ABSTRACT
The functional resemblance between kidney proximal tubular and inner ear epithelial cells which has often been pointed out in the literature led us to hypothesize that nephrotoxic agents that cause renal tubular injury might also impair the function of inner ear cells. As one of the most toxic environmental nephrotoxic agents is cadmium, we aimed to study its effects on hearing experimentally in rats. In this study, increased blood and renal cortical cadmium levels were associated with high cadmium accumulation in ear ossicles and labyrinth in rats exposed to cadmium. The changes in auditory brainstem response (ABR) and otoacoustic emission in 2-month-old male rats exposed to drinking water containing 5 and 15 ppm CdCl2 for 30 days showed that cadmium-induced nephrotoxicity was associated with signs of defective hearing at a concentration of 15 ppm CdCl2 but that 5 ppm CdCl2 caused hearing loss without affecting kidney function. The mean latency of ABR wave 1, which indicates the function of the cochlea, was 1.335 +/- 0.31 ms in the control group and 1.641 +/- 0.052 and 1.74 +/- 0.88 ms in the rats subjected to 5 and 15 ppm CdCl2, respectively (p < 0.001). In the cadmium-treated groups short interpeak wave I-III latencies (p < 0.01) indicated cochlear dysfunction and this was also supported by the distortion product otoacoustic emission results (p < 0.001). Non-significant changes in wave III and V latencies were accepted as evidence of unaltered function of the other parts of the auditory system. These results suggest that hair cells are more sensitive to cadmium than kidney tubule cells and that the cochlear component of hearing is more vulnerable to cadmium toxicity than other parts of the auditory system.