Heme oxygenase-1 expression in the guinea pig cochlea induced by intense noise stimulation

Abstract

Conclusion: These results suggest that noise induces free radical formation in the cochlea and that, in the guinea pig, heme oxygenase-1 (HO-1) may play an important role in the recovery from noise trauma in the organ of Corti. Objective: Free radicals are involved in noise-induced hearing loss. It has been demonstrated that the induction of HO-1 may protect cells exposed to oxidative challenge. The present study was designed to investigate the effect of intense noise exposure on HO-1 induction. Materials and methods: A total of 25 adult guinea pigs (body weight 200Á300 g) with a normal Preyers's reflex were used as subjects. Based on preliminary tests, the appropriate intensities and durations of noise were determined that were adequate to induce apparent threshold shifts and lead to various recovery patterns to initial thresholds. The sound was routed through a power amplifier to a speaker, which was positioned directly over the animals in a sound chamber. Auditory brainstem response (ABR) testing, Western blot analysis for HO-1, and immunohistochemical testing were done. Results: Exposure of the guinea pigs to 115 dB SPL octave band noise for 5 h induced HO-1 expression in the organ of Corti. In the organ of Corti, HO-1 expression increased mainly in the outer hair cells. Some expression of HO-1 was observed before and after noise exposure in the supporting cells. HO-1 expression in the organ of Corti was definitely increased in guinea pigs with an intense noise exposure which causes a temporary threshold shift.

Acoustic Trauma Modulates Cochlear Blood Flow and Vasoactive Factors in a Rodent Model of Noise-Induced Hearing Loss

“…Importantly, Yuan et al reported that noise-induced oxidative responses as indicated by products of lipid oxidation (4-hydroxynonenal) and protein nitration (3-nitrotyrosine) occurred in a noise-dose-dependent manner [82]. The results of this study are consistent with the literature in demonstrating that the levels of antioxidant enzymatic scavengers, including HO-1 and catalase, are increased in the cochlea (particularly the organ of Corti), in response to intense noise stimulation [83,84]. The natural defense system managed by antioxidant enzymatic scavengers seems to be overwhelmed by ROS accumulation, before or during initiation of TTS- or PTS-related damage.…”

Heat Shock Protein-Mediated Protection Against Cisplatin-Induced Hair Cell Death

“…HO-1 expression has been reported in cochlear hair cells and stria vascularis following a variety of stressors, including noise stress, heat stress, and pharmacological induction (Fairfield et al 2004;Lopez et al 2008;Kim et al 2009;Matsunobu et al 2009;Fetoni et al 2010). In the current study, CoPPIX treatment resulted in HO-1 induction primarily in resident macrophages without induction in hair cells or supporting cells (Fig.…”

“…Previously, we showed that heat shock inhibits both cisplatin-and aminoglycoside-induced hair cell death (Cunningham and Brandon 2006). In addition to heat shock, noise exposure has also been shown to induce HSPs in the inner ear (Matsunobu et al 2009;Roy et al 2013).…”

Protection by low-dose kanamycin against noise-induced hearing loss in mice: Dependence on dosing regimen and genetic background

“…The preconditioning literature across systems and tissues further implicates antioxidants, TNFα, NFκB, HO-1, and Nrf2 (Dirnagl et al, 2003; Ran et al, 2005; Gidday, 2006; Lehotsky et al, 2009),. All the above factors are known to participate in cochlear responses to stress (Rybak, 2007; So et al, 2008; Matsunobu et al, 2009; Yamamoto et al, 2009; Chance et al, 2010), some to aminoglycosides specifically (Jiang et al, 2005; Chen et al, 2008; Taleb et al, 2009). The friend-or-foe nature of some factors, in particular TNFα and NFκB (Shi and Nuttall, 2007; Yamamoto et al, 2009), may depend on when and where they are expressed (Ohlemiller, 2008).…”