Introduction: The 72 kDa heat shock protein (HSP72) had cochlear cytoprotective and anti-inflammatory roles in inner ear during noise stressful challenges. On the other hand, in the extracellular millie these proteins participate as pro-inflammatory signal.

Objectives: We argue whether noise induced hearing loss (NIHL) model promotes both intracellular (iHSP72) and extracellular (eHSP72) heat shock response.

Methods: Female Wistar rats, 90 days old, were randomly divided in Control (CON, n = 6) and NIHL group (n = 10). Auditory Brainstem Response (ABR) was evaluated before and 14 days after noise exposure (124 dB NPS for 2 h). Cochlea and plasma samples were collected to iHSP72 and eHSP72 by AMP'D® HSP70 high sensitivity ELISA kit (Analysis by Student T test).

Results: The noise exposition induced an increase in auditory threshold in NIHL group (Control = 18.3 ± 4.1 vs NIHL = 58.0 ± 9.7 dB, P < 0.0001). NIHL group showed increased levels in both iHSP72 and eHSP72 (iHSP72: Control = 4.44 ± 1.99 vs NIHL = 6.86 ± 0.94 ng/ml, P = 0.018. eHSP72: Control = 0.18 ± 0.02 vs NIHL = 4.07 ± 4.27 ng/ml, P = 0.036).

Conclusion: Our data indicates that cochlear damage induced by noise exposition is accompanied by local and systemic heat shock response. Thus, plasma levels of 72 kDa heat shock proteins can be used as biomarker of cochlear stress condition after noise exposure.