Vitamin C Mitigates Early Auditory Cortical Hyperexcitability and Antioxidant Imbalance Induced by Acute Intermittent Hypoxia

Objectives To test whether brief intermittent hypoxia (IH) induces early hyperexcitability and antioxidant imbalance in the primary auditory cortex (Au1), and whether high-dose vitamin C (VC) pretreatment mitigates these effects. Methods Adult male Sprague–Dawley rats were assigned to four groups (n = 6/group): control, IH, IH plus intraperitoneal normal saline (IH + IPNS), and IH plus intraperitoneal VC (IH + IPVC). Rats underwent a 3-h IH protocol; VC (500 mg/kg, i.p.) or saline was administered 30 min before IH. Three hours after IH, in vivo Au1 multiunit recordings quantified spontaneous firing rate (SFR). We quantified catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities and assessed apoptosis using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. Results Acute IH increased Au1 SFR versus control, and saline did not alter this response; VC pretreatment reduced SFR toward control levels. IH decreased CAT activity and increased SOD activity, with minimal change in GPx. VC increased CAT, SOD, and GPx activities relative to IH. No overt neuronal apoptosis was detected. Conclusions Brief OSA-relevant IH triggers an early stage of auditory cortical dysfunction with hyperexcitability and antioxidant imbalance. High-dose VC pretreatment attenuates hyperexcitability and enhances antioxidant enzyme activity, supporting antioxidant strategies as adjuncts for central auditory protection.