Redox metabolism reactions in humans - involving the transfer of electrons between molecules - play crucial roles in various cellular functions and physiological processes. Redox reactions are essential for energy production, antioxidant defence, cellular signalling, and maintaining the overall redox balance within cells. Redox reactions involve the transfer of electrons between molecules, resulting in the oxidation of one molecule and the reduction of another. The molecule that loses electrons is oxidized, whilst the molecule that gains electrons is reduced. These reactions are most critical in energy production through oxidative phosphorylation in the mitochondria, where electrons are transferred along the electron transport chain to generate ATP. The electron transport chain (ETC) is a critical component of redox metabolism in humans. Located in the inner mitochondrial membrane, the ETC consists of a series of protein complexes that transfer electrons from electron donors (such as NADH and FADH2) to oxygen, the final electron acceptor. This transfer of electrons drives the pumping of protons across the mitochondrial membrane, generating a proton gradient. The energy released during this process is used to produce ATP through oxidative phosphorylation. Maintaining redox homeostasis is essential for cellular health and preventing oxidative damage caused by reactive oxygen species (ROS). ROS are by-products of redox reactions that, when produced in excess, can chemically damage cellular components, including lipids, proteins, and DNA. Cells have evolved a range of antioxidant defence systems, including enzymes like superoxide dismutase, catalase, and glutathione peroxidase, which can neutralize ROS and protect cells from such oxidative stress. Redox metabolism also plays a pivotal role in cellular signalling. Redox-sensitive proteins, such as transcription factors, enzymes, and receptors, are modulated by changes in cellular redox status. For example, redox regulation of nuclear factor-kappa B (NF-κB) influences gene expression related to inflammation and immune responses, whilst high levels of ROS can oxidize and inactivate tyrosine phosphatase enzymes, reducing their ability to dephosphorylate target proteins and in turn affecting the cellular signalling pathways that depend on tyrosine phosphorylation events. Redox signalling thus participates in regulating many processes, including cell growth, apoptosis, and responses to environmental stressors. Nicotinamide adenine dinucleotide (NAD+) and its reduced form, NADH, are central players in redox metabolism processes. NAD+ functions as an electron carrier, accepting electrons during catabolic reactions and donating them during anabolic reactions. NADH is a potent reducing agent, donating electrons to the ETC during oxidative phosphorylation. The NAD+/NADH ratio thus plays a vital role in redox signalling and cellular energetics. Finally, glutathione is a tripeptide composed of cysteine, glycine, and glutamate that serves as a major antioxidant in cells. It participates in redox metabolism by donating electrons to neutralize ROS and detoxify potentially harmful compounds. Maintaining the reduced form of glutathione (GSH) is therefore crucial for cellular redox status and protection against oxidative stress. Increased oxidative stress and impaired antioxidant defence can lead to cellular damage and contribute to disease pathogenesis and ageing. We offer a wide product range of research tools for investigating redox metabolism, including Myeloperoxidase antibodies, Thyroid Peroxidase antibodies, Superoxide Dismutase 1 antibodies, Myeloperoxidase ELISA Kits, and eNOS ELISA Kits. Explore our full redox metabolism product range below and discover more, for less. Alternatively, you can explore our Oxidative Stress, Fatty Acid Oxidation, and Antioxidants product ranges.