From reactive species to disease development: Effect of oxidants and antioxidants on the cellular biomarkers

Abstract

The influence of modern lifestyle, diet, exposure to chemicals such as phytosanitary substances, together with sedentary lifestyles and lack of exercise play an important role in inducing reactive stress (RS) and disease. The imbalance in the production and scavenging of free radicals and the induction of RS (oxidative, nitrosative, and halogenative) plays an essential role in the etiology of various chronic pathologies, such as cardiovascular diseases, diabetes, neurodegenerative diseases, and cancer. The implication of free radicals and reactive species injury in metabolic disturbances and the onset of many diseases have been accumulating for several decades, and are now accepted as a major cause of many chronic diseases. Exposure to elevated levels of free radicals can cause molecular structural impact on proteins, lipids, and DNA, as well as functional alteration of enzyme homeostasis, leading to aberrations in gene expression. Endogenous depletion of antioxidant enzymes can be mitigated using exogenous antioxidants. The current interest in the use of exogenous antioxidants as adjunctive agents for the treatment of human diseases allows a better understanding of these diseases, facilitating the development of new therapeutic agents with antioxidant activity to improve the treatment of various diseases. Here we examine the role that RS play in the initiation of disease and in the reactivity of free radicals and RS in organic and inorganic cellular components.

Electrophilic Compounds in the Human Diet and Their Role in the Induction of the Transcription Factor NRF2

“…NRF2 regulates both the inflammatory response and cellular senescence [ 81 ]. Atherosclerosis, Alzheimer’s disease, and cancer are among the age-related diseases associated with chronic inflammation, a common feature of aging associated with this condition [ 82 ].…”

Polyphenols as Antioxidant/Pro-Oxidant Compounds and Donors of Reducing Species: Relationship with Human Antioxidant Metabolism

“…Additionally, quinones are able to create DNA adducts, which cause genetic mutations [49]. ROS produce DNA strand breaks and oxidatively damaged nucleobases [50]. The genotoxicity of o-quinones is aggravated by the nuclear translocation of estrogen o-quinones by the estrogen receptor and by the nuclear translocation of polycyclic aromatic o-quinones by the aryl hydrocarbon receptor [51].…”

Chemical Insights into Oxidative and Nitrative Modifications of DNA

“…These reactive species can be produced by endogenous sources, such as cellular aerobic metabolism, and can also be produced by macrophages and neutrophils at sites of infection and inflammation as well as by exposure to various physical agents, such as UV light and ionizing radiation, or chemical pollutants or carcinogens [38] (Figure 11).…”

“…hydroxyl radical ( • OH), alkoxyl radical (RO • ), peroxyradicals (RO2 • ), organic hydroper oxides (ROOH), nitric oxide (NO • ), peroxynitrite (ONOO − ), and singlet oxygen ( 1 O2) [37] These reactive species can be produced by endogenous sources, such as cellular aer obic metabolism, and can also be produced by macrophages and neutrophils at sites o infection and inflammation as well as by exposure to various physical agents, such as UV light and ionizing radiation, or chemical pollutants or carcinogens [38] (Figure 11). Endogenous or exogenous sources generate ROS (O2 •− , • OH, HO2 • , H2O2, RO2 • , and hypochlorous acid (HOCl)) and RNS (NO • , NO2 • , ONOO − , nitrous acid (HNO2), al kylperoxynitrates (RONOO), and dinitrogen trioxide (N2O3).…”