The NO/ONOO- cycle as the etiological mechanism of tinnitus.

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Int Tinnitus J. 2007;13(2):99- 104. Links

 

The NO/ONOO- cycle as the etiological mechanism of tinnitus.

 

_http://www.ncbi. nlm.nih.gov/ pubmed/18229788? dopt=AbstractPlu s_

(http://www.ncbi. nlm.nih.gov/ pubmed/18229788? dopt=AbstractPlu s)

 

Pall ML, Bedient SA.

School of Molecular Biosciences, Washington State University, Pullman,

Washington 99164-4234, USA. _martin_pall@ wsu.edu_ (martin_pall)

 

Peripheral tinnitus is a good candidate for inclusion under the NO/ONOO

cycle etiological mechanism, fitting each of the five principles of this

mechanism. Cases of tinnitus are initiated by at least 11 short-term stressors

increasing nitric oxide or other cycle mechanisms. Such cycle elements as

N-methyl-D-aspartat e activity; oxidative stress; nitric oxide; peroxynitrite;

vanilloid activity; NF-kappaB activity; and intracellular calcium levels are

all

reported to be elevated in tinnitus. Tinnitus is comorbid with some putative

NO/ONOO- cycle diseases. Most important, multiple agents that down-regulate

NO/ONOO- cycle biochemistry are reported to be helpful in the treatment of

tinnitus and related diseases. Previous studies suggested that NO/ONOO cycle

diseases may be best treated with complex combinations of agents predicted to

lower

NO/ONOO- cycle biochemistry, and such combinations may be helpful in

tinnitus treatment. Other inner-ear-related defects, such as acute or

progressive

hearing loss, vertigo, and dizziness, may also be NO/ONOO cycle diseases.

 

PMID: 18229788 [PubMed - indexed for MEDLINE]