HYDROPEROXIDES CAN MODULATE THE REDOX STATE OF PYRIDINE-NUCLEOTIDES AND THE CALCIUM BALANCE IN RAT-LIVER MITOCHONDRIA
HYDROPEROXIDES CAN MODULATE THE REDOX STATE OF PYRIDINE-NUCLEOTIDES AND THE CALCIUM BALANCE IN RAT-LIVER MITOCHONDRIA
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DOI：
10.1073/pnas.76.9.4340
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发表时间：
1979-01-01
影响因子：
11.1
通讯作者：
RICHTER, C
中科院分区：
文献类型：
--
作者：
LOTSCHER, HR;WINTERHALTER, KH;RICHTER, C
When rats are fed a selenium-deficient diet, the glutathione peroxidase activity in liver mitochondria decreases within 5 weeks to 0-6% of that of control animals fed on a diet supplemented with 0.5 ppm of selenium as sodium selenite. Analysis of the temperature dependence of energy-linked Ca2+uptake by means of Arrhenius plots reveals two breaks (at around 11°C and 24°C) in mitochondria isolated from selenium-supplemented animals, whereas in selenium-deficient rats the break at 11°C is absent. Ca2+-loaded mitochondria of selenium-supplemented rats—i.e., with active glutathione peroxidase in the matrix—lose Ca2+rapidly, with a concomitant oxidation of endogenous NAD(P)H, when exposed tot-butyl hydroperoxide or H2O2. In contrast, in selenium deficiency,t-butyl hydroperoxide and H2O2induce neither a release of Ca2+nor an oxidation of NAD(P)H. The peroxide-induced oxidation of NAD(P)H is reversible in the presence of succinate when no Ca2+has been taken up. When Ca2+has previously been accumulated, however, the oxidation of NAD(P)H is irreversible. Enzymatic analysis of mitochondrial pyridine nucleotides reveals that the peroxide-induced oxidation of NAD(P)H in Ca2+-loaded mitochondria leads to a loss of NAD+and NADP+. It is proposed that the redox state of mitochondrial pyridine nucleotides can be or is in part controlled by glutathione peroxidase and glutathione reductase and is a factor in the balance of Ca2+between mitochondria and medium.
