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. The intestine also responds to secondary reactive species formed by exposure to ozone doses, generating noxious stimuli that increase degenerative damage. This review aims to elucidate how environmental pollution, mainly by ozone, induces a state of chronic oxidative stress with the loss of regulation of the inflammatory response, both in the intestine and in the brain, where the functionality of both structures is altered and plays a determining role in some neurodegenerative and chronic degenerative diseases. For this purpose, we searched for information on sites such as the Cochrane Library Database, PubMed, Scopus, and Medscape. Reviewing the data published, we can conclude that environmental pollutants are a severe health problem. Ozone pollution has different pathways of action, both molecular and systemic, and participates in neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease as well in bowel diseases as Inflammatory Bowel Disease, Crohn’s Disease, and Irritable Bowel Syndrome.

Background. Adiponectin (APN) is an adipocyte-derived hormone that has peripheral beneficial effects. Although its receptors AdipoR1 and AdipoR2 are expressed in the brain, their function in neurons is poorly understood. The aims of this work were to describe the distribution of APN receptors in the olfactory bulb (OB) as well as the possible effects of APN injection on the insulin receptor (InsR) content and Akt kinase. Method. We performed the double immunofluorescence technique to describe the distribution of AdipoRs and the cellular type they were expressing. mRNA transcript and protein content were assessed by RT-PCR and Western blot, respectively. APN injection was performed to analyze its possible effect on the insulin pathway. Results. We found that AdipoRs were localized in all cell layers and in both neurons and astrocytes. We observed the presence of mRNA transcripts and immunoblot analysis confirmed the protein on the intact OB; APN injection in the OB resulted in a slight decrease of the total InsR and Akt phosphorylation and a reduction of phopho-InsR content. Conclusions. These data demonstrated that AdipoRs are expressed in OB regions, and APN injection could act as an insulin pathway modulator in the OB and thus possibly contribute to olfaction physiology.

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. The dysfunction of redox system and failures in control the inflammatory responses are involved in a vicious circle that maintains and increases the degenerative process. Intestine also responds to secondary reactive species formed by exposure to ozone doses, generating noxious stimuli that increase degenerative damage. This review aims to elucidate how environmental pollution, mainly by ozone, induces a state of chronic oxidative stress with the loss of regulation of the inflammatory response, both in the intestine and in the brain, where the functionality of both structures is altered and plays a determining role in some neurodegenerative and chronic degenerative diseases. For this purpose, we searched for information on sites like the Cochrane Library Database, PubMed, Scopus, and Medscape. Reviewing the data published, we can conclude that environmental pollutants are a severe health problem. Ozone pollution has different pathways of action, both molecular and systemic, and participates in neurodegenerative diseases such as Parkinson's and Alzheimer's disease as well in bowel diseases as Inflammatory Bowel Disease, Crohn's Disease and Irritable Bowel Syndrome.

This work aimed to elucidate how O₃ 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 O₃ 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 O₃. After treatment, tissues were extracted and processed using Western blotting, biochemical, and immunohistochemical techniques. The results indicated an increase in 4-hydroxynonenal (4HNE) and Cu/Zn-SOD and a decrease in Mn-SOD, and SOD activity in the substantia nigra, jejunum, and colon decreased. Furthermore, the translocation of NFκB to the nucleus increased in the different organs studied. In conclusion, repeated exposure to O₃ alters the regulation of the antioxidant and inflammatory response in the substantia nigra and the intestine. This indicates that these factors are critical in the loss of regulation in the inflammatory response; they respond to ozone pollution, which can occur in chronic degenerative diseases.

This work aimed to elucidate how O3 pollution causes loss of regulation of the immune response in both the brain and the intestine. In this work, we studied the effect of exposing rats to low doses of O3 on the association between the antioxidant response of superoxide dismutase (SOD) levels and nuclear factor kappa light chains of activated B cells (NFκB) as a marker of inflammation. Method: 72 Wistar rats were used, divided into six groups that received the following treatments: Control, 7, 15, 30, 60, and 90 days at O3, respectively. After treatment, tissues were extracted and processed using Western blotting, biochemical, and immunohistochemical techniques. The results indicated an increase in 4-hydroxynonenal (4HNE) and Cu/Zn-SOD, a decrease in Mn-SOD, and SOD activity in the substantia nigra, jejunum, and colon decrease. Furthermore, the translocation of NFκB to the nucleus increased in the different organs studied. In conclusion, repeated exposure to ozone alters the regulation of the antioxidant and inflammatory response in the substantia nigra and the intestine. This suggests that these responses are critical in the loss of regulation of the inflammatory response, and they respond to ozone pollution, which could be occurring in the progression of chronic degenerative diseases.

Adipose tissue is an organ with a high metabolic rate, functioning as a storage site for potential energy derived from food. It is a heterogeneous tissue composed of various cell types that respond differently to stimuli. Polyunsaturated fatty acids are lipids characterized by the presence of multiple double bonds in their molecular structure. These fatty acids are particularly vulnerable to oxidation by Reactive Oxygen Species, a process known as lipoperoxidation. While the oxidized lipids can serve important physiological roles within adipose tissue, they can also enter the bloodstream, where they associate with lipoproteins, leading to cellular damage and increased systemic oxidative stress. In cases of obesity, adipose tissue displays an exaggerated inflammatory and immune response that can affect multiple body systems, contributing to the onset of chronic degenerative diseases. Therefore, adipose tissue is a complex organ in which metabolic, endocrine, and immune response processes are intricately regulated and coordinated. This paper explains the role of alterations in redox balance, lipogenic, and inflammatory functions in adipose tissue as important risk factors for the development of chronic degenerative diseases, including those affecting the central nervous system. For this study, we searched multiple databases, including PubMed, Scopus, Google Scholar, the Cochrane Library, and Medscape, from 2015 to the present.