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1.
Hear Res ; 370: 16-21, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30253329

RESUMO

Cisplatin is a potent chemotherapeutic compound for which ototoxicity is a significant side effect. Cisplatin has shown sensitivity to circadian time, in that cisplatin is most effective as an anti-tumor compound, and least nephrotoxic, when given in the active (dark) period of the light-dark cycle in rodents. The objective of the study was to determine the sensitivity of cisplatin ototoxicity to circadian time. Fifty-seven Fischer 344/NHsd rats were exposed to 12 mg/kg cisplatin by intra-peritoneal injection at one of six time points on a 12 h light-12 h dark cycle: 2, 6, or 10 h after light onset or 2, 6, or 10 h after light offset. Cochlear injury was evaluated using auditory brainstem response threshold shifts and postmortem outer hair cell counts. All animals experienced threshold shift in the highest frequencies tested (30 and 40 kHz). The animals exposed to cisplatin at 6 h after light onset (the inactive period) had significantly higher mid-frequency threshold shifts and outer hair cell losses than the groups exposed during the dark hours. The results indicate that cisplatin is less likely to cause ototoxicity in the Fischer 344/NHsd rat when given during the active period. This finding is consistent with the lower nephrotoxicity that has been detected in cisplatin-exposed animals treated during the dark hours, and the magnitude of differences in threshold shifts between the light and dark exposure indicates that circadian timing has a significant impact on susceptibility to cisplatin ototoxicity.


Assuntos
Antineoplásicos/administração & dosagem , Cisplatino/administração & dosagem , Cóclea/efeitos dos fármacos , Doenças Cocleares/prevenção & controle , Cronofarmacoterapia , Animais , Antineoplásicos/toxicidade , Fadiga Auditiva/efeitos dos fármacos , Cisplatino/toxicidade , Cóclea/patologia , Cóclea/fisiopatologia , Doenças Cocleares/induzido quimicamente , Doenças Cocleares/patologia , Doenças Cocleares/fisiopatologia , Potenciais Evocados Auditivos do Tronco Encefálico/efeitos dos fármacos , Feminino , Células Ciliadas Auditivas Externas/efeitos dos fármacos , Células Ciliadas Auditivas Externas/patologia , Masculino , Fotoperíodo , Ratos Endogâmicos F344 , Fatores de Tempo
2.
Otol Neurotol ; 35(4): 743-7, 2014 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-24622028

RESUMO

PURPOSE: Gentian violet (GV) is an antimicrobial and antifungal agent that has been used widely to treat intractable discharge in the ear. The purpose of this report is to warn clinicians about the ototoxic effect of GV in the middle ear. MATERIALS AND METHODS: GV ototoxicity was evaluated by measuring compound action potentials (CAPs) in the VIIIth nerve in adult Hartley guinea pigs. The middle ear cavities of the animals were filled with GV solution (0.5% or 0.13%), and CAPs were measured after intervals of 5 and 30 minutes and 1, 2, 6, and 24 hours. After all measurements were completed, the temporal bones were harvested for histopathologic evaluation. Celloidin-embedded specimens were cut into 20-µm slices and examined using light microscopy. The bacteriostatic activity of GV was evaluated using a disk-diffusion assay. RESULTS: A 0.5% GV solution produced a mild elevation in the CAP threshold at 30 minutes, a greater reduction at 1 hour, and complete abolishment of CAP at 24 hours. A 0.13% GV solution caused mild elevation in the CAP threshold at 2 hours and severe elevation at 6 hours. Massive new bone formation was found in the middle ear cavity at 6 weeks. GV concentrations of 0.13% and 0.06% were effective against all bacteria tested, with the exception of Pseudomonas aeruginosa. CONCLUSIONS: Although GV has marked antibacterial and antifungal activities, its use should be limited to the external ear canal. GV exerts an ototoxic effect in a concentration- and time-dependent manner, and so the use of this drug in the middle ear cavity is not recommended.


Assuntos
Anti-Infecciosos/toxicidade , Cóclea/patologia , Doenças Cocleares/induzido quimicamente , Violeta Genciana/toxicidade , Estimulação Acústica , Animais , Anti-Infecciosos/farmacologia , Limiar Auditivo/efeitos dos fármacos , Bactérias/efeitos dos fármacos , Doenças Cocleares/patologia , Contagem de Colônia Microbiana , Potenciais Evocados Auditivos/fisiologia , Violeta Genciana/farmacologia , Cobaias , Testes de Sensibilidade Microbiana , Osso Temporal/patologia , Doenças do Nervo Vestibulococlear/induzido quimicamente , Doenças do Nervo Vestibulococlear/patologia
3.
Otol Neurotol ; 35(3): 533-9, 2014 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-24518411

RESUMO

HYPOTHESIS: Oral supplementation with mitoquinone (MitoQ) prevents gentamicin-induced ototoxicity in guinea pigs. BACKGROUND: Antioxidants have been shown to protect against aminoglycoside (AG)-induced ototoxicity. MitoQ, a mitochondria-targeted derivative of the antioxidant ubiquinone, is attached to a lipophilic triphenylphosphonium (TPP) cation, which enables its accumulation inside the mitochondria several hundred-fold over the untargeted antioxidant. MitoQ has improved bioavailability and can reach most tissues and has been used in Parkinson's disease and hepatitis C human trials, which demonstrated that MitoQ can be safely used in humans. Thus, MitoQ is a promising novel therapeutic approach for protecting against AG-induced ototoxicity. METHODS: Gentamicin-treated guinea pigs were supplied with water alone (control), decyl-TPP (positive control), or MitoQ-supplemented drinking water. Auditory function was assessed by auditory brainstem response. Cochlear damage was assessed using scanning electron microscopy. Western blotting was performed to evaluate changes in proteins related to apoptosis and oxidative damage in the cochlea. RESULTS: Threshold shifts at 4 and 8 kHz at 4 and 7 weeks after gentamicin treatment were smaller in animals treated with MitoQ compared with those in the control- and decyl-TPP-treated animals (p < 0.05). Protein carbonyls and levels of the proapoptotic protein Bak were lower (p < 0.05 and p = 0.008, respectively), whereas the level of the antioxidant enzyme manganese superoxide dismutase was higher (p = 0.01) in the cochlea of MitoQ-treated animals. The expression of 3-nitrotyrosine and Hrk were not different between groups (p > 0.05). CONCLUSION: Oral supplementation with MitoQ attenuated gentamicin-induced cochlear damage and hearing loss in guinea pigs. MitoQ holds promise as a means for protecting against AG ototoxicity.


Assuntos
Antioxidantes/uso terapêutico , Cóclea/efeitos dos fármacos , Doenças Cocleares/tratamento farmacológico , Potenciais Evocados Auditivos do Tronco Encefálico/efeitos dos fármacos , Perda Auditiva/tratamento farmacológico , Compostos Organofosforados/uso terapêutico , Ubiquinona/análogos & derivados , Animais , Antioxidantes/farmacologia , Apoptose/efeitos dos fármacos , Apoptose/fisiologia , Cóclea/metabolismo , Doenças Cocleares/induzido quimicamente , Doenças Cocleares/metabolismo , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia , Gentamicinas , Cobaias , Perda Auditiva/induzido quimicamente , Perda Auditiva/metabolismo , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Compostos Organofosforados/farmacologia , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/fisiologia , Superóxido Dismutase/metabolismo , Ubiquinona/farmacologia , Ubiquinona/uso terapêutico
4.
Neurotoxicology ; 34: 42-50, 2013 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-23164932

RESUMO

3-Nitropropionic acid (3-NP), a mitochondrial toxin, has been reported to induce an acute cochlear damage. Korean red ginseng (KRG) is known to have protective effects from some types of hearing loss. This study aimed to observe the protective effect of KRG in an ototoxic animal model using 3-NP intratympanic injection. BALB/c mice were classified into 5 groups (n=15) and dose-dependent toxic effects after intratympanic injection with 3-NP (300-5000 mM) on the left ear were investigated to determine the appropriate toxicity level of 3-NP. For observation of the protective effects of KRG, 23 mice were grouped into 3-NP (500 mM, n=12) and KRG+3-NP groups (300 mg/kg KRG for 7 days before 500 mM 3-NP administration, n=11). Auditory brain response (ABR) and cochlear morphological evaluations were performed before and after drug administration. The ABR thresholds in the 800-5000 mM groups exceeded the maximum recording limit at 16 and 32 kHz 1 day after 3-NP administration. The ABR threshold in the 500 mM 3-NP+KRG group was significantly lower than that in the 500 mM 3-NP group from post 1 week to 1 month. The mean type II fibrocyte counts significantly differed between the control and 3-NP groups and between the 3-NP and 3-NP+KRG groups. Spiral ganglion cell degeneration in the 3-NP group was more severe than that in the 3-NP+KRG group. This animal model exhibited a dose-dependent hearing loss with histological changes. KRG administration ameliorated the deterioration of hearing by 3-NP.


Assuntos
Cóclea/efeitos dos fármacos , Doenças Cocleares/prevenção & controle , Perda Auditiva/prevenção & controle , Nitrocompostos , Panax , Extratos Vegetais/farmacologia , Propionatos , Animais , Limiar Auditivo/efeitos dos fármacos , Cóclea/patologia , Cóclea/fisiopatologia , Doenças Cocleares/induzido quimicamente , Doenças Cocleares/patologia , Doenças Cocleares/fisiopatologia , Citoproteção , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Potenciais Evocados Auditivos do Tronco Encefálico/efeitos dos fármacos , Células Ciliadas Auditivas Externas/efeitos dos fármacos , Células Ciliadas Auditivas Externas/patologia , Audição/efeitos dos fármacos , Perda Auditiva/induzido quimicamente , Perda Auditiva/patologia , Perda Auditiva/fisiopatologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Panax/química , Extratos Vegetais/isolamento & purificação , Raízes de Plantas , Plantas Medicinais , Gânglio Espiral da Cóclea/efeitos dos fármacos , Gânglio Espiral da Cóclea/patologia , Fatores de Tempo
5.
J Neural Eng ; 8(5): 056006, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-21828906

RESUMO

Infrared neural stimulation (INS) has received considerable attention over the last few years. It provides an alternative method to artificially stimulate neurons without electrical current or the introduction of exogenous chromophores. One of the primary benefits of INS could be the improved spatial selectivity when compared with electrical stimulation. In the present study, we have evaluated the spatial selectivity of INS in the acutely damaged cochlea of guinea pigs and compared it to stimulation with acoustic tone pips in normal-hearing animals. The radiation was delivered via a 200 µm diameter optical fiber, which was inserted through a cochleostomy into the scala tympani of the basal cochlear turn. The stimulated section along the cochlear spiral ganglion was estimated from the neural responses recorded from the central nucleus of the inferior colliculus (ICC). ICC responses were recorded in response to cochlear INS using a multichannel penetrating electrode array. Spatial tuning curves (STCs) were constructed from the responses. For INS, approximately 55% of the activation profiles showed a single maximum, ∼22% had two maxima and ∼13% had multiple maxima. The remaining 10% of the profiles occurred at the limits of the electrode array and could not be classified. The majority of ICC STCs indicated that the spread of activation evoked by optical stimuli is comparable to that produced by acoustic tone pips.


Assuntos
Cóclea/fisiologia , Cóclea/efeitos da radiação , Implantes Cocleares , Colículos Inferiores/fisiologia , Raios Infravermelhos , Estimulação Acústica , Potenciais de Ação/fisiologia , Anestesia , Animais , Audiometria de Tons Puros , Calibragem , Doenças Cocleares/induzido quimicamente , Doenças Cocleares/fisiopatologia , Eletrodos Implantados , Feminino , Tecnologia de Fibra Óptica , Cobaias , Masculino , Neomicina , Estimulação Luminosa , Desenho de Prótese , Inibidores da Síntese de Proteínas , Percepção Espacial/fisiologia , Gânglio Espiral da Cóclea/fisiologia
6.
Neurotoxicology ; 31(3): 317-25, 2010 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-20226206

RESUMO

3-Nitropropionic acid (3-NP) induces hearing loss by impairing mitochondrial energy generation. Geranylgeranylacetone (GGA) is known to protect the cochlea from various injuries. The present study was designed to investigate the protective effect of GGA against acute 3-NP-induced damage to the cochlear mitochondria. Female Hartley guinea pigs were divided into 4 groups. The 3-NP vehicle was injected to control animals and in animals receiving GGA alone, only GGA was administered for 7 days. 3-NP (500 mM, 4 microl) was administered with (animals receiving both GGA and 3-NP) or without (animals receiving 3-NP alone) GGA pretreatment (800 mg/kg, 7 days). The auditory brainstem response (ABR) was recorded at click and at 8, 16 and 32 kHz before and after injection, respectively. After cochlear harvest, hematoxylin/eosin staining and immunohistochemistry for anti-HSP70 antibody were done. 3-NP exposure resulted in elevated ABR thresholds that exceeded the maximum recording limit, while GGA pretreatment before 3-NP exposure led to a significant decrease in hearing threshold shift. Histological analysis of above former group revealed loss of type II fibrocytes in the spiral ligament, hair cells in the organ of Corti, stellate fibrocytes in the spiral limbus and spiral ganglion cells, while in above latter group, these cells were preserved. Control animals revealed weak HSP70 expression in the nuclei of some supporting cells (pillar cells, Deiters' cells and Hensen's cells) and interdental cells. Animals receiving GGA alone showed strong HSP70 expression in the same area as in control animals, while animals receiving both GGA and 3-NP demonstrated slightly decreased HSP70 expression in that area. These results suggest that GGA may protect the cochlea against acute injury resulting from mitochondrial dysfunction.


Assuntos
Doenças Cocleares/induzido quimicamente , Doenças Cocleares/tratamento farmacológico , Diterpenos/uso terapêutico , Antagonistas dos Receptores H2 da Histamina/uso terapêutico , Nitrocompostos , Propionatos , Estimulação Acústica/métodos , Animais , Limiar Auditivo/efeitos dos fármacos , Doenças Cocleares/fisiopatologia , Modelos Animais de Doenças , Interações Medicamentosas , Eletroencefalografia/métodos , Potenciais Evocados Auditivos do Tronco Encefálico/efeitos dos fármacos , Feminino , Regulação da Expressão Gênica/efeitos dos fármacos , Cobaias , Proteínas de Choque Térmico HSP72/metabolismo , Órgão Espiral/metabolismo , Órgão Espiral/patologia , Órgão Espiral/ultraestrutura
7.
J Assoc Res Otolaryngol ; 9(1): 65-89, 2008 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-18157569

RESUMO

Inner ear hair cells detect environmental signals associated with hearing, balance, and body orientation. In humans and other mammals, significant hair cell loss leads to irreversible hearing and balance deficits, whereas hair cell loss in nonmammalian vertebrates is repaired by the spontaneous generation of replacement hair cells. Research in mammalian hair cell regeneration is hampered by the lack of in vivo damage models for the adult mouse inner ear and the paucity of cell-type-specific markers for non-sensory cells within the sensory receptor epithelia. The present study delineates a protocol to drug damage the adult mouse auditory epithelium (organ of Corti) in situ and uses this protocol to investigate Sox2 and Jagged1 expression in damaged inner ear sensory epithelia. In other tissues, the transcription factor Sox2 and a ligand member of the Notch signaling pathway, Jagged1, are involved in regenerative processes. Both are involved in early inner ear development and are expressed in developing support cells, but little is known about their expressions in the adult. We describe a nonsurgical technique for inducing hair cell damage in adult mouse organ of Corti by a single high-dose injection of the aminoglycoside kanamycin followed by a single injection of the loop diuretic furosemide. This drug combination causes the rapid death of outer hair cells throughout the cochlea. Using immunocytochemical techniques, Sox2 is shown to be expressed specifically in support cells in normal adult mouse inner ear and is not affected by drug damage. Sox2 is absent from auditory hair cells, but is expressed in a subset of vestibular hair cells. Double-labeling experiments with Sox2 and calbindin suggest Sox2-positive hair cells are Type II. Jagged1 is also expressed in support cells in the adult ear and is not affected by drug damage. Sox2 and Jagged1 may be involved in the maintenance of support cells in adult mouse inner ear.


Assuntos
Proteínas de Ligação ao Cálcio/metabolismo , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Proteínas de Membrana/metabolismo , Órgão Espiral/metabolismo , Fatores de Transcrição SOXB1/metabolismo , Animais , Animais Recém-Nascidos , Antibacterianos/toxicidade , Biomarcadores/metabolismo , Galinhas , Doenças Cocleares/induzido quimicamente , Modelos Animais de Doenças , Diuréticos/toxicidade , Furosemida/toxicidade , Proteína Jagged-1 , Canamicina/toxicidade , Camundongos , Camundongos Endogâmicos CBA , Órgão Espiral/efeitos dos fármacos , Proteínas Serrate-Jagged , Fatores de Tempo
8.
Eur J Neurosci ; 24(12): 3365-71, 2006 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-17229085

RESUMO

Glucocorticoid receptors are widely distributed in the cochlea but their role remains poorly known. Previous studies provided contradictory reports on a possible cochlear acoustic hypersensitivity induced by adrenal insufficiency, while several experiments agree on a significant action of glucocorticoid receptors in adverse conditions such as acoustic trauma and restraint stress. The present experiments confirmed a cochlear acoustic hypersensitivity induced by adrenalectomy and reversed by corticosterone supplementation. These observations point to a significant role of corticosteroids in basal cochlear functioning. The glucocorticoids are known to be essential for limiting and resolving inflammatory processes. The endotoxin Escherichia coli lipopolysaccharide is widely used to induce inflammatory reactions. However, in various organs several toxic processes of this endotoxin are not influenced by glucocorticoids. From previous experiments on the cochlea there is no evidence that glucocorticoids are an essential factor against endotoxin cochlear toxicity. In the present experiments it was found that adrenalectomy greatly increased the cochlear susceptibility to endotoxin; the effect was reversed by providing corticosterone supplementation. This shows the essential role of corticosterone in this cochlear inflammation model. In previous studies local administration (at the cochlear base) of endotoxin was used and losses of cochlear acoustic sensitivity were found predominantly at high frequencies; in contrast, the systemic injection used in this study produced a cochlear loss of acoustic sensitivity at all frequencies, indicating a uniform cochlear sensitivity to the toxic effects of endotoxin.


Assuntos
Adrenalectomia , Anti-Inflamatórios/administração & dosagem , Cóclea/fisiologia , Doenças Cocleares/dietoterapia , Corticosterona/administração & dosagem , Endotoxinas/toxicidade , Estimulação Acústica/métodos , Análise de Variância , Animais , Anti-Inflamatórios/sangue , Limiar Auditivo/efeitos dos fármacos , Comportamento Animal , Cóclea/efeitos dos fármacos , Cóclea/efeitos da radiação , Doenças Cocleares/induzido quimicamente , Corticosterona/sangue , Relação Dose-Resposta à Radiação , Inflamação/induzido quimicamente , Inflamação/dietoterapia , Lipopolissacarídeos , Masculino , Ratos , Ratos Sprague-Dawley
9.
Gac Med Mex ; 139(6): 529-34, 2003.
Artigo em Espanhol | MEDLINE | ID: mdl-14723047

RESUMO

This study was done to ascertain prospectively whether distortion product-evoked otoacoustic emissions (DP-EOAE) might detect changes in specific frequencies damaged in inner ear function earlier, before they become permanent after cisplatinum exposure for cancer treatment in children. Sixteen children treated with cisplatinum for various types of cancer were repeatedly evaluated after each chemotherapy session; results were compared to 44 controls. We observed a progressive damage in auditory function. In second assessment 50% of DP-EOAE studies were abnormal; in the third study, 66% were abnormal, and in the fourth test 71% were abnormal. Our results suggest that DP-EOAE are useful tests for earlier auditory changes induced by cisplatinum therapy; higher frequencies are the most affected, and we propose that DP-EOAE be a mandatory test before treatment and during cisplatinum therapy to detect or diagnose early hearing loss.


Assuntos
Antineoplásicos/efeitos adversos , Cisplatino/efeitos adversos , Doenças Cocleares/induzido quimicamente , Potenciais Evocados Auditivos , Emissões Otoacústicas Espontâneas/efeitos dos fármacos , Estimulação Acústica/métodos , Antineoplásicos/administração & dosagem , Audiometria de Tons Puros , Estudos de Casos e Controles , Pré-Escolar , Cisplatino/administração & dosagem , Doenças Cocleares/diagnóstico , Feminino , Humanos , Lactente , Masculino , Neoplasias/tratamento farmacológico , Emissões Otoacústicas Espontâneas/fisiologia , Estudos Prospectivos
10.
Am J Otol ; 21(4): 513-20, 2000 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-10912697

RESUMO

HYPOTHESIS: The goals of this investigation were to compare the efficacy of three protective agents against cisplatin-induced elevation of auditory brainstem response (ABR) thresholds and to examine whether these protective agents prevent cisplatin-induced alterations of the antioxidant defense system in the cochlea of the rat. BACKGROUND: Cisplatin is an ototoxic antitumor agent. Previous animal studies have shown that cisplatin administration causes an elevation of ABR thresholds. These auditory changes are accompanied by alterations in the concentration of glutathione and the antioxidant enzymes in the cochlea. The authors' previous work has indicated that the protective agent diethyldithiocarbamate (DDTC) prevents decrease in glutathione (GSH), alteration of antioxidant enzyme activity, and disruption of cochlear function with cisplatin administration. METHODS: Wistar rats were sedated and underwent pretreatment ABR testing using clicks and tone burst stimuli at 8, 16, and 32 kHz. Control rats received saline by intraperitoneal (i.p.) injection. Positive control rats were administered cisplatin 16 mg/kg i.p. Three groups of rats received protective agents in combination with cisplatin. The DDTC-protected rats were given 600 mg/kg of DDTC subcutaneously 1 hour after cisplatin. Animals protected by 4-methylthiobenzoic acid (MTBA) were given 250 mg/kg of this agent i.p. 30 minutes before cisplatin. Animals protected with ebselen were given 16 mg/kg i.p. one hour before cisplatin. The ABR thresholds were recorded 72 hours after cisplatin administration in all groups. Cochleas were removed, and extracts of the tissues were analyzed for GSH, activities of antioxidant enzymes (superoxide dismutase [SOD], catalase, glutathione peroxidase, and glutathione reductase) and malondialdehyde (MDA) (as an index of lipid peroxidation). RESULTS: Cisplatin-treated rats had significant ABR threshold shifts, ranging from 27 to 40 dB. Rats administered each of the three protective agents in combination with cisplatin had ABR threshold shifts of <10 dB. The cochleae of rats administered cisplatin alone had nearly a 50% depletion of glutathione and about a 50% reduction in the activities of SOD, glutathione peroxidase, and glutathione reductase, while catalase activity was reduced to 70% of control values. These changes were accompanied by a reciprocal elevation of MDA of 165%. These changes, namely, the depletion of GSH and antioxidant enzyme activity and the elevation of MDA in the cochlea, were largely attenuated by the administration of the protective agents tested. CONCLUSION: These findings suggest that cisplatin ototoxicity is related to lipid peroxidation and that the use of protective agents prevents hearing loss and lipid peroxidation by sparing the antioxidant system in the cochlea. These results suggest the possibility that the clinical use of protective agents could effectively reduce or prevent damage to the inner ear of patients receiving cisplatin chemotherapy, provided that the antitumor effect is not altered.


Assuntos
Adjuvantes Imunológicos/uso terapêutico , Antineoplásicos/efeitos adversos , Antioxidantes/uso terapêutico , Azóis/uso terapêutico , Benzoatos/uso terapêutico , Cisplatino/efeitos adversos , Doenças Cocleares/induzido quimicamente , Doenças Cocleares/prevenção & controle , Ditiocarb/uso terapêutico , Transtornos da Audição/induzido quimicamente , Transtornos da Audição/prevenção & controle , Compostos Organosselênicos/uso terapêutico , Animais , Doenças Cocleares/diagnóstico , Doenças Cocleares/enzimologia , Modelos Animais de Doenças , Avaliação Pré-Clínica de Medicamentos , Potenciais Evocados Auditivos do Tronco Encefálico/efeitos dos fármacos , Glutationa/deficiência , Glutationa/efeitos dos fármacos , Transtornos da Audição/diagnóstico , Transtornos da Audição/enzimologia , Isoindóis , Peroxidação de Lipídeos/efeitos dos fármacos , Ratos , Ratos Wistar
11.
Br J Audiol ; 32(5): 305-16, 1998 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-9845029

RESUMO

Transient evoked otoacoustic emissions (TEOAE) have been evaluated as a means of monitoring cochlear function in patients receiving the chemotherapeutic agents cisplatin and carboplatin (-cis-diammine, 1,1-cyclobutane dicarboxylate (2) -0,0-platinum). Patients receiving these drugs were monitored prospectively with pure tone audiometry (PTA), tympanometry and TEOAE. Data was collected on 22 subjects receiving cisplatin and nine subjects receiving carboplatin. Significant deterioration in both PTA thresholds and TEOAE energy levels (with no change in tympanometry) were detected in the cisplatin group. No significant deterioration in audiological parameters occurred in the carboplatin group. It is indicated that cisplatin has a significant ototoxic effect in the majority of patients, whereas any ototoxic effect of carboplatin was undetectable. Our findings were different from previous studies in that the measurable changes in TEOAE occurred later than changes in the pure tone audiogram for the cisplatin group.


Assuntos
Estimulação Acústica , Antineoplásicos/efeitos adversos , Carboplatina/efeitos adversos , Cisplatino/efeitos adversos , Cóclea/fisiologia , Doenças Cocleares/induzido quimicamente , Doenças Cocleares/diagnóstico , Adulto , Idoso , Limiar Auditivo/efeitos dos fármacos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Inquéritos e Questionários
12.
Zhongguo Zhong Xi Yi Jie He Za Zhi ; 18(6): 362-4, 1998 Jun.
Artigo em Chinês | MEDLINE | ID: mdl-11477914

RESUMO

OBJECTIVE: To observe the effect of electroacupuncture (EA) on succinate dehydrogenase (SDH) of gentamycin (GE) induced ototoxic cochlear hair cells. METHODS: Preyer's reflex normal guinea pigs were selected and divided randomly into three groups: GE group, EA group, control group. Brainstem auditory evoked potential (BAEP) and SDH in the cochlear hair cells were taken as indexes. In the animals of GE group GE was alone injected intramuscularly 80 mg.kg-1.d-1 for 20 days, while in the animals of EA group GE and additional EA was applied once a day on Tinggong (SI19), Yifeng(SJ17) and Shenshu (UB23) points. EA lasted for 15 minutes. RESULTS: In the GE group BAEP reaction threshold rose markedly, while that rose slightly in EA group. The difference was significant between two groups (P < 0.05). The change of SDH within cochlear hair cells and degree of hair cells injury in the EA group were lower than those in GE group. CONCLUSIONS: EA therapy could relieve GE ototoxicity, protect SDH in cochlear hair cells and might be a possible mechanism of action of EA.


Assuntos
Cóclea/enzimologia , Eletroacupuntura , Potenciais Evocados Auditivos do Tronco Encefálico , Gentamicinas/efeitos adversos , Succinato Desidrogenase/metabolismo , Animais , Doenças Cocleares/induzido quimicamente , Doenças Cocleares/enzimologia , Feminino , Cobaias , Células Ciliadas Auditivas/enzimologia , Masculino , Distribuição Aleatória
13.
Zhongguo Zhong Xi Yi Jie He Za Zhi ; 18(6): 365-7, 1998 Jun.
Artigo em Chinês | MEDLINE | ID: mdl-11477915

RESUMO

OBJECTIVE: To assess the antagonistic effect of Fucong Tablet (FCT) and its ingredients on ototoxicity of gentamycin in guinea pigs. METHODS: The guinea pigs were given gentamycin 80 mg/kg intramuscularly once daily for 20 days and FCT or its ingredients separately oral taken for 20 days. The auditory brain stem evoked response (ABR) threshold, vascular stria blood circulation condition, outer hair-cell count and cochlear ultrastructure of guinea pigs were observed before and after treatment to assess the antagonistic effect and protective effect of FCT on cochlear structure. RESULTS: FCT and its ingredients of tonifying Kidney, replenishing Qi and blood, promoting blood circulation could lower the impairment ratio of outer hair-cell induced by gentamycin (P < 0.05), protect morphosis and function of cochlea and lower the elevated ABR threshold (P < 0.05). CONCLUSIONS: FCT and its ingredients could reduce the toxic damage on ear induced by gentamycin effectively.


Assuntos
Cóclea/ultraestrutura , Medicamentos de Ervas Chinesas/farmacologia , Potenciais Evocados Auditivos do Tronco Encefálico , Gentamicinas/efeitos adversos , Perda Auditiva Bilateral/patologia , Animais , Cóclea/fisiopatologia , Doenças Cocleares/induzido quimicamente , Doenças Cocleares/tratamento farmacológico , Doenças Cocleares/patologia , Medicamentos de Ervas Chinesas/uso terapêutico , Feminino , Cobaias , Células Ciliadas Auditivas Externas/ultraestrutura , Perda Auditiva Bilateral/induzido quimicamente , Perda Auditiva Bilateral/tratamento farmacológico , Masculino , Distribuição Aleatória
14.
Br J Audiol ; 27(2): 85-90, 1993 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-8220286

RESUMO

Damaging influences to the cochlea are a leading cause of sensorineural hearing loss. Examples include acute or chronic noise exposure and cochleotoxic drugs such as aminoglycosides. Typically, once damage has occurred, the cochlea cannot recover. Therefore, prevention is critical. If damaging influences cannot be avoided, then secondary prevention or early detection of cochlear hearing loss becomes important. Ideally, methods for the detection of cochlear damage should be as specific and as sensitive as possible. Otoacoustic emissions satisfy these criteria and offer a means of testing aspects of cochlear function in a non-invasive and objective way. Evoked otoacoustic emissions measured either after transient stimuli or during two-tone stimulation (distortion-product otoacoustic emissions) are the types most commonly used for clinical purposes. They are stable over time within individual ears and their repeatability has been established under conditions of clinical testing using commercial equipment. Thus, they are well suited as an effective means of monitoring subtle changes in cochlear status. The possibility of making non-invasive repeated measures of cochlear function has led to the widespread use of otoacoustic emissions in animal experiments. Influences of development, anoxia, anaesthesia, noise, and drugs have been monitored. Preliminary studies in humans demonstrate that cochlear damage due to ototoxic drugs such as aminoglycosides or cisplatin and due to noise exposure can be detected using otoacoustic emissions. Comparison of such results to those available using pure-tone audiometry indicates a greater sensitivity of otoacoustic emissions for detecting early cochlear damage.(ABSTRACT TRUNCATED AT 250 WORDS)


Assuntos
Cóclea/fisiopatologia , Doenças Cocleares/induzido quimicamente , Células Ciliadas Auditivas/fisiopatologia , Estimulação Acústica , Aminoglicosídeos/efeitos adversos , Cisplatino/efeitos adversos , Cóclea/efeitos dos fármacos , Doenças Cocleares/diagnóstico , Doenças Cocleares/fisiopatologia , Feminino , Perda Auditiva Neurossensorial/induzido quimicamente , Perda Auditiva Neurossensorial/diagnóstico , Perda Auditiva Neurossensorial/fisiopatologia , Perda Auditiva Neurossensorial/prevenção & controle , Humanos , Masculino , Ruído/efeitos adversos
15.
Int J Pediatr Otorhinolaryngol ; 25(1-3): 73-80, 1993 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-8436482

RESUMO

Eight children and young adults with cancer were evaluated serially using pure tone audiometry as well as registration of click-evoked otoacoustic emissions (EOAE) 1 day prior to therapy as well as after various numbers of doses of cisplatinum. A reduction of EOAE-amplitudes following cisplatinum therapy was observed in all patients. This reduction tended to recover after the end of cisplatinum administration. Since EOAE are believed to result from cochlear bio-mechanical processes, the reduced emissions are interpreted as signs of cochlear dysfunction. We conclude, that EOAE testing may be a simple, non-invasive method that may detect early, transient functional impairment of hearing due to ototoxic agents such as cisplatinum, even in children. Further controlled trials are needed.


Assuntos
Cisplatino/efeitos adversos , Doenças Cocleares/induzido quimicamente , Transtornos da Audição/induzido quimicamente , Emissões Otoacústicas Espontâneas/fisiologia , Estimulação Acústica , Adolescente , Adulto , Audiometria de Tons Puros , Criança , Pré-Escolar , Cisplatino/uso terapêutico , Doenças Cocleares/diagnóstico , Potenciais Evocados Auditivos , Feminino , Transtornos da Audição/diagnóstico , Humanos , Masculino , Neoplasias/tratamento farmacológico
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