General Antioxidant Activity

General antioxidant activity refers to the integrated capacity of endogenous systems and exogenous substances to neutralize reactive oxygen species (ROS) and reactive nitrogen species (RNS), thereby preventing oxidative stress-induced damage to cellular macromolecules such as DNA, proteins, and lipids [1, 2]. This activity is not a single molecular target but rather a physiological process mediated by enzymatic antioxidants (e.g., superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic molecules (e.g., glutathione, vitamins C and E) [2, 3]. In disease states like cancer, atherosclerosis, and Alzheimer's disease, the balance between pro-oxidants and antioxidants is disrupted, leading to chronic oxidative damage [3, 4]. Pharmacological interventions often aim to bolster this activity through direct radical scavenging or by activating transcription factors like Nrf2, which upregulates a broad battery of protective genes [5]. However, the therapeutic application of general antioxidants faces challenges, including the 'antioxidant paradox,' where high doses may actually increase mortality or interfere with essential physiological signaling pathways [1, 6]. Because this term describes a broad functional outcome rather than a specific protein or receptor, it is generally categorized as a pharmacological effect rather than a discrete therapeutic target [4, 6]. Sources: [1] NIH Office of Dietary Supplements. "Antioxidants: In Depth." [2] Halliwell, B., & Gutteridge, J. M. C. (2015). Free Radicals in Biology and Medicine. Oxford University Press. [3] PubMed (PMID: 29130107). "Oxidative stress, inflammation, and cancer: How are they linked?" [4] PubMed (PMID: 24513140). "The antioxidant paradox: less can be more." [5] UniProt (P15923). "Nuclear factor erythroid 2-related factor 2." [6] PubMed (PMID: 30855146). "Antioxidants for preventions and treatment of cardiovascular diseases."

Other names

Antioxidant capacityFree radical scavengingReactive Oxygen Species (ROS) scavengingRedox homeostasisAntioxidant defense system

Direct neutralization of free radicals via electron donation, chelation of transition metals, and induction of endogenous antioxidant enzymes through the activation of the Nrf2-ARE signaling pathway.