Aminoglycosides, such as
gentamycin, are well known ototoxic agents. Toxicity occurs via an activation process involving the formation of an
iron-
gentamycin complex with
free radical production.
Antioxidants like
Q-ter (a soluble formulation of
coenzyme Q(10),
CoQ(10)), can limit or prevent cellular ototoxic damage. The present study was designed to investigate the possible protective effects of
Q-ter on
gentamycin ototoxicity in albino guinea pigs (250-300 g). Animals were divided into five experimental groups: I, a
sham control group given an intra-peritoneal (I.P.) injection of 0.5 ml saline (
SHAM); II,
gentamycin group (GM), treated with an injection of
gentamycin (100 mg/ kg); III,
gentamycin +
Q-ter group (GM+Q-ter), treated with
gentamycin (same dose as group II) and an I.P. injection of
coenzyme Q(10) terclatrate (
Q-ter) at 100 mg/kg
body weight; IV, injected with
gentamycin (100 mg/kg) plus saline; V, treated with
Q-ter alone (100 mg/ kg). All animals were treated for 14 consecutive days. Auditory function was evaluated by recording auditory brainstem responses (ABR) at 15 and 30 days from the beginning of treatment. Morphological changes were analyzed by
rhodamine-
phalloidine staining.
Gentamycin-induced progressive
high-frequency hearing loss of 45-55 dB SPL.
Q-ter therapy slowed and attenuated the progression of
hearing loss, yielding a threshold shift of 20 dB. The significant loss of outer hair cells (OHCs) in the cochlear medio-basal turn in
gentamycin-treated animals was not observed in the cochleae of animals protected with
Q-ter. This study supports the hypothesis that
Q-ter interferes with
gentamycin-induced
free radical formation, and suggests that it may be useful in protecting OHC function from
aminoglycoside ototoxicity, thus reducing
hearing loss.