Abstract:
:In summary, NO is capable of decreasing mitochondrial respiration in a variety of mammalian tissues. This effect is mediated primarily via binding of NO to the O2 binding site of cytochrome oxidase. This highly sensitive interaction presumably reflects a remnant homology between cytochrome oxidase and bacterial nitrate reductase. This effect has been demonstrated at physiologic levels of NO, highlighting the role for NO in the tonic control of cellular respiration. As this inhibition is dependent upon the levels figure: see text[ of NO and O2 in the tissue, various states of NO production and oxygen supply dictate the ultimate respiratory rate of the mitochondria. Furthermore, deviation from a physiologic NO: O2 may lead to an exacerbation of pathologic states, such as congestive heart failure and septic shock. Thus, NO may play a crucial role in the control of cellular respiration, providing an additional mechanism of action for this biologically diverse molecule that is distinct yet inseparable from its dilator effect on blood vessels.
journal_name
Adv Exp Med Bioljournal_title
Advances in experimental medicine and biologyauthors
Forfia PR,Hintze TH,Wolin MS,Kaley Gdoi
10.1007/978-1-4615-4717-4_46subject
Has Abstractpub_date
1999-01-01 00:00:00pages
381-8eissn
0065-2598issn
2214-8019journal_volume
471pub_type
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abstract::Tropomyosins constitute a family of highly related actin-binding proteins found in the animal kingdom from yeast to human. In vertebrates, they are encoded by a multigene family where each member can produce several isoforms through alternative splicing and for some of them with alternate promoters. Tropomyosin isofor...
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