scholarly journals Environmental Enrichment Modified Epigenetic Mechanisms in SAMP8 Mouse Hippocampus by Reducing Oxidative Stress and Inflammaging and Achieving Neuroprotection

2016 ◽  
Vol 8 ◽  
Author(s):  
Christian Griñan-Ferré ◽  
Dolors Puigoriol-Illamola ◽  
Verónica Palomera-Ávalos ◽  
David Pérez-Cáceres ◽  
Júlia Companys-Alemany ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Environmental Enrichment ◽  
Epigenetic Mechanisms ◽  
Samp8 Mouse ◽  
Mouse Hippocampus

scholarly journals Environmental Enrichment Attenuates Oxidative Stress and Alters Detoxifying Enzymes in an A53T α-Synuclein Transgenic Mouse Model of Parkinson’s Disease

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 928
Author(s):  
Jung Hwa Seo ◽  
Seong-Woong Kang ◽  
Kyungri Kim ◽  
Soohyun Wi ◽  
Jang Woo Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Olfactory Bulb ◽  
Frontal Cortex ◽  
Brain Stem ◽  
Environmental Enrichment ◽  
Brain Regions ◽  
Wild Type ◽  
Detoxifying Enzymes

Although environmental enrichment (EE) is known to reduce oxidative stress in Parkinson’s disease (PD), the metabolic alternations for detoxifying endogenous and xenobiotic compounds according to various brain regions are not fully elucidated yet. This study aimed to further understand the role of EE on detoxifying enzymes, especially those participating in phase I of metabolism, by investigating the levels of enzymes in various brain regions such as the olfactory bulb, brain stem, frontal cortex, and striatum. Eight-month-old transgenic PD mice with the overexpression of human A53T α-synuclein and wild-type mice were randomly allocated to either standard cage condition or EE for 2 months. At 10 months of age, the expression of detoxifying enzymes was evaluated and compared with wild-type of the same age raised in standard cages. EE improved neurobehavioral outcomes such as olfactory and motor function in PD mice. EE-treated mice showed that oxidative stress was attenuated in the olfactory bulb, brain stem, and frontal cortex. EE also reduced apoptosis and induced cell proliferation in the subventricular zone of PD mice. The overexpression of detoxifying enzymes was observed in the olfactory bulb and brain stem of PD mice, which was ameliorated by EE. These findings were not apparent in the other experimental regions. These results suggest the stage of PD pathogenesis may differ according to brain region, and that EE has a protective effect on the PD pathogenesis by decreasing oxidative stress.

scholarly journals Environmental enrichment prevents behavioral deficits and oxidative stress caused by chronic cerebral hypoperfusion in the rat

Life Sciences ◽  
2012 ◽  
Vol 91 (1-2) ◽  
pp. 29-36 ◽  
Author(s):  
Fernanda Cechetti ◽  
Paulo Valdeci Worm ◽  
Gisele Lovatel ◽  
Felipe Moysés ◽  
Ionara Rodrigues Siqueira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Environmental Enrichment ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Behavioral Deficits ◽  
And Oxidative Stress

scholarly journals Radiation-Induced Normal Tissue Damage: Oxidative Stress and Epigenetic Mechanisms

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jinlong Wei ◽  
Bin Wang ◽  
Huanhuan Wang ◽  
Lingbin Meng ◽  
Qin Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tissue Damage ◽  
Normal Tissue ◽  
Noncoding Rna ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Redox System ◽  
Epigenetic Mechanisms ◽  
Rna Regulation ◽  
Normal Tissue Damage ◽  
Radiation Induced

Radiotherapy (RT) is currently one of the leading treatments for various cancers; however, it may cause damage to healthy tissue, with both short-term and long-term side effects. Severe radiation-induced normal tissue damage (RINTD) frequently has a significant influence on the progress of RT and the survival and prognosis of patients. The redox system has been shown to play an important role in the early and late effects of RINTD. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are the main sources of RINTD. The free radicals produced by irradiation can upregulate several enzymes including nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), lipoxygenases (LOXs), nitric oxide synthase (NOS), and cyclooxygenases (COXs). These enzymes are expressed in distinct ways in various cells, tissues, and organs and participate in the RINTD process through different regulatory mechanisms. In recent years, several studies have demonstrated that epigenetic modulators play an important role in the RINTD process. Epigenetic modifications primarily contain noncoding RNA regulation, histone modifications, and DNA methylation. In this article, we will review the role of oxidative stress and epigenetic mechanisms in radiation damage, and explore possible prophylactic and therapeutic strategies for RINTD.

Alteration of Energy Metabolism and Antioxidative Processing in the Hippocampus of Rats Reared in Long-Term Environmental Enrichment

2016 ◽  
Vol 38 (3) ◽  
pp. 186-194 ◽  
Author(s):  
Hee Kang ◽  
Dong-Hee Choi ◽  
Su-Kang Kim ◽  
Jongmin Lee ◽  
Youn-Jung Kim
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Protein Expression ◽  
Environmental Enrichment ◽  
Synaptic Activity ◽  
Antioxidant Defenses ◽  
Laboratory Animals ◽  
Oxidative Stress Marker ◽  
Altered Expression

Environmental enrichment (EE) is a typical experimental method that promotes levels of novelty and complexity that enhance experience-dependent neuroplasticity and cognitive behavior function in laboratory animals. Early EE is associated with resilience in the face of later-life challenges. Since increased synaptic activity enhances endogenous neuronal antioxidant defenses, we hypothesized that long-term EE beginning at an early stage may alter the levels of oxidative stress. We investigated global protein expression and oxidative stress in hippocampal proteins from rats nurtured for a 6-month EE beginning in the prenatal period. The analysis of protein expression was carried out using 2-dimensional gel electrophoresis with matrix-associated laser desorption ionization time-of-flight mass spectrometry. Proteins with altered expression were involved in energy metabolism (phosphoglycerate mutase 1, α-enolase isoform 1, adenylate kinase 1, and triose phosphate isomerase) and antioxidant enzymes (superoxide dismutase 1, glutathione S-transferase ω type 1, peroxiredoxin 5, DJ-1, and glial maturation factor β). Using Western blot assays, some of the proteins with altered expression and NADPH oxidase 2 were confirmed to be decreased. Further confirmation was demonstrated with attenuated expression of 7,8-dihydro-8-oxo-deoxyguanine, a DNA oxidative stress marker, in the hippocampus of EE group rats. Our data demonstrate that a long-term EE program beginning in the prenatal and early postnatal phase of development modulates energy metabolism and reduced oxidant stress possibly through enhanced synaptic activity. We provide evidence that EE can be developed as a tool to protect the brain from oxidative stress-induced injury.

Neuroprotective effects of N-adamantyl-4-methylthiazol-2-amine against amyloid β-induced oxidative stress in mouse hippocampus

2017 ◽  
Vol 128 ◽  
pp. 22-28 ◽  
Author(s):  
Jiae Kim ◽  
Chang Hun Cho ◽  
Hoh-Gyu Hahn ◽  
Soo-Young Choi ◽  
Sung-Woo Cho
Keyword(s):  
Oxidative Stress ◽  
Amyloid Β ◽  
Neuroprotective Effects ◽  
Mouse Hippocampus

Expression of a novel gene containing ankyrin-repeat in SAMP8 mouse hippocampus

2004 ◽  
Vol 1260 ◽  
pp. 367-371
Author(s):  
Naoshi Yamamura ◽  
Nobuya Koike ◽  
Yasunobu Okuma ◽  
Takashi Uehara ◽  
Yasuyuki Nomura ◽  
...  
Keyword(s):  
Ankyrin Repeat ◽  
Novel Gene ◽  
Samp8 Mouse ◽  
Mouse Hippocampus

scholarly journals Environmental cadmium exposure: a possible factor in the pathogenesis of preeclampsia

2019 ◽  
Vol 7 (12) ◽  
pp. 4818
Author(s):  
Nnenna L. Nwobi ◽  
Joshua O. Owolabi ◽  
John O. Sotunsa ◽  
Joseph C. Nwobi ◽  
Razaq A. Abiodun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Developing Countries ◽  
Toxic Metal ◽  
Pregnancy Complication ◽  
Cadmium Exposure ◽  
Epigenetic Mechanisms ◽  
Molecular Systems ◽  
Specific Syndrome ◽  
Increased Risk ◽  
Remote Association

Cadmium is a toxic metal, an environmental contaminant and a multi-organ poison which has been implicated in the derangement of a number of biological and molecular systems. Exposure to cadmium is a serious global health threat particularly in developing countries and pregnant women are at great risk, This is because they have increased gastrointestinal absorption and retention of cadmium and the tendency for increased risk of complications owing to its toxic effects. Preeclampsia is a pregnancy complication characterized by the development of onset of hypertension and significant proteinuria after 20 weeks of gestation or during labour and/or within 48 hours of delivery. This pregnancy-specific syndrome is a leading cause of maternal death particularly in developing countries. Several reports have provided evidence of remote association between preeclampsia and cadmium but the mechanism of the involment of this toxic metal in this disease is still surrounded with uncertainty. Some possible mechanistic pathways such as induction of oxidative stress, acting as an antimetabolite to zinc and deregulation of epigenetic mechanisms have been elucidated in this article may be interconnected, work synergistically or act independently. However, pertinent to understand them in a bid to possibly prevent the disease or forestall its devastating consequences. Environmental cadmium exposure may be considered a factor that merits further serious attention in the continuous search for the precise an etiology of preeclampsia particularly in developing countries that experience uncontrolled cadmium release into the environment.

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