Browsing by Subject "Ototoxicity"
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- PublicationOpen AccessEffect of coenzyme A on outer hair cells in cisplatin ototoxicity: functional and ultrastructural study(Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Fernández Cervilla, Francisco; Martínez Martínez, María; Fernández Segura, Eduardo; Cañizares García, Francisco Javier; Crespo Ferrer, Pascual VicenteThe aim of this study was to use functional and morphological analyses to evaluate the protective effect of coenzyme A (CoA) in cisplatin-induced toxicity in outer hair cells (OHC). Three groups of 8 guinea pigs were used: control (group I), cisplatin-treated (group II) and cisplatin + CoA-treated (group III). In groups II and III, a single ototoxic dose of cisplatin (10 mg/kg) was injected intraperitoneally. Group III was co-treated with CoA (900 μg/kg per day for 7 consecutive days). Electrocochleography (ECoG) recordings were made before and after the 7-day treatment period in all groups. After ECoG on day 7, all animals were anesthetized and the cochleae were removed and fixed for ultrastructural analysis. Cell damage in OHC was observed with transmission electron microscopy. Cisplatin induced a significant increase in auditory thresholds (p<0.001) compared to group I (control). In contrast, group III (cisplatin + CoA) had significantly reduced thresholds (p<0.001) compared to the group treated with cisplatin alone (group II). We found no significant differences between the control group and animals co-treated with cisplatin and CoA. The electron microscopy findings in OHC were consistent with these results. Ultrastructural analysis of OHC in group II showed morphological indications of necrosis, i.e. cytoplasmic swelling and vacuolation, and mitochondrial swelling. In group III the cell morphology of OHC was preserved, with ultrastructural characteristics similar to the control group. In conclusion, co-treatment with cisplatin with CoA inhibited antineoplastic-induced cytotoxicity in OHC in a guinea pig model.
- PublicationOpen AccessVestibular histofluorescence could be due to accumulation of both the antibiotic and its derivative, streptidine, after acute streptomycin treatment in the guinea pig(Murcia : F. Hernández, 2001) Meza Ruiz, G.; Barba-Behrens, N.; Granados, O.; Hernandez-Cruz, A.; Toxqui, A.Acute treatment with 300 mglkg of pigmented guinea pigs with streptomycin sulfate induces an elevation of endogenous fluorescence in vestibular ampullary cristae. Fluorescence accumulates in all compartments of the epithelium, i.e., vestibular sensory and supporting cells and nerve fibers of the stroma and it was very intense 1 and 12 hours after its administration. Fli~orescence decreased to control levels 24 hours following streptomycin injection. Fluorescence levels were very low either in untreated animals or in animals injected with s a l i n e physiological solution. To investigate whether this fluorescence was an intrinsic property of the antibiotic or whether it was due to a derivative of it, or both, an in vitro fluorescence spectrum was performed with I00 ,LIM solutions of streptomycin or streptidine, or both, dissolved in various buffer solutions at 488 nm of excitation. A discrete level of fluorescence was observed in the spectrum regardless of media when separate solutions of both streptomycin or streptidine were s t u d i e d . Fluorescence notably increased at 522-532 nm when the solutions contained both streptomycin and streptidine toget her. These results suggest that streptidine putatively derived from streptomycin may contribute to the observed fluorescence accumulation in vestibular preparations after acute treatment. Thus, these metabolic properties of the inner ear which transform streptomycin into streptidine, something never considered earlier, could be claimed as partially responsible for converting a therapeutic agent into a compound which could be as harmful as STP to the inner ear.