Disruptions in nitric oxide homeostasis, lipid peroxidation-derived oxidative stress, and antioxidant defense mechanisms in spinal cord injury: elucidating biomolecular correlates of disease severity

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Abstract
Spinal cord injury (SCI) is a debilitating condition characterized by irreversible neurological deficits resulting from primary mechanical damage followed by a complex cascade of secondary injuries. Among the key molecular mechanisms driving secondary damage are oxidative stress (OS), nitric oxide (NO) homeostasis disruptions, and impaired antioxidant defense systems. This review elucidates the critical interplay between reactive oxygen and nitrogen species, lipid peroxidation (LPO)-derived aldehydes such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), and the roles of key antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Particular focus is placed on the dual role of NO as both a neuroprotective and neurotoxic agent, influenced mainly by its source and interaction with superoxide to form peroxynitrite (ONOO⁻). The paper also highlights the regulatory functions of trace elements like zinc, selenium, copper, and magnesium in modulating oxidative responses and recovery. Also, the nuclear factor erythroid 2 related factor 2 (Nrf2) pathway is discussed as a vital modulator of antioxidant gene expression. Understanding the dynamic cross-talk between NO signaling, LPO, and antioxidant mechanisms provides valuable insights into the molecular pathophysiology of SCI and unveils potential therapeutic targets aimed at mitigating oxidative damage, promoting neuroprotection, and enhancing functional recovery.

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