Diabetes-Associated Decline in Antioxidant Networks: Consequences for Immune Surveillance and Tissue Integrity

Ivan Mutebi

Department of Pharmacognosy Kampala International University Uganda

Email: ivan.mutebi@studwc.kiu.ac.ug

                                                                              ABSTRACT
Diabetes mellitus, a metabolic disorder characterized by chronic hyperglycemia, exerts broad systemic effects that extend beyond glucose dysregulation. Central to these effects is an imbalance between reactive oxygen species (ROS) production and the body’s antioxidant defense systems, leading to persistent oxidative stress. In diabetic conditions, increased ROS generation arises from glucose auto-oxidation, mitochondrial dysfunction, activation of alternative metabolic pathways, and formation of advanced glycation end products (AGEs), while antioxidant networks such as superoxide dismutase, catalase, glutathione peroxidase, and non-enzymatic antioxidants are simultaneously compromised. This redox imbalance contributes to cellular and molecular damage, impairs immune surveillance by disrupting innate and adaptive immune responses, and undermines tissue integrity through endothelial dysfunction, chronic inflammation, and genomic instability. Moreover, oxidative stress accelerates diabetic complications such as neuropathy, nephropathy, retinopathy, and macrovascular disease. Understanding these mechanisms has profound implications for prevention, early detection, and therapeutic interventions. Emerging strategies aimed at restoring antioxidant capacity and modulating immune function may mitigate the progression of diabetic complications.

Keywords: Diabetes mellitus, oxidative stress, antioxidant defenses, immune surveillance, tissue integrity.

CITE AS: Ivan Mutebi (2026). Diabetes-Associated Decline in Antioxidant Networks: Consequences for Immune Surveillance and Tissue Integrity. NEWPORT INTERNATIONAL JOURNAL OF BIOLOGICAL AND APPLIED SCIENCES 7(2):23-29. https://doi.org/10.59298/NIJBAS/2026/7.2.2329