DHA-Rich fish oil and Tualang honey reduce stress-induced oxidative damage in the brain

The effects of modafinil (MD) on behavioral and oxidative damage to protein and lipid in the brain of rats were evaluated. Wistar rats were given a single administration by gavage of water or MD (75, 150, or 300 mg/kg). Behavioral parameters were evaluated in open-field apparatus 1, 2, and 3 h after drug administration. Thiobarbituric acid reactive substances (TBARS) and protein carbonyl formation were measured in the brain. MD increased locomotor activity at the highest dose 1 and 3 h after administration. MD administration at the dose of 300 mg/kg increased visits to the center of open-field 1 h after administration; however, 3 h after administration, all administered doses of MD increased visits to the open-field center. MD 300 mg/kg increased lipid damage in the amygdala, hippocampus, and striatum. Besides, MD increased protein damage in the prefrontal cortex, amygdala, and hippocampus; however, this effect varies depending on the dose administered. In contrast, the administration of MD 75 and 300 mg/kg decreased the protein damage in the striatum. This study demonstrated that the MD administration induces behavioral changes, which was depending on the dose used. In addition, the effects of MD on oxidative damage parameters seemed to be in specific brain region and doses.

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Mn Inhibits GSH Synthesis via Downregulation of Neuronal EAAC1 and Astrocytic xCT to Cause Oxidative Damage in the Striatum of Mice

Oxidative Medicine and Cellular Longevity ◽

10.1155/2018/4235695 ◽

2018 ◽

Vol 2018 ◽

pp. 1-15 ◽

Cited By ~ 7

Author(s):

Xinxin Yang ◽

Haibo Yang ◽

Fengdi Wu ◽

Zhipeng Qi ◽

Jiashuo Li ◽

...

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Dependent Manner ◽

Protein Levels ◽

Key Factor ◽

Protein Sulfhydryl ◽

Mrna And Protein Expression ◽

The Brain

Excessive manganese (Mn) can accumulate in the striatum of the brain following overexposure. Oxidative stress is a well-recognized mechanism in Mn-induced neurotoxicity. It has been proven that glutathione (GSH) depletion is a key factor in oxidative damage during Mn exposure. However, no study has focused on the dysfunction of GSH synthesis-induced oxidative stress in the brain during Mn exposure. The objective of the present study was to explore the mechanism of Mn disruption of GSH synthesis via EAAC1 and xCT in vitro and in vivo. Primary neurons and astrocytes were cultured and treated with different doses of Mn to observe the state of cells and levels of GSH and reactive oxygen species (ROS) and measure mRNA and protein expression of EAAC1 and xCT. Mice were randomly divided into seven groups, which received saline, 12.5, 25, and 50 mg/kg MnCl2, 500 mg/kg AAH (EAAC1 inhibitor) + 50 mg/kg MnCl2, 75 mg/kg SSZ (xCT inhibitor) + 50 mg/kg MnCl2, and 100 mg/kg NAC (GSH rescuer) + 50 mg/kg MnCl2 once daily for two weeks. Then, levels of EAAC1, xCT, ROS, GSH, malondialdehyde (MDA), protein sulfhydryl, carbonyl, 8-hydroxy-2-deoxyguanosine (8-OHdG), and morphological and ultrastructural features in the striatum of mice were measured. Mn reduced protein levels, mRNA expression, and immunofluorescence intensity of EAAC1 and xCT. Mn also decreased the level of GSH, sulfhydryl, and increased ROS, MDA, 8-OHdG, and carbonyl in a dose-dependent manner. Injury-related pathological and ultrastructure changes in the striatum of mice were significantly present. In conclusion, excessive exposure to Mn disrupts GSH synthesis through inhibition of EAAC1 and xCT to trigger oxidative damage in the striatum.

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Pomegranate from Oman Alleviates the Brain Oxidative Damage in Transgenic Mouse Model of Alzheimer’s Disease

Journal of Traditional and Complementary Medicine ◽

10.4103/2225-4110.139107 ◽

2014 ◽

Vol 4 (4) ◽

pp. 232-238 ◽

Cited By ~ 40

Author(s):

Selvaraju Subash ◽

Musthafa Mohamed Essa ◽

Abdullah Al-Asmi ◽

Samir Al-Adawi ◽

Ragini Vaishnav ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Mouse Model ◽

Oxidative Damage ◽

Transgenic Mouse ◽

Transgenic Mouse Model ◽

Model Of Alzheimer’S Disease ◽

The Brain

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Resveratrol protects the brain against oxidative damage in a dopaminergic animal model of mania

Metabolic Brain Disease ◽

10.1007/s11011-019-00408-1 ◽

2019 ◽

Vol 34 (3) ◽

pp. 941-950 ◽

Cited By ~ 2

Author(s):

Samira Menegas ◽

Camila L. Ferreira ◽

José Henrique Cararo ◽

Fernanda F. Gava ◽

Gustavo C. Dal-Pont ◽

...

Keyword(s):

Animal Model ◽

Oxidative Damage ◽

The Brain

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Fish oil and 3-thia fatty acid have additive effects on lipid metabolism but antagonistic effects on oxidative damage when fed to rats for 50 weeks

The Journal of Nutritional Biochemistry ◽

10.1016/j.jnutbio.2011.08.006 ◽

2012 ◽

Vol 23 (11) ◽

pp. 1384-1393 ◽

Cited By ~ 23

Author(s):

Natalya Filipchuk Vigerust ◽

Daniel Cacabelos ◽

Lena Burri ◽

Kjetil Berge ◽

Hege Wergedahl ◽

...

Keyword(s):

Fatty Acid ◽

Lipid Metabolism ◽

Oxidative Damage ◽

Fish Oil ◽

Additive Effects ◽

Antagonistic Effects

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Oxidative damage to DNA in plaques of MS brains

Multiple Sclerosis Journal ◽

10.1177/135245859800400503 ◽

1998 ◽

Vol 4 (5) ◽

pp. 413-418 ◽

Cited By ~ 84

Author(s):

Olga Vladimirova ◽

John O'Connor ◽

Alan Cahill ◽

Hansjuerg Alder ◽

Catalin Butunoi ◽

...

Keyword(s):

Oxidative Damage ◽

Degenerative Process ◽

Oxidative Markers ◽

Normal Appearing White Matter ◽

The Central Nervous System ◽

Cortical Regions ◽

Tissue Alterations ◽

Oxidative Damage To Dna ◽

The Brain ◽

Cerebellar Symptoms

A major cause of clinical disability in multiple sclerosis (MS) is related to a degenerative process in the central nervous system (CNS) which ultimately develops from a potentially reversible inflammation and demyelination. The mechanism of this degenerative process within MS lesions is not completely understood. We hypothesize that oxidative damage to DNA secondary to inflammation may contribute to irreversible tissue alterations in a plaque. To test this assumption, we determined the level of a DNA oxidative marker, 8-hydroxy-deoxy-guanosine (8-OH-dG) in the normal appearing white matter (NAWM), plaque and cortical regions of cerebella from MS patients who suffered from severe cerebellar symptoms during the course of the disease, and in NAWM and cortical regions of cerebella from non-neurological controls. We found a significant increase in DNA oxidation within plaques compared to NAWM specimens in MS cerebella. A tendency for increase of oxidative markers in normal appearing cortical tissues located in the proximity of MS plaques was also observed when compared to those in control cortical specimens. Oxidative damage to DNA in MS lesions, and in neuron rich areas located in the proximity of these lesions is likely related to the release of reactive oxygen species (ROS) and nitric oxide (NO) during inflammation in the brain. This biochemical impairment of DNA and of other macromolecules may contribute to the development of severe clinical disability through the induction of degenerative changes within and outside of plaques in MS brains.

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Apolipoprotein E deletion has no effect on copper-induced oxidative stress in the mice brain

Bioscience Reports ◽

10.1042/bsr20180719 ◽

2018 ◽

Vol 38 (5) ◽

Author(s):

Yuan Chen ◽

Liang Wang ◽

Jiang-hui Geng ◽

Hui-feng Zhang ◽

Li Guo

Keyword(s):

Oxidative Damage ◽

Apolipoprotein E ◽

Copper Accumulation ◽

Wild Type ◽

Quinone Oxidoreductase ◽

Neuroprotective Effects ◽

Mice Brain ◽

Effect Of Copper ◽

Actin Expression ◽

The Brain

The current study was designed to investigate effect of copper administration on oxidative damage to the brain in ApoE−/− mice and to explore the putative neuroprotective effects rendered by apolipoprotein E (ApoE). Male C57BL/6 ApoE−/− and wild-type mice were randomly assigned into four groups, ApoE−/− mice wild-type mice treated with either copper or saline. Copper sulphate pentahydrate or saline (200 µl) were administered intragastrically daily for 12 weeks. Expression of malondialdehyde, superoxide dismutase (SOD), hemeoxygenase 1 (HO-1), and NAD(P)H: quinone oxidoreductase 1 (NQO1) were determined by a combination of biochemical assays. The concentration of copper in the brain of C57BL/6 mice and ApoE−/− mice treated by copper significantly increased compared with mice treated by saline (P=0.0099 and P=0.0443). Compared with the C57BL/6 mice treated by copper, the level of the ApoE−/− mice treated by copper was higher (P=0.018). TBARS and SOD activities or the expressions of NQO1 and HO-1 in the brain were not significantly different amongst the four experimental groups of mice. The relative value of NQO1/β-actin expression in the brain of the ApoE−/− mice was similar in both saline and copper administration experimental groups. However, Western blot analysis showed that NQO1 expression was significantly higher in the ApoE−/− mice brain treated with saline compared with saline treated wild-type mice (P=0.0449). ApoE does not function in protecting the brain from oxidative damage resulting from copper build-up in Wilson’s disease, but may play a role in regulating copper accumulation in the brain.

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

Journal of Applied Physiology ◽

10.1152/jappl.1997.83.2.354 ◽

1997 ◽

Vol 83 (2) ◽

pp. 354-358 ◽

Cited By ~ 68

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.

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