Exposures to large dose of kanamycin(KM) are well known to cause inner ear hair cell damage. For the monitoring of the ototoxic effect of kanamycin, eighteen guinea pigs with daily dosage of 50 mg/kg of kanamycin were evaluated by click-evoked otoacoustic emissions(CEOEs) and Preyer's reflex daily. The electron microscopic changes of cochlear hair cells were studied in three groups, such as just after negetive conversion of CEOEs, just after loss of Preyer's reflex and at the eightth week after loss of Preyer's reflex. Ther Preyer's reflex was disappeared at about 17th day of KM injection and the outer hair cells of basal and middle turn of cochlea were damaged. However, the cochlea echo of CEOEs was lost at the third day of KM jnjection and the cochlear hair cell damage was minimal on scanning electron microscope(SEM). The SEM study at the eighth week after loss of Preyer's reflex without further injection of kanamycin, revealed similar hair cell damages as those just after loss of Preyer's reflex. From this study, clinical application of CEOEs as a method for early identification and as a result, prevention of aminoglycoside-induced ototoxicity.