Background: Although styrene is an established ototoxic agent at occupational exposure levels, the mechanisms of styrene toxicity in the auditory system are still unclear. Objectives: The aim of this study was to identify the consequences of styrene chronic exposure in cochlear structures, looking for the mechanisms of ototoxicity of this organic compound and focusing on cell targets and oxidative stress/inflammatory processes. Methods: Male adult Wistar rats were exposed to styrene (400 mg/kg by gavage for 5 days/week, 3 consecutive weeks). Hearing loss was evaluated by measuring auditory brainstem responses (ABR), morphological analysis were performed to evaluate hair cell and spiral ganglion neuron survival, as well as synaptic damage. Analysis of apoptotic (p53) and inflammatory (NF-κB, TNF-α, IL-1β and IL-10) mediators were performed by immunofluorescence analysis and western blot. Results: Styrene ototoxic effects induced a hearing loss of about 35–40 dB. Immunofluorescence and western blotting analyses demonstrated that styrene administration induced redox imbalance and activated inflammatory processes, targeting sensory hair cell and neural dysfunction by a cross-talk between oxidative and inflammatory mediators. Discussion: Major findings connect styrene ototoxicity to an interplay between redox imbalance and inflammation, leading to the intriguing assumption of a mixed sensory and neural styrene-induced ototoxicity. Thus, in a clinical perspective, data reported here have important implications for styrene risk assessment in humans.

Fetoni, A. R., Paciello, F., Rolesi, R., Pisani, A., Moleti, A., Sisto, R., Troiani, D., Paludetti, G., Grassi, C., Styrene targets sensory and neural cochlear function through the crossroad between oxidative stress and inflammation, <<FREE RADICAL BIOLOGY & MEDICINE>>, 2021; 163 (163): 31-42. [doi:10.1016/j.freeradbiomed.2020.12.001] [http://hdl.handle.net/10807/171545]

Styrene targets sensory and neural cochlear function through the crossroad between oxidative stress and inflammation

Fetoni, A. R.;Paciello, F.;Rolesi, R.;Pisani, A.;Troiani, D.;Paludetti, G.;Grassi, C.
2021

Abstract

Background: Although styrene is an established ototoxic agent at occupational exposure levels, the mechanisms of styrene toxicity in the auditory system are still unclear. Objectives: The aim of this study was to identify the consequences of styrene chronic exposure in cochlear structures, looking for the mechanisms of ototoxicity of this organic compound and focusing on cell targets and oxidative stress/inflammatory processes. Methods: Male adult Wistar rats were exposed to styrene (400 mg/kg by gavage for 5 days/week, 3 consecutive weeks). Hearing loss was evaluated by measuring auditory brainstem responses (ABR), morphological analysis were performed to evaluate hair cell and spiral ganglion neuron survival, as well as synaptic damage. Analysis of apoptotic (p53) and inflammatory (NF-κB, TNF-α, IL-1β and IL-10) mediators were performed by immunofluorescence analysis and western blot. Results: Styrene ototoxic effects induced a hearing loss of about 35–40 dB. Immunofluorescence and western blotting analyses demonstrated that styrene administration induced redox imbalance and activated inflammatory processes, targeting sensory hair cell and neural dysfunction by a cross-talk between oxidative and inflammatory mediators. Discussion: Major findings connect styrene ototoxicity to an interplay between redox imbalance and inflammation, leading to the intriguing assumption of a mixed sensory and neural styrene-induced ototoxicity. Thus, in a clinical perspective, data reported here have important implications for styrene risk assessment in humans.
Inglese
Fetoni, A. R., Paciello, F., Rolesi, R., Pisani, A., Moleti, A., Sisto, R., Troiani, D., Paludetti, G., Grassi, C., Styrene targets sensory and neural cochlear function through the crossroad between oxidative stress and inflammation, <<FREE RADICAL BIOLOGY & MEDICINE>>, 2021; 163 (163): 31-42. [doi:10.1016/j.freeradbiomed.2020.12.001] [http://hdl.handle.net/10807/171545]
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/10807/171545
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