Abstract:
:Cystic fibrosis (CF) remains a major problem in human genetics and cell pathophysiology. It is a single gene trait caused by a mutation on the long arm of chromosome 7. Among its expressions are abnormal regulation of chloride channels and/or microobstructions in exocrine tissues. Here, evidence is presented that mitochondria are dysfunctional in CF: the major site of increased intracellular Ca in CF is mitochondrial, cells from subjects with CF consume more oxygen than normal, respond differentially to inhibitors of mitochondrial function, express increased electron transport activity and altered kinetics of complex I (NADH dehydrogenase) of the mitochondrial electron transport system. Patients with CF express increased total and resting energy expenditure. Some of these differences from normal occur also in asymptomatic carriers of the CF gene.
journal_name
Life Scijournal_title
Life sciencesauthors
Shapiro BLdoi
10.1016/0024-3205(89)90389-5subject
Has Abstractpub_date
1989-01-01 00:00:00pages
1327-34issue
19eissn
0024-3205issn
1879-0631pii
0024-3205(89)90389-5journal_volume
44pub_type
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