Protective effect of vitamin E, β-carotene and N-acetylcysteine from the brain oxidative stress induced in rats by lipopolysaccharide

Systemic inflammation causes brain oxidative stress, a prerequisite for neurodegeneration. In this study, we investigated the effect of the anesthetic agents propofol and fentanyl on brain oxidative stress during mild systemic endotoxemia induced by lipopolysaccharide (LPS) endotoxin. For this purpose, rats were administered LPS (400 μg/kg, intraperitoneally; i.p.), treated at the same time with different doses of propofol or fentanyl, i.p., and euthanized 4 h later. Other groups were treated with the saline, only propofol, or only fentanyl. Oxidative stress markers including malondialdehyde (MDA), nitric oxide (NO), and reduced glutathione (GSH) were determined. In addition, nuclear factor kappaB (NF-kB), paraoxonase-1 (PON-1), and butyrylcholinesterase (BChE) activities were measured in the brain tissue. Results showed that compared with the saline group, administration of LPS caused a marked and significant increase in brain MDA and NO combined with depletion of GSH and decreased PON-1 and BChE activities. Additionally, the active form of NF-kB was significantly increased in the brain of LPS only-treated rats. Treatment with propofol or fentanyl led to a marked and significant decrease in the levels of brain MDA and NO together with a significant increase in GSH and restoration of PON-1 and BChE activities. Furthermore, lower levels of active form of NF-kB were found following treatment with propofol or fentanyl compared with those in the LPS only group. Collectively, these results suggest that propofol and fentanyl exhibit an antioxidant action and attenuate the endotoxin-induced brain oxidative stress.

Download Full-text

The possible protective effects of vitamin E and selenium administration in oxidative stress caused by high doses of glucocorticoid administration in the brain of rats

Journal of Trace Elements in Medicine and Biology ◽

10.1016/j.jtemb.2017.10.005 ◽

2018 ◽

Vol 45 ◽

pp. 131-135 ◽

Cited By ~ 12

Author(s):

Ebru Beytut ◽

Seval Yilmaz ◽

Mesut Aksakal ◽

Seher Polat

Keyword(s):

Oxidative Stress ◽

Vitamin E ◽

Protective Effects ◽

Glucocorticoid Administration ◽

High Doses ◽

The Brain

Download Full-text

Protocatechuic acid protects brain mitochondrial function in streptozotocin-induced diabetic rats

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2015-0158 ◽

2015 ◽

Vol 40 (10) ◽

pp. 1078-1081 ◽

Cited By ~ 10

Author(s):

Yoswaris Semaming ◽

Jirapas Sripetchwandee ◽

Piangkwan Sa-nguanmoo ◽

Hiranya Pintana ◽

Patchareewan Pannangpetch ◽

...

Keyword(s):

Oxidative Stress ◽

Glycemic Control ◽

Mitochondrial Dysfunction ◽

Stress Reduction ◽

Mitochondrial Function ◽

Protocatechuic Acid ◽

Diabetic Rats ◽

Brain Oxidative Stress ◽

The Brain ◽

Brain Mitochondrial Function

Brain mitochondrial dysfunction has been demonstrated in diabetic animals with neurodegeneration. Protocatechuic acid (PCA), a major metabolite of anthocyanin, has been shown to exert glycemic control and oxidative stress reduction in the heart. However, its effects on oxidative stress and mitochondrial function in the brain under diabetic condition have never been investigated. We found that PCA exerted glycemic control, attenuates brain mitochondrial dysfunction, and contributes to the prevention of brain oxidative stress in diabetic rats.

Download Full-text

Effects of oral vitamin E and β-carotene supplementation on ultraviolet radiation–induced oxidative stress in human skin

American Journal of Clinical Nutrition ◽

10.1093/ajcn/80.5.1270 ◽

2004 ◽

Vol 80 (5) ◽

pp. 1270-1275 ◽

Cited By ~ 59

Author(s):

Frank McArdle ◽

Lesley E Rhodes ◽

Richard AG Parslew ◽

Graeme L Close ◽

Catherine IA Jack ◽

...

Keyword(s):

Oxidative Stress ◽

Vitamin E ◽

Ultraviolet Radiation ◽

Human Skin ◽

Oral Vitamin ◽

Radiation Induced ◽

Β Carotene

Download Full-text

Anxiety-related behavior in hyperhomocysteinemia induced by methionine nutritional overload in rats: role of the brain oxidative stress

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2015-0581 ◽

2016 ◽

Vol 94 (10) ◽

pp. 1074-1082 ◽

Cited By ~ 13

Author(s):

Dragan Hrncic ◽

Jelena Mikić ◽

Aleksandra Rasic-Markovic ◽

Milica Velimirović ◽

Tihomir Stojković ◽

...

Keyword(s):

Oxidative Stress ◽

Open Field ◽

Wistar Rats ◽

Brain Regions ◽

Oxidative Status ◽

Standard Diet ◽

Male Wistar Rats ◽

Brain Oxidative Stress ◽

The Brain

The aim of this study was to examine the effects of a methionine-enriched diet on anxiety-related behavior in rats and to determine the role of the brain oxidative status in these alterations. Adult male Wistar rats were fed from the 30th to 60th postnatal day with standard or methionine-enriched diet (double content comparing with standard diet: 7.7 g/kg). Rats were tested in open field and light–dark tests and afterwards oxidative status in the different brain regions were determined. Hyperhomocysteinemia induced by methionine-enriched diet in this study decreased the number of rearings, as well as the time that these animals spent in the center of the open field, but increased index of thigmotaxy. Oxidative status was selectively altered in the examined regions. Lipid peroxidation was significantly increased in the cortex and nc. caudatus of rats developing hyperhomocysteinemia, but unaltered in the hippocampus and thalamus. Based on the results of this research, it could be concluded that hyperhomocysteinemia induced by methionine nutritional overload increased anxiety-related behavior in rats. These proanxiogenic effects could be, at least in part, a consequence of oxidative stress in the rat brain.

Download Full-text

Experimental Chronic Prostatitis/Chronic Pelvic Pain Syndrome Increases Anxiety-Like Behavior: The Role of Brain Oxidative Stress, Serum Corticosterone, and Hippocampal Parvalbumin-Positive Interneurons

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/6687493 ◽

2021 ◽

Vol 2021 ◽

pp. 1-17

Author(s):

Nikola Šutulović ◽

Željko Grubač ◽

Sonja Šuvakov ◽

Djurdja Jerotić ◽

Nela Puškaš ◽

...

Keyword(s):

Oxidative Stress ◽

Pelvic Pain ◽

Chronic Prostatitis ◽

Chronic Pelvic Pain ◽

Chronic Pelvic Pain Syndrome ◽

Pain Syndrome ◽

Pelvic Pain Syndrome ◽

Serum Corticosterone ◽

Brain Oxidative Stress ◽

The Brain

Mechanisms of the brain-related comorbidities in chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) are still largely unknown, although CP/CPPS is one of the major urological problems in middle-aged men, while these neuropsychological incapacities considerably diminish life quality. The objectives of this study were to assess behavioral patterns in rats with CP/CPPS and to determine whether these patterns depend on alterations in the brain oxidative stress, corticosterone, and hippocampal parvalbumin-positive (PV+) interneurons. Adult male Wistar albino rats from CP/CPPS (intraprostatic injection of 3% λ-carrageenan, day 0) and sham (0.9% NaCl) groups were subjected to pain and anxiety-like behavior tests (days 2, 3, and 7). Afterwards, rats were sacrificed and biochemical and immunohistochemical analyses were performed. Scrotal allodynia and prostatitis were proven in CP/CPPS, but not in sham rats. Ethological tests (open field, elevated plus maze, and light/dark tests) revealed significantly increased anxiety-like behavior in rats with CP/CPPS comparing to their sham-operated mates starting from day 3, and there were significant intercorrelations among parameters of these tests. Increased oxidative stress in the hippocampus, thalamus, and cerebral cortex, as well as increased serum corticosterone levels and decreased number of hippocampal PV+ neurons, was shown in CP/CPPS rats, compared to sham rats. Increased anxiety-like behavior in CP/CPPS rats was significantly correlated with these brain biochemical and hippocampal immunohistochemical alterations. Therefore, the potential mechanisms of observed behavioral alterations in CP/CPPS rats could be the result of an interplay between increased brain oxidative stress, elevated serum corticosterone level, and loss of hippocampal PV+ interneurons.

Download Full-text