scholarly journals The investigation into neurotoxicity mechanisms of Nonylphenol: A narrative review

2020 ◽  
Vol 18 ◽  
Author(s):  
Mandana Lotfi ◽  
Amir Hosseyn Hasanpour ◽  
Ali Akbar Moghadamnia ◽  
Sohrab Kazemi
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Health Hazard ◽  
Learning Disorders ◽  
Inflammatory Factors ◽  
Postnatal Exposure ◽  
Memory And Learning ◽  
Nonylphenol Ethoxylate ◽  
Intracellular Calcium Ion ◽  
The Brain

Background: Nonylphenol (NP), as a chemical compound that widely used in industry, is the result of the nonylphenol ethoxylate decomposition and it is known as an estrogen-like compound. Numerous studies and researches have shown that it has many destructive functions of various organs such as the brain. This toxicant causes oxidative stress in the cortex and hippocampus cells, which are two essential regions to preserve memory and learning in the brain. Methods: This review examines recent findings to better understand the mechanisms of NP neurotoxicity. We used Scopus, Google Scholar and PubMed databases to find articles with focus on the destructive effects of NP on the oxidative stress pathway and its defense mechanisms. Results: NP has potential human health hazard associated with gestational, peri- and postnatal exposure. NP can disrupt brain homeostasis in different ways, such as activation of inflammatory factors in brain especially in hippocampus and cortex, disruption of the cell cycle, changes in neuron, dendrites and synapses morphology, disruption of extra and intracellular calcium ion balance and also memory and learning disorders

scholarly journals The Effect of a Traditional Preparation Containing Piper nigrum L. and Bunium persicum (Boiss.) B.Fedtsch. on Immobility Stress-Induced Memory Loss in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Marzieh Rashedinia ◽  
Mina Mojarad ◽  
Forouzan Khodaei ◽  
Ali Sahragard ◽  
Mohammad Javad Khoshnoud ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Motor Coordination ◽  
Black Pepper ◽  
Aqueous Extracts ◽  
Memory And Learning ◽  
Hydroalcoholic Extract ◽  
The Brain ◽  
And Oxidative Stress

Objective. Alzheimer’s disease is a progressive, age-related, and neurodegenerative disease characterized by mental decline. The exact cause of Alzheimer’s disease is unclear, but cholinergic dysfunction, protein accumulation, and oxidative stress are among the most important hypotheses. The main purpose of our study was to investigate the effects of aqueous and hydroalcoholic extract combination of these two medicinal plants, black pepper and cumin (as a related formulation in traditional Persian medicine), on memory and learning of an immobilized stress animal model. Methods. In this study, hydroalcoholic and aqueous extracts of cumin and black pepper fruits were prepared. Six groups of mice were treated orally for 2 weeks: control group, immobility stress, and stress-induced immobility mice received different doses of the hydroalcoholic extract (100 and 200 mg/kg) and aqueous extract (100 and 200 mg/kg). The shuttle box, novel object detection, and rotarod test were used to evaluate memory and learning. The activities of acetylcholinesterase, catalase (CAT), and superoxide dismutase (SOD) and the level of reduced glutathione (GSH) and malondialdehyde (MDA) were measured in the brain tissue. Results. Immobility stress significantly reduced learning and motor coordination. Furthermore, MDA levels and acetylcholinesterase activity were significantly increased, while CAT and SOD activities were significantly reduced in the brain of immobility-induced stress mice. Other findings indicated that hydroalcoholic and aqueous extracts (100 and 200 mg/kg) of cumin and black pepper fruits have an improving effect on animal motor coordination and learning ability, GSH content, and CAT, SOD, and acetylcholinesterase enzyme function in comparison with stress groups ( p < 0.05 ). Conclusion. The hydroalcoholic and aqueous extracts of cumin and black pepper fruits have protective effects against stress-induced memory deficit and oxidative stress and may have beneficial therapeutic effect in the treatment of neurodegenerative diseases.

Sulforaphane Reverses the Amyloid-β Oligomers Induced Depressive-Like Behavior

2020 ◽  
Vol 78 (1) ◽  
pp. 127-137 ◽  
Author(s):  
Wei Wang ◽  
Cuibai Wei ◽  
Meina Quan ◽  
Tingting Li ◽  
Jianping Jia
Keyword(s):  
Oxidative Stress ◽  
Memory Impairment ◽  
Molecular Mechanisms ◽  
Psychological Symptoms ◽  
Amyloid Β ◽  
Serotonergic System ◽  
Inflammatory Factors ◽  
The Relationship ◽  
The Brain ◽  
And Oxidative Stress

Background: Depression is one of the most common behavioral and psychological symptoms in people with Alzheimer’s disease (AD). To date, however, the molecular mechanisms underlying the clinical association between depression and AD remained elusive. Objective: Here, we study the relationship between memory impairment and depressive-like behavior in AD animal model, and investigate the potential mechanisms. Methods: Male SD rats were administered amyloid-β oligomers (AβOs) by intracerebroventricular injection, and then the depressive-like behavior, neuroinflammation, oxidative stress, and the serotonergic system were measured in the brain. Sulforaphane (SF), a compound with dual capacities of anti-inflammation and anti-oxidative stress, was injected intraperitoneally to evaluate the therapeutic effect. Results: The results showed that AβOs induced both memory impairment and depressive-like behavior in rats, through the mechanisms of inducing neuroinflammation and oxidative stress, and impairing the serotonergic axis. SF could reduce both inflammatory factors and oxidative stress parameters to protect the serotonergic system and alleviate memory impairment and depressive-like behavior in rats. Conclusion: These results provided insights into the biological mechanisms underlying the clinical link between depressive disorder and AD, and offered new drug options for the treatment of depressive symptoms in dementia.

scholarly journals Antioxidant Therapies for Neuroprotection-A Review

2019 ◽  
Vol 8 (10) ◽  
pp. 1659 ◽  
Author(s):  
Teleanu ◽  
Chircov ◽  
Grumezescu ◽  
Volceanov ◽  
Teleanu
Keyword(s):  
Oxidative Stress ◽  
Reactive Nitrogen Species ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
The Body ◽  
Physiological Processes ◽  
Progressive Loss ◽  
Cellular Regeneration ◽  
Brain Oxidative Stress ◽  
The Brain

Although moderate concentrations of reactive oxygen species (ROS) and reactive nitrogen species (RNS) are crucial for various physiological processes within the human body, their overproduction leads to oxidative stress, defined as the imbalance between the production and accumulation of ROS and the ability of the body to neutralize and eliminate them. In the brain, oxidative stress exhibits significant effects, due to its increased metabolical activity and limited cellular regeneration. Thus, oxidative stress is a major factor in the progressive loss of neurons structures and functions, leading to the development of severe neurodegenerative disorders. In this context, recent years have witnessed tremendous advancements in the field of antioxidant therapies, with a special emphasis for neuroprotection. The aim of this paper is to provide an overview of the oxidative stress and antioxidant defense mechanisms and to present the most recent studies on antioxidant therapies for neuroprotection.

scholarly journals Antioxidative defense mechanisms in the aging brain

2014 ◽  
Vol 66 (1) ◽  
pp. 245-252 ◽  
Author(s):  
Zorica Jovanovic
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Current Knowledge ◽  
Aging Brain ◽  
Antioxidative Defense ◽  
Neuroprotective Effects ◽  
Age Related ◽  
Antioxidant Defense Systems ◽  
High Concentrations ◽  
The Brain

Aging is an extremely complex, multifactorial process that is characterized by a gradual and continuous loss of physiological functions and responses, particularly marked in the brain. A common hallmark in aging and age-related diseases is an increase in oxidative stress and the failure of antioxidant defense systems. Current knowledge indicates that the level of glutathione progressively declines during aging. Because nerve cells are the longest-living cells that exhibit a high consumption rate of oxygen throughout an individual?s lifetime, the brain may be especially vulnerable to oxidative damage and this vulnerability increases during aging. In addition, the brain contains high concentrations of polyunsaturated fatty acids and transition metals and low antioxidative defense mechanisms. Although aging is an inevitable event, a growing volume of data confirms that antioxidant supplementation in combination with symptomatic drug treatments reduces oxidative stress and improves cognitive function in aging and age-related diseases. The present review discusses the neuroprotective effects of antioxidants in the aging brain.

scholarly journals Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
José A. Hernández ◽  
Rosa C. López-Sánchez ◽  
Adela Rendón-Ramírez
Keyword(s):  
Oxidative Stress ◽  
Cognitive Abilities ◽  
Defense Mechanisms ◽  
Neuronal Damage ◽  
Public Health Problem ◽  
Physiological Processes ◽  
Excessive Intake ◽  
The Brain ◽  
And Oxidative Stress

The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells. This metabolism of ethanol can induce the oxidation of the fatty acids in phospholipids, and the bioactive aldehydes produced are known to be associated with neurotoxicity and neurodegeneration. As such, here we will review the role of lipids in the neuronal damage induced by ethanol-related oxidative stress and the role that lipids play in the related compensatory or defense mechanisms.

scholarly journals Mechanism of Baicalein in Brain Injury After Intracerebral Hemorrhage by Inhibiting the ROS/NLRP3 Inflammasome Pathway

2021 ◽  
Author(s):  
Xuan Chen ◽  
Yue Zhou ◽  
Shanshan Wang ◽  
Wei Wang
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Water Content ◽  
Nlrp3 Inflammasome ◽  
Inflammatory Factors ◽  
Brain Water Content ◽  
Ros Scavenger ◽  
The Brain ◽  
Brain Water

Abstract Intracerebral hemorrhage (ICH) is a devastating subtype of stroke with high disability/mortality. Baicalein has strong anti-inflammatory activity. This study aims to explore the mechanism of baicalein on brain injury after ICH. The model of brain injury after ICH was established by collagenase induction, followed by the evaluation of neurological severity, brain water content, the degenerated neurons, neuronal apoptosis and reactive oxygen species (ROS). The ICH model was treated with baicalein and silencing NLRP3 to detect brain injury. The expression of NLRP3 inflammasome was detected after treatment with ROS scavenger. The expression of oxidative stress markers and inflammatory factors were detected, and the levels of components in NLRP3 inflammasome were detected. Baicalein reduced the damage of nervous system, lesion surface, brain water content and apoptosis. Baicalein inhibited malondialdehyde and increased IL-10 by inhibiting ROS in brain tissue after ICH. Baicalein inhibited the high expression of NLRP3 inflammasome in ICH. ROS scavenger inhibited the NLRP3 inflammatory response by inhibiting ROS levels. Silencing NLRP3 alleviated the brain injury after ICH by inhibiting excessive oxidative stress and inflammatory factors. Overall, baicalein alleviated the brain injury after ICH by inhibiting ROS and NLRP3 inflammasome.

Error Analysis in Neuropsychological Assessment of Verbal Memory and Learning

1995 ◽  
Vol 11 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Dietmar Heubrock
Keyword(s):  
Error Analysis ◽  
Verbal Memory ◽  
Verbal Learning ◽  
Learning Disorders ◽  
Memory And Learning ◽  
Auditory Verbal Learning Test ◽  
Additional Information ◽  
Auditory Verbal Learning ◽  
Accurate Picture ◽  
Learning Test

Performance on a German version of the Rey Auditory-Verbal Learning Test (AVLT) was investigated for 64 juvenile patients who were subdivided in 6 clinical groups. In addition to standard evaluation of AVLT protocols which is usually confined to items recalled correctly, an error analysis was performed. Differentiating between total errors (TE), repetition errors (RE), and misnamings (ME), substantial differences between clinical groups could be demonstrated. It is argued that error analysis of verbal memory and learning enriches the understanding of neuropsychological syndromes, and provides additional information for diagnostic and clinical use. Thus, it is possible to gain a more accurate picture so that patients can be appropriately retrained, and research into the functional causes of memory and learning disorders can be intensified.

Methyl jasmonate delays the latency to anoxic convulsions by normalizing the brain levels of oxidative stress biomarkers and serum corticosterone contents in mice with repeated anoxic stress

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Abayomi Ololade Adelaja ◽  
Oluwafemi Gabriel Oluwole ◽  
Oritoke Modupe. Aluko ◽  
Solomon Umukoro
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Methyl Jasmonate ◽  
Brain Injuries ◽  
Antioxidant Property ◽  
Oxidative Stress Biomarkers ◽  
Serum Corticosterone ◽  
Stress Agent ◽  
Cellular Antioxidants ◽  
The Brain

AbstractObjectivesRepeated exposure to anoxic stress damages the brain through cortisol-mediated increases in oxidative stress and cellular-antioxidants depletion. Thus, compounds with antioxidant property might confer protection against anoxic stress-induced brain injuries. In this study, we further examined the protective effect of methyl jasmonate (MJ), a potent anti-stress agent against anoxic stress-induced convulsions in mice.MethodsThirty-six male Swiss mice randomized into six groups (n=6) were given MJ (25, 50 and 100 mg/kg, i.p.) or vehicle (10 mL/kg, i.p.) 30 min before 15 min daily exposure to anoxic stress for 7 days. The latency(s) to anoxic convulsion was recorded on day 7. The blood glucose and serum corticosterone levels were measured afterwards. The brains were also processed for the determination of malondialdehyde, nitrite, and glutathione levels.ResultsMethyl jasmonate (MJ) delayed the latency to anoxic convulsion and reduced the blood glucose and serum corticosterone levels. The increased malondialdehyde and nitrite contents accompanied by decreased glutathione concentrations in mice with anoxic stress were significantly attenuated by MJ.ConclusionsThese findings further showed that MJ possesses anti-stress property via mechanisms relating to the reduction of serum contents of corticosterone and normalization of brain biomarker levels of oxidative stress in mice with anoxic stress.

scholarly journals Cytomegalovirus Infection and Inflammation in Developing Brain

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1078
Author(s):  
Fran Krstanović ◽  
William J. Britt ◽  
Stipan Jonjić ◽  
Ilija Brizić
Keyword(s):  
Cytomegalovirus Infection ◽  
Hcmv Infection ◽  
Severe Disease ◽  
Intraperitoneal Administration ◽  
Inflammatory Factors ◽  
Mcmv Infection ◽  
Newborn Mice ◽  
Organ Systems ◽  
Congenital Hcmv Infection ◽  
The Brain

Human cytomegalovirus (HCMV) is a highly prevalent herpesvirus that can cause severe disease in immunocompromised individuals and immunologically immature fetuses and newborns. Most infected newborns are able to resolve the infection without developing sequelae. However, in severe cases, congenital HCMV infection can result in life-threatening pathologies and permanent damage of organ systems that possess a low regenerative capacity. Despite the severity of the problem, HCMV infection of the central nervous system (CNS) remains inadequately characterized to date. Cytomegaloviruses (CMVs) show strict species specificity, limiting the use of HCMV in experimental animals. Infection following intraperitoneal administration of mouse cytomegalovirus (MCMV) into newborn mice efficiently recapitulates many aspects of congenital HCMV infection in CNS. Upon entering the CNS, CMV targets all resident brain cells, consequently leading to the development of widespread histopathology and inflammation. Effector functions from both resident cells and infiltrating immune cells efficiently resolve acute MCMV infection in the CNS. However, host-mediated inflammatory factors can also mediate the development of immunopathologies during CMV infection of the brain. Here, we provide an overview of the cytomegalovirus infection in the brain, local immune response to infection, and mechanisms leading to CNS sequelae.

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