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Sida 1 från 32 resultat
Use of digitonin fractionation to determine mitochondrial transmembrane ion distribution in cells during anoxia.
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A method to determine intracellular distribution of ions and metabolites under conditions of low oxygen concentration was developed. The technique involves rapid digitonin fractionation and addition of cyanide to inhibit reoxygenation. Applicability of the procedure was examined by studying the
Evidence for involvement of nonesterified fatty acid-induced protonophoric uncoupling during mitochondrial dysfunction caused by hypoxia and reoxygenation.
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BACKGROUND
Proximal tubules subjected to hypoxia in vitro under conditions relevant to ischaemia in vivo develop an energetic deficit that is not corrected even after full reoxygenation. We have provided evidence that accumulation of nonesterified fatty acids (NEFA) is the primary reason for this
Production of hydrogen peroxide in situ in cardiac myocytes during hypoxia-reoxygenation as assessed with cerium.
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Free radicals have been implicated in myocardial reperfusion injury. Hydrogen peroxide (H(2)O(2)) is one possible source of reactive oxygen intermediates. We studied the formation and toxicity of H(2)O(2) in isolated myocytes during hypoxia-reoxygenation with the use of cerium. This method involves
Substrate modulation of fatty acid effects on energization and respiration of kidney proximal tubules during hypoxia/reoxygenation.
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Kidney proximal tubules subjected to hypoxia/reoxygenation develop a nonesterified fatty acid-induced energetic deficit characterized by persistent partial mitochondrial deenergization that can be prevented and reversed by citric acid cycle substrates. To further assess the role of competition
Subsynaptosomal calcium distribution during hypoxia and 3,4-diaminopyridine treatment.
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Previous results demonstrate that hypoxia (low oxygen) diminishes calcium uptake by synaptosomes. The present studies examined the effects of low oxygen on calcium homeostasis in the digitonin-resistant (mitochondrial) and the digitonin-labile (nonmitochondrial) compartments of intact synaptosomes
Chlortetracycline-mediated continuous Ca2+ oscillations in mitochondria of digitonin-treated Tetrahymena pyriformis.
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Ca2+ transport in mitochondria was studied in situ using digitonin-permeabilized cells of the ciliate protozoan Tetrahymena pyriformis GL. In the presence of oxidizable substrates and inorganic phosphate, mitochondria were able to accumulate a large amount of the added Ca2+ without subsequent
A nitroimidazole derivative, PR-350, enhances the killing of pancreatic cancer cells exposed to high-dose irradiation under hypoxia.
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The radiosensitizing effects of PR-350, a nitroimidazole derivative, were examined concerning the cell killing of human pancreatic cancer cell lines exposed to high doses of gamma-ray irradiation in vitro. The percentages of dead cells were analyzed with a multiwell plate reader to measure the
Effects of hypoxia on the catecholamine release, Ca2+ uptake, and cytosolic free Ca2+ concentration in cultured bovine adrenal chromaffin cells.
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The purpose of the present study is to clarify the effects of hypoxia on catecholamine release and its mechanism of action. For this purpose, using cultured bovine adrenal chromaffin cells, we examined the effects of hypoxia on high (55 mM) K(+)-induced increases in catecholamine release, in
Mitochondrial transmembrane potential and pH gradient during anoxia.
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The effect of anoxia on the mitochondrial transmembrane potential and pH gradient was studied in a preparation of isolated hepatocytes. Transmembrane potential (delta psi) was calculated from the distribution of triphenylmethylphosphonium between the mitochondrial, cytosolic, and extracellular
Intracellular respiratory dysfunction and cell injury in short-term anoxia of rabbit renal proximal tubules.
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The effects of short-term anoxia and hypoxia were studied in a rabbit proximal renal tubule suspension in order to avoid the hemodynamic consequences of clamp-induced ischemia. The suspension was subjected to anoxia for 10-40 min and the effects on a number of cellular transport and respiratory
Subcellular distribution of malate-aspartate cycle intermediates during normoxia and anoxia in the heart.
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The subcellular distribution of adenine nucleotides, phosphocreatine and intermediates of the malate-aspartate cycle was investigated in adult rat heart myocytes under normoxia and anoxia. Cytosolic and mitochondrial concentrations of metabolites were determined by a fractionation method using
Anoxia induces matrix shrinkage accompanied by an increase in light scattering in isolated brain mitochondria.
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It is important to monitor mitochondrial conditions, and light scattering (LS) measurements have been applied to the detection of morphological changes in mitochondria in vivo. Little is known about the morphological and LS responses of brain mitochondria to oxygen withdrawal, a critical factor in
Susceptibility of murine periportal hepatocytes to hypoxia-reoxygenation: role for NO and Kupffer cell-derived oxidants.
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Ischemia/reperfusion (I/R) is an important problem in liver resection and transplantation that is associated with hepatocellular dysfunction and injury. This study was designed to investigate whether a difference in hepatocyte susceptibility occurs in the periportal (PP) and/or perivenous (PV) zones
Assessment of mitochondrial membrane potential in proximal tubules after hypoxia-reoxygenation.
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Proximal tubules develop a severe energetic deficit during hypoxia-reoxygenation (H/R) that previous studies using fluorescent potentiometric probes have suggested is characterized by sustained, partial mitochondrial deenergization. To validate the primary occurrence of mitochondrial deenergization
Hypoxia-reoxygenation induced increase in cellular Ca2+ in myocytes and perfused hearts: the role of mitochondria.
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Reoxygenation of isolated rat cardiac myocytes following a period of hypoxia and substrate deprivation resulted in a 1.5-2-fold increase in the total Ca2+ content which could be inhibited by 1 microM antimycin A or ruthenium red (50% inhibition at 2.5 microM). This increase in Ca2+ content was not
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