Lipid peroxidation in the brain of rats differing in resistance to emotional stress

1994 ◽  
Vol 118 (4) ◽  
pp. 1085-1087
Author(s):  
M. L. Kuklei ◽  
S. L. Stvolinskii ◽  
A. A. Boldyrev ◽  
I. V. Gannushkina
Keyword(s):  
Lipid Peroxidation ◽  
Emotional Stress ◽  
The Brain

Lipid peroxidation and antioxidant enzymes in the brain of rats exposed to acute emotional stress: Effect of interleukin-1β

1995 ◽  
Vol 120 (3) ◽  
pp. 884-886 ◽  
Author(s):  
S. S. Pertsov ◽  
T. S. Balashova ◽  
A. A. Kubatiev ◽  
A. S. Sosnovskii ◽  
G. V. Pirogova ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Emotional Stress ◽  
Interleukin 1Β ◽  
Stress Effect ◽  
Acute Emotional Stress ◽  
The Brain

The brain 3β-HSD up-regulation in response to deteriorating effects of background emotional stress: an animal model of multiple sclerosis

2021 ◽  
Author(s):  
Sogol Meknatkhah ◽  
Monireh-Sadat Mousavi ◽  
Pouya Sharif Dashti ◽  
Leila Azizzadeh Pormehr ◽  
Gholam Hossein Riazi
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Emotional Stress ◽  
The Brain

scholarly journals C60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Olga O. Gonchar ◽  
Andriy V. Maznychenko ◽  
Nataliya V. Bulgakova ◽  
Inna V. Vereshchaka ◽  
Tomasz Tomiak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Expression ◽  
Restraint Stress ◽  
Stress Condition ◽  
Rat Tissues ◽  
Stress Exposure ◽  
The Brain ◽  
Nrf2 Protein

The effects of C60FAS (50 and 500 μg/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O2⋅−, H2O2, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST, γ-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes γ-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C60FAS attenuates ROS generation and O2⋅− and H2O2 releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C60FAS supplementation has dose-dependent and tissue-specific effects. C60FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C60FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an in vivo model, when C60FAS (50 and 500 μg/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the in vivo model, C60FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition.

scholarly journals Decreased glucorticoid sensitivity as a factor of stressogenic shifts in the activity of monoamine oxidase, lipid peroxidation, and behavior in rats

2003 ◽  
Vol 49 (5) ◽  
pp. 48-51 ◽  
Author(s):  
I. A. Volchegorsky ◽  
V. E. Tseilikman ◽  
D. S. Smirnov ◽  
S. A. Ship ◽  
A. V. Borisenkov
Keyword(s):  
Lipid Peroxidation ◽  
Monoamine Oxidase ◽  
Brain Tissue ◽  
Behavioral Disorders ◽  
Immobilization Stress ◽  
Glucocorticoid Hormones ◽  
And Behavior ◽  
The Brain

Four episodes of immobilization stress cause a decrease in the sensitivity to glucocorticoid hormones, followed by anxiogenic be­havioral disorders, enhanced monoamine oxidase-В (МАО-В) activity and simultaneously increased lipid peroxidation (LPO) in the brain tissue of rats. Concurrently, there is an increase in renal МАО-В activity, as well as renal and hepatic accumulation of LPO products. Administration of kenalog (2 mg/kg), a phar­macological analogue of glucocorticoid hormones, prevents the poststress МАО-В activation and LPO and attenuates anxiogen­ic behavioral disorders in the rats.

scholarly journals Intracerebral Injection of Heme Induces Lipid Peroxidation, Neuroinflammation, and Sensorimotor Deficits

Stroke ◽  
2021 ◽  
Author(s):  
Luiz Ricardo C. Vasconcellos ◽  
Letícia Martimiano ◽  
Danillo Pereira Dantas ◽  
Filipe Mota Fonseca ◽  
Hilton Mata-Santos ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Signaling Pathway ◽  
Brain Damage ◽  
Autologous Blood ◽  
Mapk Signaling ◽  
Heme Oxygenase 1 ◽  
Dependent Manner ◽  
In Vivo Models ◽  
Sensorimotor Deficits ◽  
The Brain

Background and Purpose: Heme is a red blood cell component released in the brain parenchyma following intracerebral hemorrhage. However, the study of the pathophysiological mechanisms triggered by heme in the brain is hampered by the lack of well-established in vivo models of intracerebral heme injection. This study aims to optimize and characterize a protocol of intrastriatal heme injection in mice, with a focus on the induction of lipid peroxidation, neuroinflammation and, ultimately, sensorimotor deficits. We also evaluated the involvement of NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3), an inflammasome sensor, in the behavior deficits induced by heme in this model. Methods: Mice were injected with heme in the striatum for the evaluation of neuroinflammation and brain damage through histological and biochemical techniques. Immunoblot was used to evaluate the expression of proteins involved in heme/iron metabolism and antioxidant responses and the activation of the MAPK (mitogen-activated protein kinase) signaling pathway. For the assessment of neurological function, we followed-up heme-injected mice for 2 weeks using the rotarod, elevated body swing, and cylinder tests. Mice injected with the vehicle (sham), or autologous blood were used as controls. Results: Heme induced lipid peroxidation and inflammation in the brain. Moreover, heme increased the expression of HO-1 (heme oxygenase-1), ferritin, p62, and superoxide dismutase 2, and activated the MAPK signaling pathway promoting pro-IL (interleukin)-1β production and its cleavage to the active form. Heme-injected mice exhibited signs of brain damage and reactive astrogliosis around the injection site. Behavior deficits were observed after heme or autologous blood injection in comparison to sham-operated controls. In addition, behavior deficits and IL-1β production were reduced in Nlrp3 knockout mice in comparison to wild-type mice. Conclusions: Our results show that intracerebral heme injection induces neuroinflammation, and neurological deficits, in an NLRP3-dependent manner, suggesting that this is a feasible model to evaluate the role of heme in neurological disorders.

scholarly journals Protective Effects of a New C-Jun N-terminal Kinase Inhibitor in the Model of Global Cerebral Ischemia in Rats

Molecules ◽  
2019 ◽  
Vol 24 (9) ◽  
pp. 1722 ◽  
Author(s):  
Mark B. Plotnikov ◽  
Galina A. Chernysheva ◽  
Oleg I. Aliev ◽  
Vera I. Smol’iakova ◽  
Tatiana I. Fomina ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cerebral Ischemia ◽  
Endothelial Dysfunction ◽  
Neurological Deficit ◽  
Neuroprotective Effect ◽  
Global Cerebral Ischemia ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Area ◽  
Ca1 Area ◽  
The Brain

c-Jun N-terminal kinase (JNK) is activated by various brain insults and is implicated in neuronal injury triggered by reperfusion-induced oxidative stress. Some JNK inhibitors demonstrated neuroprotective potential in various models, including cerebral ischemia/reperfusion injury. The objective of the present work was to study the neuroprotective activity of a new specific JNK inhibitor, IQ-1S (11H-indeno[1,2-b]quinoxalin-11-one oxime sodium salt), in the model of global cerebral ischemia (GCI) in rats compared with citicoline (cytidine-5′-diphosphocholine), a drug approved for the treatment of acute ischemic stroke and to search for pleiotropic mechanisms of neuroprotective effects of IQ-1S. The experiments were performed in a rat model of ischemic stroke with three-vessel occlusion (model of 3VO) affecting the brachiocephalic artery, the left subclavian artery, and the left common carotid artery. After 7-min episode of GCI in rats, 25% of animals died, whereas survived animals had severe neurological deficit at days 1, 3, and 5 after GCI. At day 5 after GCI, we observing massive loss of pyramidal neurons in the hippocampal CA1 area, increase in lipid peroxidation products in the brain tissue, and decrease in local cerebral blood flow (LCBF) in the parietal cortex. Moreover, blood hyperviscosity syndrome and endothelial dysfunction were found after GCI. Administration of IQ-1S (intragastrically at a dose 50 mg/kg daily for 5 days) was associated with neuroprotective effect comparable with the effect of citicoline (intraperitoneal at a dose of 500 mg/kg, daily for 5 days).The neuroprotective effect was accompanied by a decrease in the number of animals with severe neurological deficit, an increase in the number of animals with moderate degree of neurological deficit compared with control GCI group, and an increase in the number of unaltered neurons in the hippocampal CA1 area along with a significant decrease in the number of neurons with irreversible morphological damage. In rats with IQ-1S administration, the LCBF was significantly higher (by 60%) compared with that in the GCI control. Treatment with IQ-1S also decreases blood viscosity and endothelial dysfunction. A concentration-dependent decrease (IC50 = 0.8 ± 0.3 μM) of tone in isolated carotid arterial rings constricted with phenylephrine was observed after IQ-1S application in vitro. We also found that IQ-1S decreased the intensity of the lipid peroxidation in the brain tissue in rats with GCI. 2.2-Diphenyl-1-picrylhydrazyl scavenging for IQ-1S in acetonitrile and acetone exceeded the corresponding values for ionol, a known antioxidant. Overall, these results suggest that the neuroprotective properties of IQ-1S may be mediated by improvement of cerebral microcirculation due to the enhanced vasorelaxation, beneficial effects on blood viscosity, attenuation of the endothelial dysfunction, and antioxidant/antiradical IQ-1S activity.

Acutely administered melatonin reduces oxidative damage in lung and brain induced by hyperbaric oxygen

1997 ◽  
Vol 83 (2) ◽  
pp. 354-358 ◽  
Author(s):  
Marta I. Pablos ◽  
Russel J. Reiter ◽  
Jin-Ing Chuang ◽  
Genaro G. Ortiz ◽  
Juan M. Guerrero ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Hyperbaric Oxygen ◽  
Antioxidative Enzymes ◽  
Melatonin Receptors ◽  
Cellular Damage ◽  
Oxygen Exposure ◽  
Glutathione Status ◽  
Hyperbaric Oxygen Exposure ◽  
The Brain

Pablos, Marta I., Russel J. Reiter, Jin-Ing Chuang, Genaro G. Ortiz, Juan M. Guerrero, Ewa Sewerynek, Maria T. Agapito, Daniela Melchiorri, Richard Lawrence, and Susan M. Deneke. Acutely administered melatonin reduces oxidative damage in lung and brain induced by hyperbaric oxygen. J. Appl. Physiol. 83(2): 354–358, 1997.—Hyperbaric oxygen exposure rapidly induces lipid peroxidation and cellular damage in a variety of organs. In this study, we demonstrate that the exposure of rats to 4 atmospheres of 100% oxygen for 90 min is associated with increased levels of lipid peroxidation products [malonaldehyde (MDA) and 4-hydroxyalkenals (4-HDA)] and with changes in the activities of two antioxidative enzymes [glutathione peroxidase (GPX) and glutathione reductase (GR)], as well as in the glutathione status in the lungs and in the brain. Products of lipid peroxidation increased after hyperbaric hyperoxia, both GPX and GR activities were decreased, and levels of total glutathione (reduced+oxidized) and glutathione disulfide (oxidized glutathione) increased in both lung and brain areas (cerebral cortex, hippocampus, hypothalamus, striatum, and cerebellum) but not in liver. When animals were injected with melatonin (10 mg/kg) immediately before the 90-min hyperbaric oxygen exposure, all measurements of oxidative damage were prevented and were similar to those in untreated control animals. Melatonin’s actions may be related to a variety of mechanisms, some of which remain to be identified, including its ability to directly scavenge free radicals and its induction of antioxidative enzymes via specific melatonin receptors.

scholarly journals Defensive role of silibinin against arsenic induced oxidative stress mediated dyslipidemia and neurotoxicity in rats

2016 ◽  
Vol 4 (1) ◽  
pp. 78 ◽  
Author(s):  
Muthumani Muthu ◽  
Sumedha Naroem Chanu ◽  
Shagirtha Kalist ◽  
Milton Prabu
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Properties ◽  
Brain Regions ◽  
Lipid Profiles ◽  
Antioxidant Enzyme Activities ◽  
Enzymatic Antioxidants ◽  
Ros Production ◽  
Protein Carbonyl Content ◽  
Defensive Role ◽  
The Brain

Arsenic (As) is an environmental toxic metalloid that is present in everywhere such as air, water and soil. Generally, inorganic arsenic has a tendency to be more toxic than organic arsenic. The present study was designed to determine whether oral administration of silibinin (SB), which has been shown to have substantial antioxidant properties, when pre-administered (75 mg/kg body weight) once daily for 4 weeks along with arsenic (5 mg/kg) would prevent arsenic-induced changes in antioxidant defense system, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX),glutathione-S-transferase (GST),glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), reduced glutathione (GSH), total sulfhydryl groups (TSH) and vitamin C in rat brain regions such as cortex, striatum, cerebellum, hippocampus and brain stem. Our study also examined the effect of SB over arsenic-induced reactive oxygen species (ROS) production and lipid peroxidation level (LPO) and protein carbonyl content (PC) in distinct brain regions of rats. Moreover, As also alters the lipid profiles such as total lipids, phospholipids, cholesterol, cerebrosides and gangliosides in various regions of the brain. Pre-administration of SB restores the altered enzymatic and non-enzymatic antioxidants, lipid profiles and also markedly reduced the ROS, LPO, PC and accumulation of As in various regions of the brain. These results suggested that arsenic-induced deficits in antioxidant enzyme activities and increase in ROS production and lipid peroxidation levels in brain regions can be remarkably prevented by pre-administration of SB. 

Effects of diazinon on acetylcholinesterase activity and lipid peroxidation in the brain of Oreochromis niloticus

2006 ◽  
Vol 21 (3) ◽  
pp. 241-245 ◽  
Author(s):  
Nevin Üner ◽  
Elif Özcan Oruç ◽  
Yusuf Sevgiler ◽  
Nesli Şahin ◽  
Hülya Durmaz ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Oreochromis Niloticus ◽  
Acetylcholinesterase Activity ◽  
The Brain
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