Abstract

Antioxidants are central to cellular defense against oxidative stress, a critical driver of obesity-associated 
carcinogenesis. Excess adiposity generates chronic inflammation, insulin resistance, and elevated production of 
reactive oxygen species, which contribute to DNA damage and tumorigenesis. Antioxidants from dietary and 
endogenous sources are thought to counteract these effects, offering potential protection against cancer. However, 
emerging evidence suggests paradoxical roles: under certain conditions, antioxidants may promote tumor 
progression by enabling cancer cell survival, interfering with apoptosis, or altering redox-sensitive signaling 
pathways. This duality complicates the therapeutic promise of antioxidants in obesity-driven cancer risk. This 
review explores the mechanistic basis of antioxidant action in obesity-related carcinogenesis, highlighting protective 
effects and paradoxical outcomes. It examines evidence from preclinical and clinical studies, discusses the role of 
dietary, pharmacological, and endogenous antioxidants, and outlines implications for prevention and therapy. 
Ultimately, antioxidants should be viewed as a double-edged sword, with context-dependent effects that warrant 
careful evaluation in obesity-associated cancer management.