The protective effects of allopurinol and superoxide dismutase on noise‐induced cochlear damage

TLDR

Noise exposure induces cochlear vasoconstriction, reducing blood flow, causing hypoxia and free oxygen radical formation. The study tests whether antioxidants that scavenge or block free oxygen radicals can protect the cochlea from noise‑induced damage. Rats received 60 h of 90 dB SPL broadband noise and were treated with SOD‑PEG, allopurinol, or vehicle. Noise produced significant auditory threshold shifts, but SOD‑PEG and allopurinol markedly attenuated these shifts, indicating that free oxygen radicals contribute to cochlear injury.

Abstract

Several studies have demonstrated that noise exposure may result in local vasoconstriction of cochlear vessels. The subsequent decrease in cochlear blood flow may lead to hypoxia and predispose to the formation of free oxygen radicals (FORs). If hypoxia occurs in response to noise exposure, then drugs that scavenge or block the formation of FORs should protect the cochlea from damage resulting from hypoxic or ischemic events as well as noise trauma. Rats were exposed to 60 hours of continuous broad‐band noise (90 dB SPL) and treated with superoxide dismutase — Polyethylene glycol (SOD‐PEG), allopurinol, or a control vehicle. Exposure to noise resulted in significant threshold shifts at each frequency tested (3, 8, 12, and 18 kHz) as measured by tone burst‐evoked compound action potentials and cochlear microphonics recorded from the round window. Both of these thresholds In drug‐treated animals were attenuated compared with animals exposed to noise alone. These findings show that SOD‐PEG and allopurinol may preserve cochlear sensitivity associated with noise exposure. This suggests that noise‐induced damage to the cochlea may be related to the activity of FORs.