[Sodium salicylate induced intracellular Ca2+ concentration change in guinea pig outer hair cells].

OBJECTIVE

In order to explore the mechanism of sodium salicylate ototoxicity the effect of sodium salicylate on intracellular Ca2+ ([Ca2+]i) of the outer hair cells (OHCs) and the effects of calcium channel antagonist on sodium salicylate-induced [Ca2+]i changes of the OHCs were examined.

METHODS

The OHCs of guinea pig cochlear were isolated using an enzyme-machine methods and loaded with 10 mumol/L Fluo-3/AM for 30 min at 37 degrees C. Individual Fluo-3 loaded OHC was examined with a confocal microscope (ACAS Ultima, USA) using a 20 x objective lens and linear scan mean. The fluorescent images, collected each 5-sec for 300 sec, were stored in a computer. The fluorescent intensity of the OHCs were analyzed by the software cooperated with the confocal microscope, and a curve of fluorescent intensity changes trend against time was obtained.

RESULTS

The [Ca2+]i of OHCs were steady under normal extracellular liquid perfusion. Salicylate increased [Ca2+]i in OHCs in calcium-free medium(10/10) and standard medium (8/10). 3 mmol/L lidocaine inhibited [Ca2+]i increase in OHCs induced by salicylate(0/10). The [Ca2+]i increase in OHCs induced by salicylate could be blocked by flunarizine(3/12). Nimodipin failed to block the [Ca2+]i increase of OHCs induced by salicylate (7/7).

CONCLUSION

Sodium salicylate can result in [Ca2+]i increase in OHC markedly, which may be due to the Ca2+ release from intracellular calcium stores. The effects of salicylate on [Ca2+]i in OHCs might be one of the mechanisms of salicylate ototoxicity.