Accumulation of Alpha-Synuclein and Increase in the Inflammatory Response in the , Jejunum, and Colon in a Model of O Pollution in Rats.

This work aimed to study the effect of repeated exposure to low doses of ozone on alpha-synuclein and the inflammatory response in the , jejunum, and colon. Seventy-two male Wistar rats were divided into six groups. Each group received one of the following treatments: The control group was exposed to air.

Changes in SOD and NF-κB Levels in and the Intestine through Oxidative Stress Effects in a Wistar Rat Model of Ozone Pollution.

This work aimed to elucidate how O pollution causes a loss of regulation in the immune response in both the brain and the intestine. In this work, we studied the effect of exposing rats to low doses of O based on the association between the antioxidant response of superoxide dismutase (SOD) levels and the nuclear factor kappa light chains of activated B cells (NFκB) as markers of inflammation. Method: Seventy-two Wistar rats were used, divided into six groups that received the following treatments: Control and 7, 15, 30, 60, and 90 days of O.

Ozone Environmental Pollution: Relationship between the Intestine and Neurodegenerative Diseases.

Repeated exposure to environmental ozone causes a chronic state of oxidative stress. This state is present in chronic degenerative diseases and induces a loss of control of the inflammatory response. Redox system dysfunction and failures in control of inflammatory responses are involved in a vicious circle that maintains and increases the degenerative process.

Ozone Pollution, Oxidative Stress, Regulatory T Cells and Antioxidants.

Ozone pollution, is a serious health problem worldwide. Repeated exposure to low ozone doses causes a loss of regulation of the oxidation-reduction systems, and also induces a chronic state of oxidative stress. This fact is of special importance for the regulation of different systems including the immune system and the inflammatory response.

Chronic exposure to ozone induces cardiac antioxidant response and overexpression of either mitochondrial fision protein DRP1 and hipertrophyc-related proteins.

Pollution is considered a risk factor for cardiovascular disease; however, the mechanisms to explain this relationship are not well understood; ozone is one of the most abundant and studied air contaminants. Our study aimed to evaluate the effect of chronic exposition of rats to controlled low doses of ozone on oxidative stress, apoptosis, mitochondrial dynamics, and cardiac hypertrophy. Male Wistar rats were daily exposed to low ozone doses during 7, 15, 30, and 60 days, 4 h/day.

Oxidative Stress Caused by Ozone Exposure Induces Changes in P2X7 Receptors, Neuroinflammation, and Neurodegeneration in the Rat Hippocampus.

Low-ozone doses cause alterations in the oxidation-reduction mechanisms due to the increase in reactive oxygen species, alter cell signaling, and produce deleterious metabolic responses for cells. Adenosine 5'triphosphate (ATP) can act as a mediator in intercellular communication between neurons and glial cells. When there is an increase in extracellular ATP, a modification is promoted in the regulation of inflammation, energy metabolism, by affecting the intracellular signaling pathways that participate in these processes.

5-S-cysteinyl-dopamine, a neurotoxic endogenous metabolite of dopamine: Implications for Parkinson's disease.

Parkinson's disease (PD) is the second most common neurodegenerative disease worldwide and is characterized for being an idiopathic and multifactorial disease. Extensive research has been conducted to explain the origin of the disease, but it still remains elusive. It is well known that dopamine oxidation, through the endogenous formation of toxic metabolites, is a key process in the activation of a cascade of molecular events that leads to cellular death in the hallmark of PD.

Effect of Chronic Oxidative Stress on Neuroinflammatory Response Mediated by CD4T Cells in Neurodegenerative Diseases.

In a state of oxidative stress, there is an increase of reactive species, which induce an altered intracellular signaling, leading to dysregulation of the inflammatory response. The inability of the antioxidant defense systems to modulate the proinflammatory response is key to the onset and progression of neurodegenerative diseases. The aim of this work is to review the effect of the state of oxidative stress on the loss of regulation of the inflammatory response on the microglia and astrocytes, the induction of different CD4T cell populations in neuroinflammation, as well as its role in some neurodegenerative diseases.

Structural Changes of Amyloid Beta in Hippocampus of Rats Exposed to Ozone: A Raman Spectroscopy Study.

The aim of this work was to study the effect of oxidative stress on the structural changes of the secondary peptide structure of amyloid beta 1-42 (Aβ 1-42), in the dentate gyrus of hippocampus of rats exposed to low doses of ozone. The animals were exposed to ozone-free air (control group) and 0.25 ppm ozone during 7, 15, 30, 60, and 90 days, respectively.

The Effect of Chronic Ozone Exposure on the Activation of Endoplasmic Reticulum Stress and Apoptosis in Rat Hippocampus.

The chronic exposure to low doses of ozone, like in environmental pollution, leads to a state of oxidative stress, which has been proposed to contribute to neurodegenerative disorders, including Alzheimer's disease (AD). It induces an increase of calcium in the endoplasmic reticulum (ER), which produces ER stress. On the other hand, different studies show that, in diseases such as Alzheimer's, there exist disturbances in protein folding where ER plays an important role.

Obesity, Oxidative Stress, and Their Effect on Serum Heme Oxygenase-1 Concentrations and Insulin in Children Aged 3 to 5 Years in a Pediatric Hospital of the Ministry of Health CDMX.

Background: Obesity during early stages of life may condition states of oxidative stress. Heme oxygenase-1 (HO-1) is an enzyme involved in oxidative metabolism; it has antioxidant and anti-inflammatory functions and is related in sensitivity to insulin. However, a high concentration of this enzyme has been described to cause alterations such as insulin resistance.

Syntaxin 5 Overexpression and β-Amyloid 1-42 Accumulation in Endoplasmic Reticulum of Hippocampal Cells in Rat Brain Induced by Ozone Exposure.

Oxidative stress is a risk factor for Alzheimer's disease and it is currently accepted that oxidative damage precedes the overproduction of A42 peptide. We have reported that ozone causes oxidative stress inducing neurodegeneration in the brain of rats. It is associated with A42 overproduction and intracellular accumulation in hippocampus.

Vitamin C in Health and Disease: Its Role in the Metabolism of Cells and Redox State in the Brain.

Ever since Linus Pauling published his studies, the effects of vitamin C have been surrounded by contradictory results. This may be because its effects depend on a number of factors such as the redox state of the body, the dose used, and also on the tissue metabolism. This review deals with vitamin C pharmacokinetics and its participation in neurophysiological processes, as well as its role in the maintenance of redox balance.

CHANGES IN C-REACTIVE PROTEIN AND BIOCHEMICAL PROFILE IN PRESCHOOL CHILDREN WITH OBESITY.

Introduction: the childhood obesity is a serious public health problem because if weight gain continues, complications such as insulin resistance, dyslipidemia, orthopedic disorders, sleep apnea, and metabolic syndrome may occur in other stages of child development.

Objective: the objective of this study was to evaluate C-reactive protein (CRP) concentrations, lipid profiles, and glucose levels in obese children three to five years of age and compare them to eutrophic children.

Methods: in this study, 100 children aged three to five years were selected and divided into two groups (n = 50 per group): a group of eutrophic children (< 84th percentile) and a group of obese children (> 95th percentile).

Oxidative Stress State Is Associated with Left Ventricular Mechanics Changes, Measured by Speckle Tracking in Essential Hypertensive Patients.

The oxidative stress state is characterized by an increase in oxygen reactive species that overwhelms the antioxidant defense; we do not know if these pathological changes are correlated with alterations in left ventricular mechanics. The aim was correlating the oxidative stress state with the left ventricular global longitudinal strain (GLS) and the left ventricular end diastolic pressure (LVEDP). Twenty-five patients with essential hypertension and 25 controls paired by age and gender were studied.

Oxidative stress-dependent changes in immune responses and cell death in the substantia nigra after ozone exposure in rat.

Parkinson's disease has been associated with the selective loss of neurons in the substantia nigra pars compacta. Increasing evidence suggests that oxidative stress plays a major role. The resulting increase in reactive oxygen species triggers a sequence of events that leads to cell damage, activation of microglia cells and neuroinflammatory responses.

Deciphering an interplay of proteins associated with amyloid β 1-42 peptide and molecular mechanisms of Alzheimer's disease.

Extracellular and intracellular accumulation of amyloid beta 1-42 peptide in different states of aggregation has been involved in the development and progression of Alzheimer's disease. However, the precise mechanisms involved in amyloid beta peptide neurotoxicity have not been fully understood. There exists a wide variety of studies demonstrating the binding of amyloid beta peptide to a great variety of macromolecules and that such associations affect the cellular functions.

Oxidative stress activates the transcription factors FoxO 1a and FoxO 3a in the hippocampus of rats exposed to low doses of ozone.

The exposure to low doses of ozone induces an oxidative stress state, which is involved in neurodegenerative diseases. Forkhead box O (FoxO) family of transcription factors are activated by oxidative signals and regulate cell proliferation and resistance to oxidative stress. Our aim was to study the effect of chronic exposure to ozone on the activation of FoxO 1a and FoxO 3a in the hippocampus of rats.

Neuroprotective effects of tibolone against oxidative stress induced by ozone exposure.

Introduction: Oxidative stress increases brain lipid peroxidation, memory and motor deficits and progressive neurodegeneration. Tibolone, a treatment for menopausal symptoms, decreases lipid peroxidation levels and improves memory and learning.

Aim: To study the effect of chronic administration of tibolone on lipid peroxidation, memory and motor deficits in ozone induced oxidative stress.

Sepsis, mitochondrial failure and multiple organ dysfunction.

Purpose: The purpose of this review is to consider the state of oxidative stress, failure of the antioxidant systems and mitochondrial failure as the main physiopathological mechanisms leading to multiple organ dysfunction during sepsis.

Principal Findings: Sepsis is a clinical syndrome caused by a severe infection that triggers an exaggerated inflammatory response. Involved in the pathogenesis of sepsis are the activation of inflammatory, immune, hormonal, metabolic and bioenergetic responses.

Estradiol prevents olfactory dysfunction induced by A-β 25-35 injection in hippocampus.

Background: Some neurodegenerative diseases, such as Alzheimer and Parkinson, present an olfactory impairment in early stages, and sometimes even before the clinical symptoms begin. In this study, we assess the role of CA1 hippocampus (structure highly affected in Alzheimer disease) subfield in the rats' olfactory behavior, and the neuroprotective effect of 17 beta estradiol (E2) against the oxidative stress produced by the injection of amyloid beta 25-35.

Results: 162 Wistar rats were ovariectomized and two weeks after injected with 2 μl of amyloid beta 25-35 (A-β25-35) in CA1 subfield.

Oxidative stress caused by ozone exposure induces loss of brain repair in the hippocampus of adult rats.

Oxidative stress is involved in many neurodegenerative diseases. Chronic ozone exposure causes a secondary increase of reactive oxygen species, which cause an oxidative stress state in the organism. Ozone is one of the main components of photochemical pollution.

Effect of growth hormone on Cyclooxygenase-2 expression in the hippocampus of rats chronically exposed to ozone.

The aim of this study was to determine GH-effects on Cyclooxygenase-2 (COX-2) expression on hippocampus alterations caused by ozone exposure. Seventy male rats were divided into: (1) control; (2) exposed to ozone for 7, 15, and 30 days; (3) exposed to ozone and treated with GH, for 7, 15, and 30 days. Results showed that lipoperoxidation levels and number of COX-2-positive cells increased in all groups exposed to ozone compared to control.