Oxidative Mechanisms in Biological Systems

Reactive oxygen species (ROS) such as superoxide anion, hydrogen peroxide and hydroxyl radical arise from oxygen metabolism and serve both as signalling molecules and potential agents of cellular damage. Oxidative mechanisms underlie fundamental processes including defence against pathogens, regulation of gene expression and apoptosis. Central to these processes is the balance between oxidant generation and antioxidant defences, comprising enzymatic systems such as superoxide dismutases, catalase and peroxidases, and small-molecule scavengers like glutathione and ascorbate. Transition metals, notably iron and copper, catalyse formation of highly reactive radicals via the Fenton reaction, driving lipid peroxidation, protein oxidation and DNA modification. These oxidative modifications can disrupt membrane integrity, enzyme activity and genomic stability, contributing to ageing and disease. In parallel, reversible oxidative post-translational modifications of cysteine residues function in redox signalling, modulating protein function and cellular adaptation to stress. Emerging research also highlights interactions between oxidative and nitrosative pathways, generating peroxynitrite and other reactive nitrogen species that further influence cell fate. Understanding these interconnected pathways is critical for the development of therapies targeting oxidative stress in conditions such as neurodegeneration, cardiovascular disease and cancer. Biological systems have evolved compartmentalised redox networks and repair mechanisms to manage oxidant flux, underscoring the global significance of oxidative mechanisms in health and disease.

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Oxidative Mechanisms in Biological Systems publication trend

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Technical terms

Reactive oxygen species (ROS): Partially reduced oxygen derivatives that include superoxide anion, hydrogen peroxide and hydroxyl radical, capable of oxidising biomolecules.
Fenton reaction: Iron-catalysed conversion of hydrogen peroxide into hydroxyl radical and hydroxide ion, a key generator of reactive radicals.
Lipid peroxidation: Free-radical-mediated oxidative degradation of polyunsaturated lipids, leading to membrane damage and bioactive aldehyde formation.
Redox homeostasis: The dynamic equilibrium between oxidant production and antioxidant defences that maintains cellular redox balance.
Thiol–disulfide exchange: Reversible redox modification of cysteine residues, central to antioxidant defence and redox signalling.

References

1. Prediction of Antioxidant Capacity of Thiolate–Disulfide Systems Using Species-Specific Basicity Values. Antioxidants (2024).
2. The Colorimetric Detection of the Hydroxyl Radical. International Journal of Molecular Sciences (2023).
3. Iron-catalyzed hydroxyl radical formation. Stringent requirement for free iron coordination site.. Journal of Biological Chemistry (1984).