What Does Redox Do To Your Body?

Redox reactions are a fundamental part of life, and they play a key role in many aspects of human health, including:

• Cell survival: Redox reactions are essential for cell survival and proliferation. 
•  
• Brain function: Redox homeostasis is involved in all aspects of brain development, function, aging, and disease. 
•  
• Inflammation: Redox products and enzymes may help control inflammation. 
•  
• Cancer: Redox products and enzymes may help control cancer formation and spread. 
•  
• Cardiovascular disease: A buildup of plaque in the arteries can lead to cardiovascular disease symptoms like chest pain, shortness of breath, fatigue, and heart attacks. 
•  

Redox homeostasis is the balance of physiological levels of nonradical reactive oxygen species (ROS). When the balance is disrupted, it can lead to oxidative stress (OS), which can damage biomolecules and contribute to disease. 

Some factors that can contribute to an imbalance in redox homeostasis include:

• Eating a diet high in refined starch, sugar, saturated fatty acids, and trans fatty acids
• Not getting enough exercise

What is the redox theory of aging?

The redox theory of aging is that aging is a decline in plasticity of genome–exposome interaction that occurs as a consequence of execution of differentiation and exposure memory systems.

Redox theory of aging

Abstract

Metazoan genomes encode exposure memory systems to enhance survival and reproductive potential by providing mechanisms for an individual to adjust during lifespan to environmental resources and challenges. These systems are inherently redox networks, arising during evolution of complex systems with O2 as a major determinant of bioenergetics, metabolic and structural organization, defense, and reproduction. The network structure decreases flexibility from conception onward due to differentiation and cumulative responses to environment (exposome). The redox theory of aging is that aging is a decline in plasticity of genome–exposome interaction that occurs as a consequence of execution of differentiation and exposure memory systems. This includes compromised mitochondrial and bioenergetic flexibility, impaired food utilization and metabolic homeostasis, decreased barrier and defense capabilities and loss of reproductive fidelity and fecundity. This theory accounts for hallmarks of aging, including failure to maintain oxidative or xenobiotic defenses, mitochondrial integrity, proteostasis, barrier structures, DNA repair, telomeres, immune function, metabolic regulation and regenerative capacity.

Introduction

Hundreds of philosophers and scientists have addressed the topics of longevity and aging, and many theories have been advanced. These have been recently reviewed, and I make no attempt to further summarize these important contributions. Rather, the present article provides a conceptual review based upon the emerging concept that redox systems function as a critical interface between the genome and the exposome, . Relying extensively upon emerging understanding of redox systems biology, acquired epigenetic memory systems, and deductive reasoning, a simple theory is derived that aging is the decline of the adaptive interface of the functional genome and exposome that occurs due to cell and tissue differentiation and cumulative exposures and responses of an organism. This theory is not limited to redox processes but has a redox-dependent character due to the over-riding importance of electron transfer in energy supply, defense, reproduction and molecular dynamics of protein and cell signaling.

Several years ago, I presented a redox hypothesis of oxidative stress in which I concluded that oxidative stress is predominantly a process involving 2-electron, non-radical reactions rather than commonly considered 1-electron, free radical reactions. The central arguments were that  experimental measures showed that non-radical flux substantially exceeds free radical flux under most oxidative stress conditions,  radical scavenger trials in humans failed to show health benefits, and normal cell functions involving sulfur switches are readily disrupted by non-radical oxidants. The redox hypothesis is thus founded upon the concept that oxidative stress includes disruption of redox circuitry in addition to the macromolecular damage resulting from an imbalance of prooxidants and antioxidants.

The redox hypothesis of oxidative stress contained four postulates:

• 1.
  All biologic systems contain redox elements [e.g., redox-sensitive cysteines], which function in cell signaling, macromolecular trafficking and physiologic regulation.
• 2.
  Organization and coordination of the redox activity of these elements occurs through redox circuits dependent upon common control nodes (e.g., thioredoxin, GSH).
• 3.
  The redox-sensitive elements are spatially and kinetically insulated so that “gated” redox circuits can be activated by translocation/aggregation and/or catalytic mechanisms.
• 4.
  Oxidative stress is a disruption of the function of these redox circuits caused by specific reaction with the redox-sensitive thiol elements, altered pathways of electron transfer, or interruption of the gating mechanisms controlling the flux through these pathways.

The current article represents an extension and development of these concepts into a redox theory of aging. This redox theory is not exclusively limited to redox reactions but rather emphasizes the key role of electron transfer in supporting central energy currencies (ATP, phosphorylation, acetylation, acylation, methylation and ionic gradients across membranes) and providing the free energy to support metabolism, cell structure, biologic defense mechanisms and reproduction. Importantly, improved understanding of the integrated nature of redox control and signaling in complex, multicellular organisms  provide a foundation for this generalized theory.

Dean P. Jones

James Eckurg

REDOX SIGNALING HEALTH