Figure 4
From: Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway
Sequential GMTR fluorescence in the middle cochlear turn examined at 30, 90, and 180 min after 125 mg/kg GM/GMTR injection in the control (a–c) and 30-min ischemic cochlea (d–f). GMTR fluorescence in outer hair cells was depicted 30 min after injection of GMTR in both groups (a, d). At 90 min after application of GMTR, gentamicin fluorescence was still negligibly labeled at the inner hair cell of the control (b) but visible in those of the 30-min ischemic cochlea. Diffusion of GMTR fluorescence into hair cell cytoplasm could be found, especially in the ischemic cochlea (e). After 180 min, diffused GMTR fluorescence was labeled in the outer hair cells cytoplasm and some soma of inner hair cells (c, f), in which more intense GMTR fluorescence was labeled in 30-min ischemic cochlea (f). (g) Comparison of the sequential hair cells fluorescence differences between control and ischemic cochleae (n=4 in each group). The GMTR fluorescence is more intense in the outer hair cells. In addition, the hair cells in the ischemic cochleae exhibit more fluorescent intensity that those in the control cochleae at least 90 min after GMTR injection. The y axis indicates the relative fluorescence intensity ratioed against that of the first row of OHCs 30 min after 125 mg/kg GM/GMTR injection in the control cochlea. The x axis indicates the different hair cell types. The value with error bar in each point indicates mean±s.e. (*P<0.05) GM: gentamicin; GMTR: conjugate of gentamicin and Texas-Red esters. Bar=20 μm.
