Vitamin C mitigates early auditory cortical hyperexcitability and antioxidant imbalance induced by acute intermittent hypoxia.

To test whether brief intermittent hypoxia (IH) induces early hyperexcitability and antioxidant imbalance in the primary auditory cortex (Au1) of rats, and whether high-dose vitamin C (VC) pretreatment mitigates these effects. 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 single 3 h IH protocol; VC (500 mg/kg, intraperitoneal injection) 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. 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 in Au1. Acute IH induces early Au1 dysfunction characterized by hyperexcitability and antioxidant imbalance. High-dose VC pretreatment attenuates hyperexcitability and enhances antioxidant enzyme activity, suggesting a potential protective role of antioxidant strategies in the central auditory system.