Oxygen (O₂)
Description
Greek: ὀξύς (oxys) - acid + γενής (gen) - produce
Oxygen (O₂) is a colorless, odorless, and tasteless diatomic gas that constitutes about 21% of Earth's atmosphere by volume. It is essential for aerobic respiration in most living organisms and acts as a strong oxidizing agent. Oxygen has an atomic number of 8 and belongs to the chalcogen group on the periodic table. It exists primarily as a diatomic molecule (O₂) with a double bond between the atoms and also forms ozone (O₃) in the atmosphere.
Summary
Oxygen is essential for aerobic metabolism in human tissues. It is inhaled into the lungs, where it diffuses across the alveolar-capillary membrane into the bloodstream. In blood, oxygen binds reversibly to hemoglobin in red blood cells, forming oxyhemoglobin, which transports oxygen to peripheral tissues. Cells utilize oxygen in mitochondria during oxidative phosphorylation to produce ATP, the primary energy source for cellular functions. Oxygen delivery and consumption are critical for maintaining cellular homeostasis and organ function. Hypoxia, a deficiency in oxygen supply, can lead to cellular injury and organ dysfunction. Clinical monitoring of oxygenation includes measurement of arterial oxygen partial pressure (PaO₂) and oxygen saturation (SpO₂).
Absorption of Oxygen
Oxygen is absorbed into the body through the respiratory system. During inhalation, oxygen-rich air reaches the alveoli in the lungs, where oxygen diffuses across the thin alveolar-capillary membrane into pulmonary capillaries due to a partial pressure gradient. In the blood, oxygen binds reversibly to hemoglobin in red blood cells, forming oxyhemoglobin for transport. Oxygen is delivered to tissues via systemic circulation, where it diffuses into cells to support aerobic metabolism. Carbon dioxide, a metabolic waste product, diffuses from tissues into the bloodstream, transported primarily as bicarbonate ions, dissolved CO₂, or carbaminohemoglobin, and is eliminated through exhalation via the lungs.
Functions
Supports aerobic cellular respiration, enabling ATP production in mitochondria.
Facilitates oxidative phosphorylation as the final electron acceptor in the electron transport chain.
Maintains tissue and organ viability by ensuring adequate oxygen delivery.
Enables immune defense via reactive oxygen species production in phagocytes.
Assists in metabolic detoxification processes.
Chemical Structure
Molecular formula: O₂
Molecular mass: ~32 atomic mass units (amu)
Atomic composition: Two oxygen atoms (each atomic number 8)
Bond type: Double covalent bond (one sigma (σ) bond + one pi (π) bond)
Bond order: 2
Bond length: Approximately 121 picometers (pm)
Electron configuration (O atom): 1s² 2s² 2p⁴
Molecular orbital configuration:
Electrons fill bonding (σ2s, σ2s, σ2p, π2p) and antibonding (π2p) orbitals
Two unpaired electrons in antibonding π* orbitals → paramagnetic behavior
Polarity: Nonpolar molecule (identical atoms, no dipole moment)
Magnetic property: Paramagnetic due to unpaired electrons
Bond dissociation energy: ~498 kJ/mol
Physiological Functions
Cellular Energy Production
Aerobic Respiration:
Oxygen is the final electron acceptor in the mitochondrial electron transport chain.
Enables oxidative phosphorylation, producing ATP—the primary energy source for cellular processes.
One glucose molecule yields up to ~36–38 ATP molecules in the presence of oxygen, compared to just 2 ATP via anaerobic glycolysis.
Mitochondrial Function:
Sustained oxygen availability is critical for mitochondrial efficiency and cellular viability.
Oxygen deficiency (hypoxia) impairs ATP generation, leading to metabolic acidosis and cell injury.
Tissue Oxygenation and Organ Function
Oxygen Transport:
Inhaled O₂ diffuses across alveolar membranes into pulmonary capillaries.
~98% of O₂ binds reversibly to hemoglobin (forming oxyhemoglobin); the rest is dissolved in plasma.
Hemoglobin releases O₂ to tissues according to local metabolic demand (Bohr effect).
Tissue Perfusion:
Adequate oxygenation supports high-demand organs (brain, heart, kidneys) and prevents ischemic injury.
Hypoxia triggers compensatory mechanisms (e.g., increased ventilation, erythropoietin release).
Cellular Metabolism and Waste Removal
Oxidative Metabolism:
Oxygen drives the breakdown of macronutrients (glucose, fats, proteins) for ATP production.
Also contributes to thermogenesis (heat generation) in brown adipose tissue.
CO₂ Removal:
Carbon dioxide (CO₂), a metabolic byproduct of aerobic respiration, diffuses into the bloodstream.
Transported primarily as bicarbonate ions (HCO₃⁻), with smaller amounts bound to hemoglobin or dissolved in plasma.
Exhaled through the lungs during ventilation.
Immune Function and Host Defense
Respiratory Burst in Phagocytes:
Neutrophils and macrophages use O₂ to produce reactive oxygen species (ROS) (e.g., superoxide, hydrogen peroxide) during phagocytosis.
These ROS destroy engulfed pathogens and help regulate inflammatory responses.
Redox Signaling and Cellular Regulation
Reactive Oxygen Species (ROS):
While toxic at high levels, controlled ROS production is essential for cell signaling, apoptosis, and gene expression.
Oxygen balance is tightly regulated by antioxidants (e.g., glutathione, superoxide dismutase) to prevent oxidative damage.
Wound Healing and Tissue Repair
Angiogenesis and Collagen Synthesis:
Oxygen is crucial for fibroblast function, collagen cross-linking, and new blood vessel formation.
Hypoxic tissues heal poorly due to impaired cellular activity and matrix remodeling.
Clinical Relevance
Hypoxia: Leads to fatigue, organ dysfunction, lactic acidosis, and in severe cases, death.
Hyperoxia: Excessive oxygen can cause oxidative stress and tissue damage, especially in neonates and patients on supplemental oxygen.
Pulse oximetry and arterial blood gas (ABG) measurements are used to assess oxygenation status in clinical settings.
References
Arora, S. & Tantia, P. (2019) Physiology of Oxygen Transport and its Determinants in Intensive Care Unit, Indian Journal of Critical Care Medicine, 23(Suppl 3), pp. S172–S177.
Crystal, G. J. & Pagel, P. S. (2019) The Physiology of Oxygen Transport by the Cardiovascular System: Evolution of Knowledge, Journal of Cardiothoracic and Vascular Anesthesia, 33(5), pp. 1270–1281.
Fitzgerald, R. S. & Rocher, A. (2021) Physiology and Pathophysiology of Oxygen Sensitivity, Antioxidants, 10(7), 1114. DOI: 10.3390/antiox10071114.
Mori, M. P. M. et al. (2022) Mitochondria and oxygen homeostasis, The FEBS Journal. DOI: 10.1111/febs.16115.
Poole, D. C. et al. (2023) Capillary‑Mitochondrial Oxygen Transport in Muscle: Paradigm Shifts, Comprehensive Physiology, 13(1).
Sjöberg, T. et al. (2013) The medical use of oxygen: a time for critical reappraisal, Journal of Internal Medicine, 274(5), pp. 483–498. DOI: 10.1111/joim.12139.
Wigerup, C., Påhlman, S. & Bexell, D. (2016) Systems biology of oxygen homeostasis, WIREs Systems Biology and Medicine, 8(6), e1382. DOI: 10.1002/wsbm.1382.