Hypoxia-Induced Lipid Peroxidation in the Brain During Postnatal Ontogenesis

Reactive oxygen species (ROS) are common products of the physiological metabolic reactions, which are associated with cell signaling and with the pathogenesis of various nervous disorders. The brain tissue has the high rate of oxidative metabolic activity, high concentration of polyunsaturated fatty acids in membrane lipids, presence of iron ions and low capacity of antioxidant enzymes, which makes the brain very susceptible to ROS action and lipid peroxidation formation. Membranes of brain cortex show a higher production of thiobarbituric acid-reactive substances (TBARS) in prooxidant system (ADP.Fe3+/NADPH) than membranes from the heart or kidney. Lipid peroxidation influences numerous cellular functions through membrane-bound receptors or enzymes. The rate of brain cortex Na+,K+-ATPase inhibition correlates well with the increase of TBARS or conjugated dienes and with changes of membrane fluidity. The experimental model of short-term hypoxia (simulating an altitude of 9000 m for 30 min) shows remarkable increase in TBARS in four different parts of the rat brain (cortex, subcortical structures, cerebellum and medulla oblongata) during the postnatal development of Wistar rat of both sexes. Young rats and males are more sensitive to oxygen changes than adult rats and females, respectively. Under normoxia or hypobaric hypoxia both ontogenetic aspects and sex differences play a major role in establishing the activity of erythrocyte catalase, which is an important part of the antioxidant defense of the organism. Rats pretreated with L-carnitine (and its derivatives) have lower TBARS levels after the exposure to hypobaric hypoxia. The protective effect of L-carnitine is comparable with the effect of tocopherol, well-known reactive species scavenger. Moreover, the plasma lactate increases after a short-term hypobaric hypoxia and decreases in L-carnitine pretreated rats. Acute hypobaric hypoxia and/or L-carnitine-pretreatment modify serum but not brain lactate dehydrogenase activity. The obtained data seem to be important because the variations in oxygen tension represent specific signals of regulating the activity of many specific systems in the organism.

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Intermittent Hypobaric Hypoxic Preconditioning Provides Neuroprotection by Increasing Antioxidant Activity, Erythropoietin Expression and Preventing Apoptosis and Astrogliosis in the Brain of Adult Rats Exposed to Acute Severe Hypoxia

International Journal of Molecular Sciences ◽

10.3390/ijms22105272 ◽

2021 ◽

Vol 22 (10) ◽

pp. 5272

Author(s):

Débora Coimbra-Costa ◽

Fernando Garzón ◽

Norma Alva ◽

Tiago C. C. Pinto ◽

Fernando Aguado ◽

...

Keyword(s):

Oxidative Stress ◽

Hypobaric Hypoxia ◽

Hypoxic Preconditioning ◽

Severe Hypoxia ◽

Efficient Tool ◽

Adult Rats ◽

Therapeutic Benefits ◽

Background Exposure ◽

The Brain ◽

Apoptotic Cascade

Background: Exposure to intermittent hypoxia has been demonstrated to be an efficient tool for hypoxic preconditioning, preventing damage to cells and demonstrating therapeutic benefits. We aimed to evaluate the effects of respiratory intermittent hypobaric hypoxia (IHH) to avoid brain injury caused by exposure to acute severe hypoxia (ASH). Methods: biomarkers of oxidative damage, mitochondrial apoptosis, and transcriptional factors in response to hypoxia were assessed by Western blot and immunohistochemistry in brain tissue. Four groups of rats were used: (1) normoxic (NOR), (2) exposed to ASH (FiO2 7% for 6 h), (3) exposed to IHH for 3 h per day over 8 days at 460 mmHg, and (4) ASH preconditioned after IHH. Results: ASH animals underwent increased oxidative-stress-related parameters, an upregulation in apoptotic proteins and had astrocytes with phenotype forms compatible with severe diffuse reactive astrogliosis. These effects were attenuated and even prevented when the animals were preconditioned with IHH. These changes paralleled the inhibition of NF-κB expression and the increase of erythropoietin (EPO) levels in the brain. Conclusions: IHH exerted neuroprotection against ASH-induced oxidative injury by preventing oxidative stress and inhibiting the apoptotic cascade, which was associated with NF-κB downregulation and EPO upregulation.

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Antioxidant activity of catecholamines as a chane of them antistress effect

Reviews on Clinical Pharmacology and Drug Therapy ◽

10.17816/rcf12243-46 ◽

2014 ◽

Vol 12 (2) ◽

pp. 43-46 ◽

Cited By ~ 1

Author(s):

Georgii Nolianovich Shilov ◽

Vladislav Adamovich Ivanyutin

Keyword(s):

Lipid Peroxidation ◽

Antioxidant Activity ◽

Brain Cortex ◽

Malonic Dialdehyde ◽

Receptor Activation ◽

Antioxidant Effect ◽

Water Soluble ◽

Antioxidant Mechanism ◽

Antistress Effect ◽

The Brain

The antioxidant activity of some native catecholamines (adrenaline, noradrenaline, dopamine), water-soluble antioxidant emoxipine, agonist (apomorphine) and antagonist (haloperidol) of dopamine receptors was assessed as their influence on malonic dialdehyde content and products of lipid peroxidation in homogenates and suspension of the rat cortical brain cells. All catecholamines (adrenaline, noradrenaline, dopamine in concentrations of 10-4 M and 10-5 M) possessed a high (compartable with emoxipine) antioxidant activity. The most antioxidant effect was registered in apomorphine. The inhibitory action of apomorphine on lipid peroxidation in the brain cortex can be a result from both dopamine receptor activation and “direct” antioxidant mechanism.

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Expression of GFRα-1, receptor for GDNF, in rat brain capillary during postnatal development of the BBB

AJP Cell Physiology ◽

10.1152/ajpcell.2000.279.2.c361 ◽

2000 ◽

Vol 279 (2) ◽

pp. C361-C368 ◽

Cited By ~ 43

Author(s):

Hiroyuki Utsumi ◽

Hideki Chiba ◽

Yasuhiro Kamimura ◽

Makoto Osanai ◽

Yo Igarashi ◽

...

Keyword(s):

Postnatal Development ◽

Evans Blue ◽

Brain Cortex ◽

Reciprocal Relation ◽

Adult Rats ◽

Brain Capillary ◽

Old Rats ◽

Porcine Endothelial Cells ◽

The Brain ◽

Junction Proteins

It is well known that the blood-brain barrier (BBB) matures at ∼2 wk after birth in the rat. Recently, we showed that glial cell line-derived neurotrophic factor (GDNF) enhances the barrier function of porcine endothelial cells forming the BBB in culture. In the present study, we examined the relation between permeability of the BBB, using Evans blue as a tracer, and expression of the GDNF family receptor (GFRα-1) during postnatal development of the BBB. Morphometric analysis showed that exudation of Evans blue from capillaries of the cerebral cortex progressively decreased until postnatal day 21. Inversely, immunohistochemical examinations showed expression of GFRα-1 in the capillaries at postnatal day 3 and expression that reached the same levels as observed in adult rats by postnatal day 10. However, c- ret, which is thought to mediate a signal evoked by binding of GDNF to GFRα-1, was not expressed in the capillaries of the brain cortex in 3-mo-old rats. On the other hand, the tight junction proteins occludin and ZO-1 appeared to be fully expressed at birth. The reciprocal relation between GFRα-1 expression and the permeability of the BBB strongly suggests active participation of GDNF in postnatal development of the BBB, although the mechanism(s) involved is still veiled.

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Effect of diets with goat milk fat supplemented with exercise on anxiety and oxidative stress in the brains of adult rats

Food & Function ◽

10.1039/c7fo01764b ◽

2018 ◽

Vol 9 (5) ◽

pp. 2891-2901 ◽

Cited By ~ 5

Author(s):

Mayara Queiroga Barbosa ◽

Rita de Cássia Ramos Egypto Queiroga ◽

Camila Carolina de Menezes Santos Bertozzo ◽

Daline Fernandes de Souza Araújo ◽

Louise Iara Gomes Oliveira ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Milk Fat ◽

Goat Milk ◽

Anxiolytic Effect ◽

Adult Rats ◽

Exercise Induced ◽

The Brain ◽

And Oxidative Stress

Goat milk fat induced anxiolytic effect in sedentary animals; exercise promoted lipid peroxidation in the brain; exercise induced anxiety.

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Effects of 17β-estradiol and antioxidant administration on oxidative stress and insulin resistance in ovariectomized rats

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y11-053 ◽

2011 ◽

Vol 89 (7) ◽

pp. 497-504 ◽

Cited By ~ 27

Author(s):

Amr M. Abbas ◽

Ayman Z. Elsamanoudy

Keyword(s):

Insulin Resistance ◽

Lipid Peroxidation ◽

Superoxide Dismutase ◽

Vitamin E ◽

Brain Cortex ◽

Fasting Glucose ◽

Ovariectomized Rats ◽

Ovx Rats ◽

17Β Estradiol ◽

The Brain

The prevalence of insulin resistance syndrome increases during menopause with the overproduction of reactive oxygen species and impairment of the free radical scavenger function. Therefore, we investigated the effects of 17β-estradiol (E2) and vitamin E, as an antioxidant, on lipid peroxidation and antioxidant levels in the brain cortex and liver of ovariectomized rats as well as on insulin resistance in those rats. Forty female Sprague–Dawley rats, 3 months of age and weighing 231.5 ± 9.4 g, were divided into 4 groups: sham, ovariectomized (OVX), OVX treated with E2 (40 µg/kg subcutaneously), and OVX treated with E2 and vitamin E (100 mg/kg intraperitoneally). The 4 groups received the appropriate treatment every day for 8 weeks. Levels of glutathione, glutathione peroxidase, superoxide dismutase , catalase, and malondialdehyde in the brain cortex and liver of ovariectomized rats were measured. Also, fasting plasma insulin, glucose, and homeostatis model assessment of insulin resistance (HOMA-IR) were determined. Malondialdehyde increased and antioxidants (glutathione, glutathione peroxidase, catalase, superoxide dismutase) decreased in the brain cortex and liver of OVX rats. Also, fasting glucose, insulin, and HOMA-IR increased in OVX rats. E2 and E2 plus vitamin E decreased malondialdehyde and increased antioxidants in the brain cortex and liver of OVX rats. Moreover, they decreased fasting glucose, insulin, and HOMA-IR in ovariectomized rats. This study demonstrates that E2 and E2 plus vitamin E supplementation to OVX rats may improve insulin resistance, strengthen the antioxidant system, and reduce lipid peroxidation.

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Melatonin modulates 900 MHz microwave-induced lipid peroxidation changes in rat brain

Toxicology and Industrial Health ◽

10.1191/0748233706th263oa ◽

2006 ◽

Vol 22 (5) ◽

pp. 211-216 ◽

Cited By ~ 45

Author(s):

Halis Köylü ◽

Hakan Mollaoglu ◽

Fehmi Ozguner ◽

Mustafa Nazýroölu ◽

Namýk Delibap

Keyword(s):

Lipid Peroxidation ◽

Brain Cortex ◽

Treated Group ◽

Male Rats ◽

Control Group ◽

Protective Effects ◽

Sprague Dawley ◽

Melatonin Administration ◽

Anti Oxidant ◽

The Brain

Microwaves (MW) from cellular phones may affect biological systems by increasing free radicals, which may enhance lipid peroxidation levels of the brain, thus leading to oxidative damage. Melatonin is synthesized in and secreted by the pineal gland at night and exhibits anti-oxidant properties. Several studies suggest that supplementation with anti-oxidant can influence MW-induced brain damage. The present study was designed to determine the effects of MW on the brain lipid peroxidation system, and the possible protective effects of melatonin on brain degeneration induced by MW. Twenty-eight Sprague-Dawley male rats were randomly divided into three groups as follows: (1) sham-operated control group (N-8); (2) study 900-MHz MW-exposed group (N-8); and (3) 900-MHz MW-exposed-melatonin (100 mg/kg sc before daily MW exposure treated group) (N-10). Cortex brain and hippocampus tissues were removed to study the levels of lipid peroxidation as malonyl dialdehyde. The levels of lipid peroxidation in the brain cortex and hippocampus increased in the MW group compared with the control group, although the levels in the hippocampus were decreased by MW-melatonin administration. The brain cortex lipid peroxidation levels were unaffected by melatonin treatment. We conclude that melatonin may prevent MW-induced oxidative changes in the hippocampus by strengthening the anti-oxidant defense system, by reducing oxidative stress products.

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Polychlorinated biphenyl induced hepatocyte alterations

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010012789x ◽

1987 ◽

Vol 45 ◽

pp. 716-717

Author(s):

D.N. Collins ◽

J.N. Turner ◽

K.O. Brosch ◽

R.F. Seegal

Keyword(s):

Lipid Droplets ◽

Wistar Rats ◽

Homovanillic Acid ◽

Polychlorinated Biphenyl ◽

Corn Oil ◽

Environmental Pollutants ◽

Short Term ◽

Pcb Congeners ◽

Urinary Levels ◽

The Brain

Polychlorinated biphenyls (PCBs) are a ubiquitous class of environmental pollutants with toxic and hepatocellular effects, including accumulation of fat, proliferated smooth endoplasmic recticulum (SER), and concentric membrane arrays (CMAs) (1-3). The CMAs appear to be a membrane storage and degeneration organelle composed of a large number of concentric membrane layers usually surrounding one or more lipid droplets often with internalized membrane fragments (3). The present study documents liver alteration after a short term single dose exposure to PCBs with high chlorine content, and correlates them with reported animal weights and central nervous system (CNS) measures. In the brain PCB congeners were concentrated in particular regions (4) while catecholamine concentrations were decreased (4-6). Urinary levels of homovanillic acid a dopamine metabolite were evaluated (7).Wistar rats were gavaged with corn oil (6 controls), or with a 1:1 mixture of Aroclor 1254 and 1260 in corn oil at 500 or 1000 mg total PCB/kg (6 at each level).

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Melatonin reduces high levels of lipid peroxidation induced by potassium iodate in porcine thyroid

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000628 ◽

2019 ◽

pp. 1-7 ◽

Cited By ~ 1

Author(s):

Paulina Iwan ◽

Jan Stepniak ◽

Malgorzata Karbownik-Lewinska

Keyword(s):

Lipid Peroxidation ◽

Oxidative Damage ◽

Membrane Lipids ◽

Chemical Properties ◽

Iodine Concentration ◽

Free Radical Scavenger ◽

Radical Scavenger ◽

Protective Effects ◽

Potassium Iodate ◽

Hormone Synthesis

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.

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Morphological Changes in the Brain of Acutely Ill and Weight-Recovered Patients with Anorexia Nervosa

Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie ◽

10.1024/1422-4917/a000265 ◽

2014 ◽

Vol 42 (1) ◽

pp. 7-18 ◽

Cited By ~ 56

Author(s):

Jochen Seitz ◽

Katharina Bühren ◽

Georg G. von Polier ◽

Nicole Heussen ◽

Beate Herpertz-Dahlmann ◽

...

Keyword(s):

Anorexia Nervosa ◽

Cognitive Deficits ◽

Time Course ◽

Morphological Changes ◽

Meta Analysis ◽

Short Term ◽

Clinical Prognosis ◽

Qualitative Review ◽

Brain Changes ◽

The Brain

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.

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