Study uncovers potential drug treatment for noise-induced
hearing loss
July 2010
Editor: This is certainly good news in the effort to find better ways to
treat hearing loss, but I think there's still a long ways to go before
viable commercial treatment becomes a reality. Here's the press release.
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Researchers from the University of Auckland, New Zealand, have discovered
that a potent new drug restores hearing after noise-induced hearing loss in
rats. The landmark discovery found that injection of an agent called 'ADAC',
activates adenosine receptors in cochlear tissues, resulting in recovery of
hearing function. The finding paves the way for effective non-surgical
therapies to restore hearing loss after noise-induced injury. Dr. Srdjan
Vlajkovic and his team's work[1] is published in a special edition of
Springer's journal Purinergic Signalling, focusing on the inner ear.
Hearing loss from noise exposure is a leading occupational disease with
up to five percent of the population at risk worldwide. It is particularly
common in the military and in industrial settings (construction workers,
mining, forestry and airline industry). At the present time, the only
treatment strategies for hearing loss are hearing aids and cochlear
implants. Drug therapies for noise-induced hearing loss have only recently
been proposed and, to date, there are virtually no treatments that can
repair the damage to the inner ear and reduce the impact of hearing loss.
Vlajkovic and his team's study investigates the potential of adenosine
amine congener (ADAC) - a selective A1 adenosine receptor agonist - in the
treatment of noise-induced hearing loss. Wistar rats were exposed to
narrow-band noise for 2 - 24 hours in an acoustic chamber to induce cochlear
damage and permanent hearing loss. ADAC or placebo control was then
administered by injection(s) in the abdomen, either as a single injection at
six hours or multiple daily injections. The researchers measured the hearing
in the rats before and after the treatments using a technique known as
auditory brainstem response (ABR). They also used histological techniques to
determine the number of missing cochlear sensory hair cells after noise
exposure and the noise-induced production of free radicals.
Their results show that cochlear injury and hearing loss in rats exposed
to narrow-band noise can be substantially restored by ADAC administration
after noise exposure. Early treatment starting six hours after noise
exposure was the most effective and provided greater recovery than late
treatment starting 24 hours after noise exposure. The most sustainable
treatment strategy was the one involving multiple injections of ADAC for
five days after noise exposure. This therapy significantly attenuated
noise-induced hearing loss and improved sensory hair cell survival.
The authors conclude: "This study underpins an important role of
adenosine signaling in mitigation of cochlear injury caused by oxidative
stress. ADAC in particular emerges as an attractive pharmacological agent
for therapeutic interventions in noise-induced cochlear injury in instances
of both acute and extended noise exposures."