Introduction: Reactive oxygen species (ROS) are highly reactive oxygen-derived molecules that function as both potent inducers of cellular damage and essential signalling mediators. In a physiological setting, normal ROS levels control vital functions like immune responses, cell division, and proliferation. However, oxidative stress, which is a major factor in the onset and spread of cancer, is caused by a disturbance in redox equilibrium. Methods: The published literature on ROS, antioxidant defense mechanisms, redox-sensitive signalling pathways, and the anticancer potential of natural substances was summarised and critically assessed in this review. A systematic analysis of peer-reviewed research on molecular mechanisms, signalling cascades, and therapeutic implications was conducted. Results: DNA damage, lipid peroxidation, and protein oxidation are caused by excessive ROS production or impaired antioxidant defenses, which encourage genomic instability and oncogenic transformation. Increased ROS levels impact apoptosis, proliferation, and tumour growth by activating several redox-sensitive pathways such as NF-κB, PI3K/Akt, and MAPK. Both enzymatic and non-enzymatic antioxidants shield cells from oxidative damage, but they can also act as pro-oxidants in certain situations. By altering reactive oxygen levels, suppressing oncogenic signalling, and promoting apoptosis, natural compounds like curcumin, resveratrol, lycopene, and marine-derived metabolites show promising anticancer activity. Discussion: The intricacy of redox control in cancer is highlighted by the dualistic involvement of ROS as tumour promoters and suppressors. Opportunities for redox-based therapeutic interventions are presented by cancer cells, related oxidative stress, and increased reliance on antioxidant systems. Conclusion: A precise understanding of ROS-driven mechanisms can help design targeted redox-based strategies for effective cancer prevention and treatment.
Irfan et al. (Wed,) studied this question.