Cochlear injury and adaptive plasticity of the auditory cortex

Growing evidence suggests that cochlear stressors as noise exposure and aging can induce homeostatic/maladaptive changes in the central auditory system from the brainstem to the cortex. Studies centered on such changes have revealed several mechanisms that operate in the context of sensory disruption after insult (noise trauma, drug-, or age-related injury). The oxidative stress is central to current theories of induced sensory-neural hearing loss and aging, and interventions to attenuate the hearing loss are based on antioxidant agent. The present review addresses the recent literature on the alterations in hair cells and spiral ganglion neurons due to noise-induced oxidative stress in the cochlea, as well on the impact of cochlear damage on the auditory cortex neurons. The emerging image emphasizes that noise-induced deafferentation and upward spread of cochlear damage is associated with the altered dendritic architecture of auditory pyramidal neurons. The cortical modifications may be reversed by treatment with antioxidants counteracting the cochlear redox imbalance. These findings open new therapeutic approaches to treat the functional consequences of the cortical reorganization following cochlear damage

Molecular targets for anticancer redox chemotherapy and cisplatin-induced ototoxicity: the role of curcumin on pSTAT3 and Nrf-2 signalling

In oncology, an emerging paradigm emphasises molecularly targeted approaches for cancer prevention and therapy and the use of adjuvant chemotherapeutics to overcome cisplatin limitations. Owing to their safe use, some polyphenols, such as curcumin, modulate important pathways or molecular targets in cancers. This paper focuses on curcumin as an adjuvant molecule to cisplatin by analysing its potential implications on the molecular targets, signal transducer and activator of transcription 3 (STAT3) and NF-E2 p45-related factor 2 (Nrf-2), in tumour progression and cisplatin resistance in vitro and the adverse effect ototoxicity in vivo

Protective properties of antioxidant drugs in noise-induced hearing loss in the guinea pig

Oxidative stress plays a significant role in noise-induced hearing loss (NIHL), as it largely participates in the mechanisms that underlie cell death after noise exposure and lead to sensorineural hearing loss. Many antioxidant drugs have been tested to prevent NIHL. We present three molecules with antioxidant properties (vitamin E, idebenone, N-L-acetylcysteine) that have been studied in our laboratory, and compare their protective effects. We induced acoustic trauma in treated guinea pigs, evaluated their hearing function via electrophysiological measurements at 1, 7 and 21 days, and performed morphological studies with scanning electron microscopy and TUNEL assay. All molecules had a certain effect in protecting hair cells from oxidative stress; vitamin E offered almost complete protection (8095%), N-L-acetylcysteine and idebenone also significantly reduced the threshold shift and hair cell loss. Our results support the effectiveness of antioxidant drugs in protecting against NIHL and provide a rationale for exploring therapeutic strategies in humans