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Special Issue Editors

Special Issue Information

Dear Colleagues,

Inflammation and oxidative stress research cover all the way to medicine and health and disease research involving cell biology, biochemistry, chemistry, physiology and pathophysiology related mechanisms. Inflammation and oxidative stress are closely related in all these processes considering that one of which can be easily induced by another and, when not properly regulated, contributes to the development of many diseases that collectively represent the leading causes of disability and mortality worldwide Thus, both processes are simultaneously found in many, often chronic, pathological conditions (e.g. neurodegenerative diseases, cardiovascular diseases, diabetes, chronic kidney disease, liver disease, cancer, aging). Many factors are recognized as “triggering events” for chronic inflammation and oxidative stress such as xenobiotics.

Xenobiotics (e.g. drugs, dietary compounds, environmental chemicals and pollutants) can induce inflammation by a variety of different mechanisms often resulting in cell injury, degeneration and/or necrosis, either directly or indirectly, by parent or metabolite. Importantly, xenobiotics-dependent effects have significant relevance in food safety, considering that exposure of the general population to most of them occurs mainly by food. Xenobiotics may also activate inflammatory/immune cells to release inflammatory mediators in nonspecific ways, or by stimulating a specific immune response. Moreover, certain xenobiotics and/or their metabolites can also directly mediate the formation of reactive oxygen species damaging biomolecules and/or affecting signaling pathways.

The aim of this Special Issue is to provide an updated point of view about the relationship between inflammation and/or oxidative stress-related response and modulation by xenobiotics. In addition, contributes focused on bioactives able to counteract xenobiotics-induced inflammation and oxidative stress will be also considered.

Dr. Stefania Marzocco
Dr. Stefano Lorenzetti
Guest Editors

Manuscript Submission Information

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Keywords

inflammation
oxidative stress
chronic diseases
xenobiotics
bioactives
pollutants
endocrine disruptors
drugs

Published Papers (2 papers)

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Research

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17 pages, 3969 KiB

Open AccessArticle

Revealing the Therapeutic Targets and Mechanism of Ginsenoside Rg1 for Liver Damage Related to Anti-Oxidative Stress Using Proteomic Analysis

by Jiying Hou, Ruoxiang Ma, Shisheng Zhu and Yaping Wang

Int. J. Mol. Sci. 2022, 23(17), 10045; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231710045 - 02 Sep 2022

Cited by 6 | Viewed by 1644

Abstract

Ginsenoside Rg1 is an important active substance isolated from the root of ginseng. In previous studies, Rg1 has shown excellent therapeutic effects in antioxidant, anti-inflammatory, and metabolic modulation. However, the therapeutic targets of Rg1 are still unknown. In this study, we investigated the therapeutic effects of Rg1 on oxidative stress-related liver damage. The oxidative stress damage model was achieved by intraperitoneal injection of D-galactose (D-gal) for 42 consecutive days in C57BL/6J mice. Rg1 treatment started on Day 16. Body weight, liver weight, degree of hepatic oxidative stress damage, serum lipid levels, and hepatic lipid and glucose metabolism were measured. Proteomics analysis was used to measure liver protein expression. The differential expression proteins were analyzed with bioinformatics. The results showed that Rg1 treatment attenuated liver damage from oxidative stress, reduced hepatic fat accumulation, promoted hepatic glycogen synthesis, and attenuated peripheral blood low-density lipoprotein (LDL), cholesterol (CHO), and triglycerides (TG) levels. Proteomic analysis suggested that Rg1 may regulate hepatocyte metabolism through ECM–Receptor, the PI3K-AKT pathway. The epidermal growth factor receptor (EGFR) and activator of transcription 1 (STAT1) may be the key protein. In conclusion, this study provides an experimental basis for further clarifying the specific mechanism of Rg1 in the treatment of oxidative stress damage-related liver disease. Full article

(This article belongs to the Special Issue Inflammation and Oxidative Stress in Xenobiotic-Induced Damage)

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Review

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15 pages, 849 KiB

Open AccessReview

Oxidative Stress and Air Pollution: Its Impact on Chronic Respiratory Diseases

by Martha Patricia Sierra-Vargas, Josaphat Miguel Montero-Vargas, Yazmín Debray-García, Juan Carlos Vizuet-de-Rueda, Alejandra Loaeza-Román and Luis M. Terán

Int. J. Mol. Sci. 2023, 24(1), 853; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24010853 - 03 Jan 2023

Cited by 8 | Viewed by 3106

Abstract

Redox regulation participates in the control of various aspects of metabolism. Reactive oxygen and nitrogen species participate in many reactions under physiological conditions. When these species overcome the antioxidant defense system, a distressed status emerges, increasing biomolecular damage and leading to functional alterations. Air pollution is one of the exogenous sources of reactive oxygen and nitrogen species. Ambient airborne particulate matter (PM) is important because of its complex composition, which includes transition metals and organic compounds. Once in contact with the lungs’ epithelium, PM components initiate the synthesis of inflammatory mediators, macrophage activation, modulation of gene expression, and the activation of transcription factors, which are all related to the physiopathology of chronic respiratory diseases, including cancer. Even though the pathophysiological pathways that give rise to the development of distress and biological damage are not fully understood, scientific evidence indicates that redox-dependent signaling pathways are involved. This article presents an overview of the redox interaction of air pollution inside the human body and the courses related to chronic respiratory diseases. Full article

(This article belongs to the Special Issue Inflammation and Oxidative Stress in Xenobiotic-Induced Damage)

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