Redox

Redox short for oxidation-reduction, is a type of chemical reaction where electrons are transferred between molecules or atoms, causing a change in oxidation states.

A study focused on oxidative stress is typically referred to as redox biology or oxidative stress biology. These terms encompass the broader study on oxidation-reduction (redox) reactions influence biological systems, including the effects of oxidative stress. Oxidative stress itself is defined as an imbalance between oxidants and antioxidants in favour of oxidants, leading to potential damage to cells and tissues. 

A more detailed breakdown:

Redox Biology  is a field that investigates the role of redox reactions in biological processes, including the impact of oxidative stress. 

Oxidation–reduction reactions, commonly known as redox reactions, are reactions that involve the transfer of electrons from one species to another. 

The species losing electrons is said to be oxidized, while the species gaining electrons is said to be reduced.

Redox biology investigates the reversible oxidation–reduction reactions fundamental cellular processes. 

Redox biology refers to low levels of ROS that activate signalling pathways to initiate biological processes.

Oxidative Stress  denotes redox state deviation.

Oxidative stress is an attribute of aerobic metabolism. Oxidative stress evokes stress responses. Oxidative stress activates molecular redox switches, the state of imbalance where the production of reactive oxygen species (ROS) overwhelms the body's antioxidant defences, leading to potential damage. oxidative stress denotes high levels of ROS that incur damage to DNA, protein or lipids. The redox potential of the human internal environment ranges between -100 mV and -200 mV, i.e. in an antioxidant environment. This means that antioxidants, or OH- ions, predominate and the organism protects itself with enough electrons.

Oxidative Stress Biology refers to the study of harmful effects of excessive oxidation in biological systems with general signs like fatigue and brain fog to more specific issues like muscle pain, memory loss, and increased susceptibility to infections. Additionally, oxidative stress can contribute to premature aging, visible through wrinkles and skin damage.

Redox Signalling the cellular communication process that utilizes redox reactions (oxidation-reduction) to regulate various biological processes, modifications act as molecular switches, influencing protein function, downstream signalling pathways. Redox signalling is implicated in various disease relevance, including cardiovascular diseases, cancer, and neurodegenerative disorders. Understanding redox signalling pathways provides potential targets for therapeutic interventions aimed at restoring redox balance. Molecules, such as H2O2, superoxide anion (O2•−), and nitric oxide (NO), act as messengers in redox signalling.

(1) Redox signalling plays vital roles in numerous physiological processes, including: 

(2) Growth and differentiation: Regulates cell growth, proliferation, and differentiation.

(3) Metabolism: Influences energy metabolism and adaptation to metabolic stress. 

(4) Immune response: Mediates innate, adaptive immunity, affecting inflammation and pathogen defence.

(5) Cardiovascular function: Modulates vascular tone, blood pressure, adaptation to hypoxia/ischemia.

(6) Aging: Is involved in regulating cellular senescence and influencing lifespan. 

Antioxidants are molecules that counteract the damaging effects of oxidant, maintaining redox balance.

Oxidative stress in detail 

A great number of physiological functions in living systems are mediated by electron transfer (redox) reactions shifted from thermodynamic equilibrium. Transfer of electrons is involved in cell bioenergetics, oxidative phosphorylation, DNA damage, enzymatic catalysis, metabolism of drugs, other processes. The direct consequence of the electron transfer reactions in living systems is the transient presence of free radicals as ROS (Reactive Oxygen Species) and RNS (Reactive Nitrogen Species) both highly reactive molecules involved in cellular signalling and stress responses in living organisms.

The role of ROS/RNS in biological systems is  associated with the term oxidative stress, a phenomenon responsible for oxidative damage, oxidative stress is a “double edge sword” for living systems, as it is important for physiological signalling mediated by physiological concentrations of ROS, termed “oxidative eustress”, while it can be responsible for oxidative damage to biomolecules, a process termed “oxidative (di)stress”, mediated by increased ROS concentration.

Oxidative stress is characterized by multiple mechanisms by which ROS cause cellular damage; the major mechanism is damage to biomolecules their direct oxidation by ROS such as hydroxyl radical or peroxynitrite. Another important mechanism of oxidative stress-mediated damage is disturbed redox signalling. Diabetes mellitus is an example where both these mechanisms occur simultaneously. Oxidative stress as the primary cause and secondary consequence of the disease.

Oxidative stress as the primary cause has been observed in atherosclerosis and radiation-induced diseases such as lung injury. The primary cause of oxidative stress has also been observed in herbicide paraquat poisoning, characterized by a redox cycling mechanism involving superoxide radical anion formation triggered by exogenous NADPH in pulmonary endothelial cells. Oxidative stress as a second line of attack occurs after the onset of initial pathology, documented for example, by the formation of superoxide radicals and hydrogen peroxide by NADPH oxidases, for example, in the response to injury-mediated inflammation.

Oxidative stress is responsible for disturbed signalling pathways, for example, molecular mechanisms of apoptosis induction, impairment of mitochondrial function, protein modification. All disorders have in common the occurrence of oxidative stress via multiple pathways. Organisms have evolved a complex system of defence against oxidative stress as to detoxify oxidants but also repair oxidative damage.