Homeostasis

To counteract oxidative stress and associated brain diseases, antioxidant systems rescue neuronal cells from oxidative stress by neutralizing reactive oxygen species and preserving gene regulation. It is necessary to understand the communication and interactions between brain cells, including neurons, astrocytes and microglia, to understand oxidative stress and antioxidant mechanisms. Here, the role of glia in the protection of neurons against oxidative injury and glia–neuron crosstalk to maintain antioxidant defense mechanisms and brain protection are reviewed. The first part of this review focuses on the role of glia in the morphological and physiological changes required for brain homeostasis under oxidative stress and antioxidant defense mechanisms. The second part focuses on the essential crosstalk between neurons and glia for redox balance in the brain for protection against oxidative stress.

scholarly journals Ultraviolet-B Radiation Damage on Kentucky Bluegrass. III. Cultivar Effects

HortScience ◽  
2004 ◽  
Vol 39 (6) ◽  
pp. 1475-1477 ◽  
Author(s):  
Erik H. Ervin ◽  
Xunzhong Zhang ◽  
John H. Fike
Keyword(s):  
Chlorophyll A ◽  
Defense Mechanisms ◽  
Poa Pratensis ◽  
Photochemical Efficiency ◽  
Correlation Coefficients ◽  
Kentucky Bluegrass ◽  
Ultraviolet B ◽  
Antioxidant Systems ◽  
Turf Quality ◽  
Antioxidant Defense Systems

Plants possess various constitutive and inducible defense mechanisms such as pigment and antioxidant systems for protection against stresses such as ultraviolet-B (UV-B; 290 to 320 nm) radiation. Our previous research has indicated that higher chlorophyll, carotenoid, and anthocyanin concentrations were associated with greater tolerance of UV-B stress by `Georgetown' kentucky bluegrass (Poa pratensis L.). The objectives of this study were to determine if kentucky bluegrass cultivars with darker leaf color possessed greater pigment and antioxidant defense systems and if such increases were associated with greater resistance to UV-B. Eight cultivars exhibiting a range of green color intensity (`Apollo', `Brilliant', `Julius', Limerick', `Midnight', `Moonlight', `Nuglade', and `Total Eclipse') were selected and subjected to continuous, artificial UV-B radiation (70 μmol·m-2·s-1). UV-B irradiation reduced turf quality (55% to 62%) and photochemical efficiency (37% to 70%) when measured 5 days after initiation of UV-B exposure. Significant differences in turf color, photochemical efficiency, chlorophyll a, chlorophyll b, chlorophyll a+b, and carotenoids were found among the cultivars. `Moonlight' had greatest photochemical efficiency, chlorophyll, carotenoids, and turf quality. Positive correlations of pigment concentration with photochemical efficiency and turf color were observed under UV-B radiation stress, with correlation coefficients ranging from 0.49 to 0.62. The results of this study suggests that selecting cultivars with higher concentrations of chlorophyll and carotenoids and photochemical efficiency may be an effective way for turfgrass managers and sod producers to improve sod establishment and quality in environments with higher UV-B radiation.

scholarly journals Antioxidant Supplementation in Renal Replacement Therapy Patients: Is There Evidence?

2019 ◽  
Vol 2019 ◽  
pp. 1-23 ◽  
Author(s):  
Vassilios Liakopoulos ◽  
Stefanos Roumeliotis ◽  
Andreas Bozikas ◽  
Theodoros Eleftheriadis ◽  
Evangelia Dounousi
Keyword(s):  
Free Radicals ◽  
Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Defense Mechanisms ◽  
White Blood Cells ◽  
Significant Loss ◽  
Antioxidant Systems ◽  
Omega 3 ◽  
Natural Defense ◽  
Increased Risk

The disruption of balance between production of reactive oxygen species and antioxidant systems in favor of the oxidants is termed oxidative stress (OS). To counteract the damaging effects of prooxidant free radicals, all aerobic organisms have antioxidant defense mechanisms that are aimed at neutralizing the circulating oxidants and repair the resulting injuries. Antioxidants are either endogenous (the natural defense mechanisms produced by the human body) or exogenous, found in supplements and foods. OS is present at the early stages of chronic kidney disease, augments progressively with renal function deterioration, and is further exacerbated by renal replacement therapy. End-stage renal disease patients, on hemodialysis (HD) or peritoneal dialysis (PD), suffer from accelerated OS, which has been associated with increased risk for mortality and cardiovascular disease. During HD sessions, the bioincompatibility of dialyzers and dialysate trigger activation of white blood cells and formation of free radicals, while a significant loss of antioxidants is also present. In PD, the bioincompatibility of solutions, including high osmolality, elevated lactate levels, low pH, and accumulation of advanced glycation end-products trigger formation of prooxidants, while there is significant loss of vitamins in the ultrafiltrate. A number of exogenous antioxidants have been suggested to ameliorate OS in dialysis patients. Vitamins B, C, D, and E, coenzyme Q10, L-carnitine, a-lipoic acid, curcumin, green tea, flavonoids, polyphenols, omega-3 polyunsaturated fatty acids, statins, trace elements, and N-acetylcysteine have been studied as exogenous antioxidant supplements in both PD and HD patients.

scholarly journals Structural, neuronal, and functional adaptive changes in atrophic rat ileum

Gut ◽  
1999 ◽  
Vol 45 (2) ◽  
pp. 236-245 ◽  
Author(s):  
K M Ekelund ◽  
E Ekblad
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Interstitial Cells Of Cajal ◽  
In Situ Hybridisation ◽  
Neuronal Cell ◽  
Interstitial Cells ◽  
Rat Ileum ◽  
Adaptive Changes ◽  
Functional Changes ◽  
Cells Of Cajal

BACKGROUNDInactivity of the gut leads to atrophic changes of which little is known.AIMSTo investigate structural, neuronal, and functional changes occurring in bypassed rat ileum.METHODSMorphometry was used to characterise the atrophic changes. The numbers of enteric neurones, their expression of neurotransmitters, and the presence of interstitial cells of Cajal were studied using immunocytochemistry and in situ hybridisation. Motor activity was studied in vitro.RESULTSAdaptive changes in bypassed ileum include atrophy and remodelling of the gut wall. The total numbers of submucous and myenteric neurones per unit length increased one and four weeks after bypass but were identical to sham operated intestine 10 weeks after bypass. Neurones expressing vasoactive intestinal peptide, neuropeptide Y, or pituitary adenylate cyclase activating peptide decreased gradually in number in bypassed ileum. Nitric oxide synthase expressing neurones were increased, particularly in the myenteric ganglia. No change in the frequency and distribution of interstitial cells of Cajal was noted. The contractile response elicited by electrical stimulation of sham operated ileum consisted of a fast cholinergic twitch followed by a slower non-adrenergic, non-cholinergic contraction. In the bypassed ileum an identical biphasic contraction was elicited; however, the entire response was non-adrenergic, non-cholinergic. The relaxatory response to electrical stimulation in sham operated ileum was nitric oxide mediated; after bypass it was non-nitrergic.CONCLUSIONSNotable atrophic changes were seen in the rat ileum after bypass. The enteric nervous system reacted with neuronal cell death and plasticity in terms of release and expression of neurotransmitters.

scholarly journals THE STATE OF ANTIOXIDANT SYSTEM AND CYTOKINE PROFILE AT DIFFERENT PERIODS OF A PHYSIOLOGICALLY ONGOING PREGNANCY

2020 ◽  
Vol 10 (2) ◽  
pp. 40-47
Author(s):  
I. I. Pavlyuchenko ◽  
O. S. Bezrukova ◽  
V. Ya. Zobenko ◽  
E. E. Esaulenko ◽  
A. A. Basov ◽  
...  
Keyword(s):  
Antioxidant System ◽  
Mitochondrial Respiratory Chain ◽  
Normal Pregnancy ◽  
Antioxidant Systems ◽  
Tissue Respiration ◽  
Functional Changes ◽  
Cytokine Balance ◽  
Preg Nancy ◽  
Additional Amount ◽  
Oxidative Homeostasis

Pregnancy is accompanied by physiologically adaptive changes necessary for the normal vital functioning of preg- nant woman and for the growth and development of the fetus. During pregnancy, structural and functional changes in all body systems begin, including in the immune and antioxidant systems. In the normal course of pregnancy, the cytokine balance shifts toward the immunosuppressive Th-2 cytokines (IL-4, IL-10, TGF-β). Violation of an adequate restructuring cytokine balance can cause complications during pregnancy. It was noted that high levels of Th1 cyto- kines can significantly affect the course of pregnancy and that cytokines are sensitive markers of spontaneous abortion in women. Activation of metabolic processes, increased energy metabolism, the initiation of tissue respiration occurs in preg- nancy. Disruptions in the functioning of the mitochondrial respiratory chain, changes in hemodynamics and tissue oxy- genation induce the formation of reactive oxygen species (ROS) that often cause a violation of oxidative homeostasis and the formation of oxidative stress (OS). This requires activation of the antioxidant system and an additional amount of antioxidants to restore balance in the pro/antioxidant system. It should be noted that at different stages of pregnancy imbalance of pro/antioxidants and pro/anti-inflammatory cytokines systems are individual and the limits of physiological changes during normal pregnancy of particular indica- tors of these systems are poorly understood.

scholarly journals Impact of Mycotoxins on Animals’ Oxidative Status

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 214
Author(s):  
Alexandros Mavrommatis ◽  
Elisavet Giamouri ◽  
Savvina Tavrizelou ◽  
Maria Zacharioudaki ◽  
George Danezis ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Detrimental Effect ◽  
Economic Losses ◽  
Antioxidant Systems ◽  
Integrated Monitoring ◽  
Animal Products ◽  
Agriculture Sector ◽  
By Products

Mycotoxins appear to be the “Achilles’ heel” of the agriculture sector inducing enormous economic losses and representing a severe risk to the health of humans and animals. Although novel determination protocols have been developed and legislation has been implemented within Europe, the side effects of mycotoxins on the homeostatic mechanisms of the animals have not been extensively considered. Feed mycotoxin contamination and the effects on the antioxidant status of livestock (poultry, swine, and ruminants) are presented. The findings support the idea that the antioxidant systems in both monogastrics and ruminants are challenged under the detrimental effect of mycotoxins by increasing the toxic lipid peroxidation by-product malondialdehyde (MDA) and inhibiting the activity of antioxidant defense mechanisms. The degree of oxidative stress is related to the duration of contamination, co-contamination, the synergetic effects, toxin levels, animal age, species, and productive stage. Since the damaging effects of MDA and other by-products derived by lipid peroxidation as well as reactive oxygen species have been extensively studied on human health, a more integrated monitoring mechanism (which will take into account the oxidative stability) is urgently required to be implemented in animal products.

scholarly journals Response of Endolithic Chroococcidiopsis Strains From the Polyextreme Atacama Desert to Light Radiation

2021 ◽  
Vol 11 ◽  
Author(s):  
María Cristina Casero ◽  
Carmen Ascaso ◽  
Antonio Quesada ◽  
Hanna Mazur-Marzec ◽  
Jacek Wierzchos
Keyword(s):  
Oxidative Stress ◽  
Solar Radiation ◽  
Defense Mechanisms ◽  
Atacama Desert ◽  
Antioxidant Systems ◽  
Light Radiation ◽  
High Solar Radiation ◽  
Ultrastructural Damage ◽  
Term Response

Cyanobacteria exposed to high solar radiation make use of a series of defense mechanisms, including avoidance, antioxidant systems, and the production of photoprotective compounds such as scytonemin. Two cyanobacterial strains of the genus Chroococcidiopsis from the Atacama Desert – which has one of the highest solar radiation levels on Earth- were examined to determine their capacity to protect themselves from direct photosynthetically active (PAR) and ultraviolet radiation (UVR): the UAM813 strain, originally isolated from a cryptoendolithic microhabitat within halite (NaCl), and UAM816 strain originally isolated from a chasmoendolithic microhabitat within calcite (CaCO3). The oxidative stress induced by exposure to PAR or UVR + PAR was determined to observe their short-term response, as were the long-term scytonemin production, changes in metabolic activity and ultrastructural damage induced. Both strains showed oxidative stress to both types of light radiation. The UAM813 strain showed a lower acclimation capacity than the UAM816 strain, showing an ever-increasing accumulation of reactive oxygen species (ROS) and a smaller accumulation of scytonemin. This would appear to reflect differences in the adaptation strategies followed to meet the demands of their different microhabitats.

scholarly journals Efficient Vpu-Mediated Tetherin Antagonism by an HIV-1 Group O Strain

2017 ◽  
Vol 91 (6) ◽  
Author(s):  
Katharina Mack ◽  
Kathrin Starz ◽  
Daniel Sauter ◽  
Simon Langer ◽  
Frederic Bibollet-Ruche ◽  
...  
Keyword(s):  
Defense Mechanisms ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Restriction Factor ◽  
Independent Manner ◽  
Adaptive Changes ◽  
Short Isoforms ◽  
Human Tetherin ◽  
Cd4 Cell ◽  
Hiv 1

ABSTRACT Simian immunodeficiency viruses (SIVs) use their Nef proteins to counteract the restriction factor tetherin. However, a deletion in human tetherin prevents antagonism by the Nef proteins of SIVcpz and SIVgor, which represent the ape precursors of human immunodeficiency virus type 1 (HIV-1). To promote virus release from infected cells, pandemic HIV-1 group M strains evolved Vpu as a tetherin antagonist, while the Nef protein of less widespread HIV-1 group O strains acquired the ability to target a region adjacent to this deletion. In this study, we identified an unusual HIV-1 group O strain (RBF206) that evolved Vpu as an effective antagonist of human tetherin. While both RBF206 Vpu and Nef exert anti-tetherin activity in transient-transfection assays, mainly Vpu promotes RBF206 release in infected CD4+ T cells. Although mutations distinct from the adaptive changes observed in group M Vpus (M-Vpus) were critical for the acquisition of its anti-tetherin activity, RBF206 O-Vpu potently suppresses NF-κB activation and reduces CD4 cell surface expression. Interestingly, RBF206 Vpu counteracts tetherin in a largely species-independent manner, degrading both the long and short isoforms of human tetherin. Downmodulation of CD4, but not counteraction of tetherin, by RBF206 Vpu was dependent on the cellular ubiquitin ligase machinery. Our data present the first example of an HIV-1 group O Vpu that efficiently antagonizes human tetherin and suggest that counteraction by O-Nefs may be suboptimal. IMPORTANCE Previous studies showed that HIV-1 groups M and O evolved two alternative strategies to counteract the human ortholog of the restriction factor tetherin. While HIV-1 group M switched from Nef to Vpu due to a deletion in the cytoplasmic domain of human tetherin, HIV-1 group O, which lacks Vpu-mediated anti-tetherin activity, acquired a Nef protein that is able to target a region adjacent to the deletion. Here we report an unusual exception, identifying a strain of HIV-1 group O (RBF206) whose Vpu protein evolved an effective antagonism of human tetherin. Interestingly, the adaptive changes in RBF206 Vpu are distinct from those found in M-Vpus and mediate efficient counteraction of both the long and short isoforms of this restriction factor. Our results further illustrate the enormous flexibility of HIV-1 in counteracting human defense mechanisms.

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