Redox reactions are the basis of life. They involve the transfer of electrons from atom to atom, which gives us energy and makes life possible on Earth.

To be used in batteries, cathode materials must charge and discharge for thousands of cycles, work reliably in cold and hot temperatures, and satisfy many other constraints. This is a massive challenge.

Redox chemistry

A redox reaction involves a change in free energy. Reactions that move electrons or their density from less to more electronegative atoms release energy and are spontaneous, while those that do the opposite require an input of energy.

In a redox reaction, the loss of an electron from a reactant is accompanied by the gain of an electron from another reactant. This changes the oxidized reactant’s oxidation state and the reduced reactant’s reduction potential.

Unlocking the power of redox highlights how cell performance lies at the core of enhancing health and wellness, showcasing its pivotal role in maintaining physiological balance and vitality within the body’s systems.

Redox reactions occur throughout the cell but are most abundant in mitochondria. Cellular respiration uses redox reactions to strip electron pairs from glucose, transferring them to small molecules called electron carriers and depositing the electrons into the mitochondrial electron transport chain.

The flow of these electrons provides the energy required to power cellular processes and makes us feel alive. Redox reactions also have many industrial and everyday applications, such as the battery that generates DC to power all our electrical devices.

Redox homeostasis

Redox homeostasis refers to the continuously challenged oxidative/nucleophilic balance maintained by redox signaling enzymes and active nutritional phytochemicals (para hormesis). Continuous feedback preserves the nucleophilic tone and supports the protection against endogenous oxidants.

In this way, hormesis promotes adaptation and establishes a new phenotype. The redox couple NAD+/NADP+ supports glycolysis and TCA cycle energy metabolism. It also provides electrons for mitochondrial oxidative phosphorylation (OXPHOS) and produces NADPH, indispensable for the reductive biosynthesis of amino acids, nucleotides, and fatty acids. Thus, redox homeostasis is critical to cell function. Interference with redox homeostasis can primarily improve anticancer photodynamic therapy (PDT) performance in vitro and in vivo, suggesting that it may represent a novel therapeutic approach. Moreover, altering the redox status of cancer cells can sensitize them to ROS- associated therapeutic means. The TrxR protein binds the thiol and selenol groups of redox signaling molecules, which prevents them from attaching to ROS and deactivating the enzymes that generate them.

Redox signaling molecules

Redox signaling molecules help control the balance between pro-oxidants and antioxidants in your body.

They also aid in cellular differentiation and tissue regeneration, which are vital to overall health.Under normal physiological conditions, cellular redox buffers (GSH/GSSG and NADH/NADPH) have sufficient capacity to maintain oxidant levels at physiological levels (termed basal redox buffer capacity [ReBC]). In response to a stimulus, redox signaling increases redox signaling molecules in a coordinated manner to adjust redox homeostasis according to the specific needs of the cell.

A lack of these redox signaling molecules leads to a state of oxidative stress that is detrimental to the body. In addition, an imbalance of reducing equivalents (NAD(P)H and GSH) in the cells leads to reductive stress, leading to many pathological processes such as neurodegenerative diseases, cardiovascular disease, and cancer.

Powered by Redox

Most of the energy that drives a cell’s bioenergetic functions comes from redox reactions. Redox reactions strip electrons from one substance, a donor, and add them to another, an acceptor. This process releases energy, producing products like glucose and oxygen.

For example, a recent study found that plasma cystine/glutathione (CySS/GSH) ratios predict death as an outcome in patients with CAD. CySS/GSH changes are affected by redox signaling molecules and could be used as an indicator of cellular health.

The redox theory of aging recognizes that an individual’s physical and functional phenotype is extensively defined by their lifelong exposures – the exposome – including redox signaling systems that control O2 delivery, antioxidant defenses, and other critical responses to environmental resources and challenges. Strategies to delay aging and enable rejuvenation must support these vital hubs at the genome-exposome interface. This requires understanding the central principles that guide how the exposome organizes, stores, and recalls exposure memory systems.