Noise & health
-
The role of glutathione in carboplatin ototoxicity was investigated in the chinchilla. Chinchillas hearing was tested with both distortion product otoacoustic emissions (DPOAE) and evoked potentials recorded from a chronic electrode in the inferior colliculus (IC). All subjects had an osmotic pump fitted to their right ear and it received buthionine sulfoximine (BSO) at a dose of 15 mM delivered at 5 ml per hour for 14 days. ⋯ The pump was implanted three days before the carboplatin dose. The BSO treated ears showed a greater loss in both evoked potential and DPOAE measures, as well as substantially fewer missing hair cells. The results implicate reactive oxygen species (ROS) as a common factor in ototoxic reactions because suppression of glutathione antioxidant leads to greater ototoxic reactions.
-
Carboplatin, a second-generation antineoplastic drug, is much less ototoxic than cisplatin in humans and many laboratory animals. However, when a moderate dose of carboplatin is administered to chinchillas, it can selectively destroy inner hair cells (IHCs) and type-I ganglion neurons without damaging the outer hair cells (OHCs). One of the earliest signs of injury from carboplatin is damage to type I, spiral ganglion neurons. ⋯ IHC loss leads to a reduction in neural input (i.e., sensory deprivation) to the central auditory system. Surprisingly, although the neural input to the central auditory system is reduced, evoked response amplitudes recorded from the auditory cortex are often enhanced. These results indicate that when the neural input to the central auditory brain is reduced, the central auditory system compensates for the reduced input by increasing its gain.