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While nutritional VC intake demonstrates chemopreventive effects by scavenging carcinogen-induced reactive oxygen species (ROS) and maintaining genomic stability, high-dose intravenous VC acts as a prooxidant to selectively kill tumor cells via ROS-mediated deoxyribonucleic acid (DNA) damage, adenosine triphosphate (ATP) depletion, and HIF-1 degradation

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In the brain, these cells interact with antigen-presenting cells and release inflammatory cytokines such IL-17, IFN-, and TNF-, leading to neuroinflammation and dopaminergic neuron death [105]

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