Membrane disruption: an early event of hair cell apoptosis induced by exposure to intense noise.
Membrane leakage has been found in hair cells undergoing apoptosis following exposure to intense noise. However, it is not known whether this membrane damage is the consequence of apoptotic degeneration or direct mechanical stress. The current study was designed to investigate whether membrane damage occurred before the onset of apoptosis and to determine the level of the membrane damage. Chinchillas were exposed to an impulse noise at 155 dB peak SPL. The noise-induced membrane damage was assessed functionally, using membrane tracers with graded molecular sizes (propidium iodide and FITC-dextrans with molecular sizes of 3, 40, 500, and 2000 kDa), and morphologically, using DiO staining and semithin sections. The study revealed two major findings. First, exposure to intense noise caused a rapid increase in membrane permeability, and the onset of membrane leakage preceded the manifestation of nuclear condensation. This indicates that the early membrane damage observed in apoptosis is the direct consequence of mechanical stress. Second, the level of membrane damage was severe, allowing the entry of 3 kDa and 40 kDa FITC-dextrans, but the membrane was not completely broken down, as evidenced by the preservation of the ability to exclude 500 kDa and 2000 kDa FITC-dextran molecules and the maintenance of the cell boundary. Notably, despite the membrane damage, hair cells continue to undergo the apoptotic process, leading to the generation of a type of apoptosis with early membrane damage.
Hu
Bo Hua
BH
Center for Hearing and Deafness, State University of New York at Buffalo, 137 Cary Hall, 3435 Main Street, Buffalo, NY 14214, USA. bhu@acsu.buffalo.edu
Zheng
Gui Liang
GL
D000161:Acoustic Stimulation; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002462:Cell Membrane / Q000473:pathology / Q000502:physiology*; D002463:Cell Membrane Permeability / Q000502:physiology; D002467:Cell Nucleus / Q000473:pathology / Q000502:physiology; D002682:Chinchilla; D003051:Cochlea / Q000166:cytology / Q000473:pathology / Q000502:physiology; D003911:Dextrans / Q000493:pharmacokinetics; D004781:Environmental Exposure / Q000009:adverse effects*; D016650:Fluorescein-5-isothiocyanate / Q000031:analogs & derivatives / Q000493:pharmacokinetics; D005456:Fluorescent Dyes / Q000493:pharmacokinetics; D006198:Hair Cells, Auditory / Q000166:cytology / Q000473:pathology / Q000502:physiology*; D018072:Hair Cells, Auditory, Outer / Q000166:cytology / Q000473:pathology / Q000502:physiology; D009336:Necrosis / Q000473:pathology / Q000503:physiopathology; D009622:Noise / Q000009:adverse effects*; D011419:Propidium; D013314:Stress, Mechanical; D013997:Time Factors
D003911:Dextrans; D005456:Fluorescent Dyes; C015219:fluorescein isothiocyanate dextran; D011419:Propidium; D016650:Fluorescein-5-isothiocyanate
Hear Res. 2006 Jan;211(1-2):16-25
16219436
Am J Pathol. 1995 Jan;146(1):3-15
7856735
J Acoust Soc Am. 1985 Sep;78(3):833-60
4040933
Hear Res. 2005 Oct;208(1-2):14-25
15950415
Acta Otolaryngol. 2000 Jan;120(1):19-24
10779180
Eur J Neurosci. 2004 Jul;20(1):41-50
15245477
Hear Res. 2003 May;179(1-2):21-32
12742235
J Acoust Soc Am. 1986 Aug;80(2):569-84
3745686
Hear Res. 1987;25(2-3):153-71
3104269
Hear Res. 2001 Nov;161(1-2):10-22
11744276
Hear Res. 1984 Mar;13(3):229-47
6735931
Hear Res. 2003 Jan;175(1-2):82-100
12527128
Neuroscience. 2002;111(3):635-48
12031350
J Assoc Res Otolaryngol. 2003 Dec;4(4):466-77
14534835
J Neurosci. 2002 May 15;22(10):3939-52
12019313
Otol Neurotol. 2004 Jul;25(4):627-32
15241246
Apoptosis. 2007 Jun;12(6):1025-36
17268771
Arch Histol Cytol. 1995 Jun;58(2):139-49
7576866
Hear Res. 2002 Apr;166(1-2):33-43
12062756
Hear Res. 1998 Jan;115(1-2):93-100
9472738
Hear Res. 2004 Oct;196(1-2):69-76
15464303
Neurosci Lett. 2002 Mar 1;320(1-2):73-6
11849767
Neuroreport. 2003 May 23;14(7):1025-9
12802196
Hear Res. 2002 Apr;166(1-2):62-71
12062759
Hear Res. 2007 Jan;223(1-2):61-70
17141990