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Title:
Effects of quinine on K+ transport in heart mitochondria | Journal of Bioenergetics and Biomembranes
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Quinine inhibits the respiration-dependent extrusion of K+ from Mg2+-depleted heart mitochondria and the passive osmotic swelling of these mitochondria in K+ and Na+ acetate at alkaline pH. These observations concur with those of Nakashima and Garlid (J. Biol. Chem. 257, 9252, 1982) using rat liver mitochondria. Quinine also inhibits the respiration-dependent contraction of heart mitochondria swollen passively in Na+ or K+ nitrate and the increment of elevated respiration associated with the extrusion of ions from these mitochondria. Quinine, at concentrations up to 0.5 mM, inhibits the respiration-dependent42K+/K+ exchange seen in the presence of mersalyl, but higher levels of the drug produce increased membrane permeability and net K+ loss from the matrix. These results are all consistent with an inhibition of the putative mitochondrial K+/H+ antiport by quinine. However, quinine has other effects on the mitochondrial membrane, and possible alternatives to this interpretation are discussed.
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google, scholar, brierley, article, biol, chem, mitochondria, garlid, biophys, quinine, biochem, mitochondrial, privacy, cookies, content, journal, research, heart, publish, search, access, jurkowitz, arch, data, information, log, effects, farooqui, utz, inhibits, nakashima, rat, discover, chavez, download, springer, optional, personal, parties, policy, find, track, bioenergetics, biomembranes, transport, articles, cite, dennis, tahira, eric,
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month download article/chapter substrate-mediated mitochondrial respiration mg2+-depleted heart mitochondria rat liver mitochondria privacy choices/manage cookies related subjects heart mitochondria access full article pdf mitochondrial membrane european economic area cytosolic free zn2+ conditions privacy policy passive osmotic swelling eric utzย &ย gerald accepting optional cookies putative mitochondrial respiration-dependent extrusion respiration-dependent contraction journal finder publish main content log heart mitochondria higher levels article journal ohio dennis article log brierley rights privacy policy personal data article jung check access latest articles article cite instant access books a optional cookies manage preferences journal publish elevated respiration respiration-dependent42k+/ data protection essential cookies cookies skip subscription content similar content biomembranes aims institution subscribe usage analysis social media varying standards december 1984 volumeย 16
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headline:Effects of quinine on K+ transport in heart mitochondria
description:Quinine inhibits the respiration-dependent extrusion of K+ from Mg2+-depleted heart mitochondria and the passive osmotic swelling of these mitochondria in K+ and Na+ acetate at alkaline pH. These observations concur with those of Nakashima and Garlid (J. Biol. Chem.
257, 9252, 1982) using rat liver mitochondria. Quinine also inhibits the respiration-dependent contraction of heart mitochondria swollen passively in Na+ or K+ nitrate and the increment of elevated respiration associated with the extrusion of ions from these mitochondria. Quinine, at concentrations up to 0.5 mM, inhibits the respiration-dependent42K+/K+ exchange seen in the presence of mersalyl, but higher levels of the drug produce increased membrane permeability and net K+ loss from the matrix. These results are all consistent with an inhibition of the putative mitochondrial K+/H+ antiport by quinine. However, quinine has other effects on the mitochondrial membrane, and possible alternatives to this interpretation are discussed.
datePublished:
dateModified:
pageStart:379
pageEnd:390
sameAs:https://doi.org/10.1007/BF00743233
keywords:
Quinine
quinacrine
mitochondrial K+/H+ antiport
swelling and contraction of heart mitochondria
Bioorganic Chemistry
Biochemistry
general
Animal Anatomy / Morphology / Histology
Animal Biochemistry
Organic Chemistry
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headline:Effects of quinine on K+ transport in heart mitochondria
description:Quinine inhibits the respiration-dependent extrusion of K+ from Mg2+-depleted heart mitochondria and the passive osmotic swelling of these mitochondria in K+ and Na+ acetate at alkaline pH. These observations concur with those of Nakashima and Garlid (J. Biol. Chem.
257, 9252, 1982) using rat liver mitochondria. Quinine also inhibits the respiration-dependent contraction of heart mitochondria swollen passively in Na+ or K+ nitrate and the increment of elevated respiration associated with the extrusion of ions from these mitochondria. Quinine, at concentrations up to 0.5 mM, inhibits the respiration-dependent42K+/K+ exchange seen in the presence of mersalyl, but higher levels of the drug produce increased membrane permeability and net K+ loss from the matrix. These results are all consistent with an inhibition of the putative mitochondrial K+/H+ antiport by quinine. However, quinine has other effects on the mitochondrial membrane, and possible alternatives to this interpretation are discussed.
datePublished:
dateModified:
pageStart:379
pageEnd:390
sameAs:https://doi.org/10.1007/BF00743233
keywords:
Quinine
quinacrine
mitochondrial K+/H+ antiport
swelling and contraction of heart mitochondria
Bioorganic Chemistry
Biochemistry
general
Animal Anatomy / Morphology / Histology
Animal Biochemistry
Organic Chemistry
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