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Calcium‐mediated alterations in the oxidation—reduction state of pyridine nucleotides in isolated liver cells
Author(s) -
Ontko Joseph A.,
Otto David A.
Publication year - 1975
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(75)80040-8
Subject(s) - foundation (evidence) , library science , medical school , medicine , citation , gerontology , political science , medical education , law , computer science
In isolated mitochondrial systems calcium ions cause pyridine nucleotide oxidation and increased oxygen consumption, concurrent with energy-dependent calcium accumulation [ 1,2]. A variety of oxidizable substrates support this process. In the absence of phosphate or other actively permeant anions, calcium causes reduction of cytochrome b, described as State 6 [3,4], and, when ATP is present, pyridine nucleotide reduction also occurs [ 11. It has recently been observed that the addition of calcium to intact liver cells incubated with NAD-linked substrates causes gradual elevation in the mitochondrial NADH/NAD, most prominent with fatty acid substrate [5,6]. In contrast, when the hepatocytes are incubated with succinate, calcium decreases the mitochondrial NADI-I/NAD [ 61. The redox state of cellular pyridine nucleotides is of major importance in the control of metabolic processes. In view of apparent differences between the action of calcium in isolated mitochondrial systems and that observed in intact liver cells, the influence of calcium on the NAD oxidation-reduction state in hepatocytes was further examined. As reported herein, pyridine nucleotides, catalaseHZ O2 and -cyanide complexes and cytochrome oxidase in this isolated hepatocyte preparation were responsive to agents affecting these systems in the perfused liver.