Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P42574 (caspase-3)
 45,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been known for some time that noise-induced outer hair cell (OHC) death in the cochlea continues well after the termination of a noise exposure. However, the underlying mechanisms leading to the expansion of a cochlear lesion are not fully understood. Here we report involvement of the apoptotic pathway in the progression of OHC death in the chinchilla cochlea following exposure to a 4 kHz narrow band noise at 110 dB SPL for 1 h. Morphological examination of OHC nuclei revealed nuclear condensation and fragmentation, typical morphological features of apoptosis. OHC apoptosis developed asymmetrically toward the apical and basal parts of the cochleas following the noise exposure. Two days after the noise exposure, there was still active OHC pathology with condensed and fragmented nuclei in the basal part of the cochleas. Detection of caspase-3 activation, an intracellular marker for apoptosis, showed a spatial agreement between the apoptotic nuclei and activated caspase-3. These results clearly implicate the apoptotic pathway in the post-exposure progression of OHC demise.
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PMID:Involvement of apoptosis in progression of cochlear lesion following exposure to intense noise. 1206 59

We have reported that by 2 days after noise exposure the size of cochlear lesion was expanding by outer hair cells (OHCs) dying either by apoptosis or necrosis. The current study was designed to compare the prevalence of the two cell death pathways as a function of time after exposure to noises of different levels. Chinchillas were exposed to a narrow band noise at either 104 or 108 dB SPL for 1 h. At three time points (1, 4 and 30 days) after the noise exposure, the numbers of missing, apoptotic and necrotic OHCs in the cochleas were identified and documented with a combination of TUNEL, caspase-3 and propidium iodide labeling. The subjects exposed to the 108-dB noise showed significantly more apoptotic OHCs than necrotic OHCs in the cochleas examined at days 1 and 4 after the noise exposure. By day 30, apoptotic and necrotic pathologies continued, although in small quantity, with no significant difference in quantity between two types of cell death. The subjects exposed to the 104-dB noise showed a significant difference in the numbers of apoptotic and necrotic OHCs at day 1 after the noise exposure, whereas the difference became statistically insignificant at day 4 and day 30 after the noise exposure. The results of the study indicate that the early expansion of cochlear lesion is attributed primarily to apoptosis, whereas the later stage of lesion expansion is likely the result of an equal contribution from apoptosis and necrosis.
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PMID:Quantitative analysis of apoptotic and necrotic outer hair cells after exposure to different levels of continuous noise. 1546 3