Abstract:
The elimination of cisplatin ototoxicity is an
ongoing concern. This experimental study was undertaken
to investigate the effect of oral erdosteine in
ameliorating cisplatin-induced ototoxicity. Twenty-eight
adult female Wistar albino rats were randomly divided
into four equal groups. Group A received an oral carrier
vehicle of the drug erdosteine with 0.2 ml of 0.9% saline.
Group B was administered only erdosteine (per oral
10 mg/kg twice a day) for 6 days. Group C was injected
with cisplatin intraperitoneally (i.p.) on day 0 (16 mg/kg
body weight), once only. Group D was given erdosteine
(per oral 10 mg/kg/day) 1 day before and for 5 days
consecutively after cisplatin injection (16 mg/kg, i.p.).
Distortion product otoacoustic emissions (DPOAEs)
were elicited in different frequency regions, ranging from
1,001 to 6,299 Hz as DPgram and input/output (I/O)
functions from the control and experimental animals.
All experimental animals were killed under general
anesthesia on day 5, following the last otoacoustic
emission measurements. Prior to death, blood samples
were drawn for measurement of superoxide dismutase,
xanthine oxidase (XO), malondialdehyde and nitric
oxide. Initial DPgram and I/O function baseline measurements
were similar in all groups prior to any drug
administration (P>0.05). On day 5, intra-subject measurement
parameters of DPgrams and I/O functions
in the cisplatin group showed significant deterioration
(P <0.05). The other groups revealed no differences
between their pre- and post-test drug administration
DPgrams and I/O functions at any test frequency
(P>0.05). Comparison of the amplitudes of DPgrams
and I/O functions between the cisplatin and control
groups showed significant changes (P <0.05). Biochemical
studies noted an increased XO activity following
cisplatin administration (P <0.007). The other
biochemical results did not show significant differences
between the study and control groups. This study demonstrates
that, in rats, erdosteine is protective for cochlear
function against the disruptive effects of cisplatin
as measured by DPOAEs.
