ABSTRACT
OBJECTIVE: To evaluate the effect and safety of intratympanic dexamethasone administration on cisplatin-induced ototoxicity in adult male guinea pigs and to assess the differences between early and late protection from this ototoxicity. METHODS: Forty eight adult male guinea pigs were divided as follows: group I served as control group. Group II was subjected to intratympanic saline (subgroup IIa) or dexamethasone (subgroup IIb) injection. Group III was intraperitoneally injected with cisplatin. Groups IV and V were subjected first to intratympanic dexamethasone administration in both ears for 5 days starting 1 day and 1h - respectively - before cisplatin intraperitoneal injection. RESULTS: Dexamethasone intratympanic injection revealed similar functional and structural results compared with control. Cisplatin intraperitoneal injection resulted in a profound cochlear functional and structural damage in group III. Non-significant otoprotection resulted from intratympanic dexamethasone administration one day before cisplatin. Intratympanic dexamethasone injection 1h before cisplatin treatment resulted in a significant preservation of the functional and structural properties of the cochlea. CONCLUSION: Intratympanic dexamethasone administration is a safe, easy and efficient way to protect from cisplatin ototoxicity especially when administered 1h before cisplatin treatment.
Subject(s)
Antineoplastic Agents/adverse effects , Cisplatin/adverse effects , Cochlea/drug effects , Dexamethasone/administration & dosage , Glucocorticoids/administration & dosage , Hearing Loss/prevention & control , Acoustic Stimulation , Animals , Antineoplastic Agents/administration & dosage , Auditory Threshold/drug effects , Cisplatin/administration & dosage , Cochlea/pathology , Disease Models, Animal , Evoked Potentials, Auditory, Brain Stem , Guinea Pigs , Hearing Loss/chemically induced , Injections , Male , Microscopy , Microscopy, Electron, Scanning , Tympanic MembraneABSTRACT
It had been suggested that chronic exposure to Schistosoma mansoni prevents the onset of Th1-mediated diseases such as diabetes mellitus. The present study was carried out on four groups of mice: (1) control group, (2) group infected with S. mansoni, (3) group injected with streptozotocin to induce diabetes, and (4) group infected and then 3 months postinfection injected with streptozotocin. No differences were detected between the infected non-diabetic and infected diabetic groups regarding worm burden, tissue egg count, and oogram. At the same time, results showed a reducing effect of S. mansoni infection on the rate of glucose uptake by the diaphragm with reduction in glycogen content of soleus muscle. This an important issue since skeletal muscle is the primary site for insulin-stimulated glucose disposal. In conclusion, because of the detected depressed peripheral glucose uptake by the diaphragm, the protecting effect of helminths infection in diabetes should be reconsidered, to be able to devise therapeutic strategies for the treatment of autoimmune diseases.
