ototoxicity/glutathione

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Comparison of the effects of lipoic acid and glutathione against cisplatin-induced ototoxicity in auditory cells.

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OBJECTIVE The aims of this study were to examine lipoic acid (LA)- or glutathione (GSH)-mediated protection against cytotoxicity following cisplatin exposure in HEI-OC1 auditory cells and measure the potential of LA and GSH to scavenge reactive oxygen species (ROS). This study also compares their

Cisplatin-induced ototoxicity in pediatric solid tumors: the role of glutathione S-transferases and megalin genetic polymorphisms.

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Cisplatin-induced ototoxicity, an important dose-limiting side effect, has proven high interindividual variability. Glutathione S-transferases (GSTs) are isoenzymes involved in cellular detoxification processes. Megalin has been demonstrated to bind aminoglycosides, known to be similar to cisplatin

Influence of glutathione s-transferase on the ototoxicity caused by aminoglycosides.

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The process of hair cell damage and death as a result of exposure to noise and ototoxins seems to be mediated by reactive oxygen species. OBJECTIVE To investigate the relationship between genetic polymorphisms in the Glutathione S-transferase and the susceptibility to hearing loss induced by

Potentiation of ototoxicity by glutathione depletion.

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The combination of 10 mg/kg ethacrynic acid (ETA) and 100 mg/kg kanamycin (KA) caused neither morphologic damage to the cochlea nor change in the auditory brain stem response of the chinchilla. However, after pretreatment with a single dose of buthionine sulfoximine (BSO; 800 mg/kg

Attenuation of aminoglycoside ototoxicity by glutathione.

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Aminoglycoside antibiotics are commonly used for the treatment of serious gram-negative infections despite a high incidence of associated ototoxicity. Attempts to elucidate the mechanisms of toxicity or prevent the adverse effects have previously been unsuccessful. Recently, the damaging effects of

Glutathione ester but not glutathione protects against cisplatin-induced ototoxicity in a rat model.

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Glutathione (GSH) provides an important antioxidant and detoxification pathway. We tested to determine if direct administration of GSH or GSH ester could reduce cisplatin- (CDDP) induced ototoxicity. We tested eight groups of five rats each: a control group, a group receiving 16 mg/kg ip CDDP

The role of glutathione in carboplatin ototoxicity in the chinchilla.

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The role of glutathione in carboplatin ototoxicity was investigated in the chinchilla. Chinchillas hearing was tested with both distortion product otoacoustic emissions (DPOAE) and evoked potentials recorded from a chronic electrode in the inferior colliculus (IC). All subjects had an osmotic pump

Attenuation of gentamicin ototoxicity by glutathione in the guinea pig in vivo.

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The effect of glutathione co-therapy on the expression of gentamicin ototoxicity was tested in pigmented guinea pigs. The first group of animals was injected with gentamicin (100 mg/kg body weight/day) for two weeks followed by 10 weeks of rest. A second group received glutathione by gastric gavage

Glutathione protection against gentamicin ototoxicity depends on nutritional status.

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This study demonstrates that gentamicin ototoxicity depends on dietary factors and correlates with tissue glutathione levels. After 15 days of gentamicin injections (100 mg/kg/day s.c.) guinea pigs on a regular protein diet (18.5% protein) had an average hearing loss of 9 dB at 3 kHz, 31 dB at 8 kHz

Cellular glutathione content in the organ of Corti and its role during ototoxicity.

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Glutathione (GSH) is the major scavenger of reactive oxygen species (ROS) inside cells. We used live confocal imaging in order to clarify the role of GSH in the biology of the organ of Corti, the sensory epithelium of the cochlea, before, during and after the onset of hearing and in ~1 year old

Glutathione S-transferase P1 single nucleotide polymorphism predicts permanent ototoxicity in children with medulloblastoma.

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BACKGROUND Glutathione S-transferase (GST) enzymes are involved in detoxifying chemotherapy and clearing reactive oxygen species formed by radiation. We explored the relationship between the host GSTP1 105 A > G polymorphism (rs1695), tumor GSTpi protein expression, and clinical outcomes in

Cochlear detoxification: Role of alpha class glutathione transferases in protection against oxidative lipid damage, ototoxicity, and cochlear aging

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Age-related hearing loss (AHL) is the most common form of hearing impairment. AHL is thought to be a multifactorial condition resulting from the interaction of numerous causes including aging, genetics, exposure to noise, and exposure to endogenous and exogenous toxins. Cells possess many

Maturation of cochlear glutathione-S-transferases correlates with the end of the sensitive period for ototoxicity.

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The developing mammalian cochlea is especially sensitive to chemical toxins. In rats, the period of increased sensitivity falls roughly between postnatal days (P) 8 and 28. One unexplored hypothesis for this 'sensitive period' is that young cochleas may have immature complements of detoxification

Nutritional status, glutathione levels, and ototoxicity of loop diuretics and aminoglycoside antibiotics.

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Chinchillas deprived of food for 48 h prior to the administration of a combined dose of ethacrynic acid (10 mg/kg) and kanamycin (100 mg/kg) suffered a profound hearing loss. Fed animals did not demonstrate any hearing loss at the same dose levels. Drug metabolism may be the common pathway by which

Bucillamine prevents cisplatin-induced ototoxicity through induction of glutathione and antioxidant genes.

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Bucillamine is used for the treatment of rheumatoid arthritis. This study investigated the protective effects of bucillamine against cisplatin-induced damage in auditory cells, the organ of Corti from postnatal rats (P2) and adult Balb/C mice. Cisplatin increases the catalytic activity of caspase-3

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