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[The experimental study of the anti-damage effect of iminoethyl-lysine on noise-induced cochlea damage in guinea pig].

OBJECTIVE
To investigate the anti-damage effect of iminoethyl-lysine on noise-induced cochlea damage in guinea pig.


METHODS
40 healthy red eye guinea pigs were randomly divided into 4 groups: Group A, normal control group; Group B, noise group; Group C, noise and drug group; Group D, iminoethyl-lysine group. Guinea pigs of both group B and group C were exposed to 115 dB white noise for 6 hours/day for 6 days. Group C and Group D were treated with iminoethyl-lysine(10 mg/kg) intraperitoneally, while Group B were treated with the same volume of physiological saline. ABR hearing threshold was measured in all animals before and after experiment. The expression of inducible nitric oxide synthase(NOS II) in the cochlea was examined by the method of immunohistochemistry. Also the cochlea of four groups were examined with scanning electronic microscope. ABR hearing threshold, expression of NOS II and structure of cochlea of four groups were compared with each other.


RESULTS
There was no significant difference in ABR hearing threshold among four groups before the experiment(P > 0.05). There was no significant ABR hearing threshold shift in Group A and Group D after the experiment(P > 0.05), and there was significant ABR hearing threshold shift in Group B and Group C(P < 0.05). After the experiment, the ABR hearing threshold of group B(60.23 +/- 11.23) dB, was higher than that of Group C(38.46 +/- 7.24) dB, P < 0.05. The expression of NOS II was negative in the cochlea of Group A and Group D, but was stronger in Group B than that in Group C. The damage of outer hair cells of cochlea of Group B was more severe than that of Group C.


CONCLUSIONS
The expression of NOS II in the guinea pig's cochlea damaged by noise is positive. Iminoethyl-lysine could inhibit the activity of NOS II and has the anti-damage effect on noise-induced cochlea damage. It is indicated that nitric oxide plays an important role in the pathogenesis of noise-induced hearing loss.