Energy charge of the adenylate pool as a regulatory parameter.  Interaction with feedback modifiers

Atkinson, Daniel E.

doi:10.1021/bi00851a033

Cited by 2,318 publications

(965 citation statements)

References 13 publications

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“…The plasma membrane peroxidations favor an unregulated increase in intracellular calcium ion levels (Orrenius et al, 1989;Farber et al, 1990;Farber, 1994;Sakagami and Satoh, 1997), which, along with thiol oxidations, poison mitochondria. That damage decreases the output of ATP (Saurin et al, 2004) necessary to maintain the homeostatic cell energy charge (Atkinson, 1968) and to assist in repairing the ongoing damage associated with the peroxidations (Stadtman, 1992). Mitochondrial alterations have already been reported following VC, VK3, and VC:VK 3 treatment (Gilloteaux et al, 1995(Gilloteaux et al, , 2001a(Gilloteaux et al, , 2001b(Gilloteaux et al, , 2001cJamison et al, 1997).…”

Section: Cytotoxicity Of Ascorbatementioning

confidence: 95%

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Gilloteaux¹,

Jamison²,

Arnold³

et al. 2005

Anat. Rec.

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Feulgen and actin-phalloidin staining as well as gel electrophoresis have been employed in conjunction with cell ultrastructure to describe the effects of 1-, 2-, and 4-hr ascorbate (VC), menadione (VK 3 ), and ascorbate:menadione (VC:VK 3 ) treatments on the T24 human bladder carcinoma cell line. T24 cells exposed to VC alone display blebs and other superficial membrane defects related to membrane alterations and to superficial cytoskeleton changes. VK 3 treatment damages the cell nucleus and organelles, leads to the redistribution of the organelles in the perikaryon as a consequence of cytoskeletal damage, and results in cytoplasmic self-excisions. After VC:VK 3 treatment, the cells show exaggerated alterations characteristic of each vitamin treatment alone, including damaged mitochondria, self-excision of organelle-free pieces of cytoplasm, and extrusion of the perikaryon containing a nucleus surrounded by the damaged organelles. The nuclear envelope appears intact and contains chromatin that decondenses and dissipates. During the cellular demise that concludes with apparent karyolysis, the cells significantly decrease their size and alter their shape. However, the cisterns of rough endoplasmic reticulum are undamaged, but may become dilated. Since the cellular phenomena leading to cell death differ morphologically from apoptosis and necrosis, but entail selfcutting without nuclear bodies, this new form of cell death was called autoschizis. In addition, gel electrophoresis and Feulgen staining demonstrate that autoschizis is accompanied by random DNA degeneration.

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Section: Cytotoxicity Of Ascorbatementioning

confidence: 95%

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Gilloteaux¹,

Jamison²,

Arnold³

et al. 2005

Anat. Rec.

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“…Cerebral energy charge potential. The cerebral energy charge potential (ECP)-the charge of the phosphory lated adenine nucleotide pool-was derived from the for mula of Atkinson (1968):…”

Section: Calculationsmentioning

confidence: 99%

Lactate Reverses Insulin-Induced Hypoglycemic Stupor in Suckling—Weanling Mice: Biochemical Correlates in Blood, Liver, and Brain

Thurston

Hauhart

Schiro

1983

J Cereb Blood Flow Metab

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Summary:The recovery of weanling mice from insulin induced hypoglycemic stupor-coma after injection of so dium -L( + )-lactate (18 mmoUkg) was as rapid (10 min) as in litter-mates treated with glucose (9 mmoUkg). Stimu lated by this dramatic action, we studied the effects of lactate injection on brain carbohydrate and energy me tabolism in normal and hypoglycemic mice; blood and liver tissue were also studied. Te n minutes after lactate injection in normal mice, plasma lactate levels increased by 15 mmoUL; plasma glucose levels were unchanged, but the f3-hydroxybutyrate concentration fell 59%. In the brains of these animals, glucose levels increased 2.3-fold, and there were significant increases in brain glycogen (10%), glucose-6-phosphate (27%), lactate (68%), pyru vate (37%), citrate (12%), and malate (19%); the increase in (I-ketoglutarate (32%) was not significant. Lactate in jection reduced the cerebral glucose-use rate 40%. These changes were not due to lactate-induced increases in blood [HCO 31 and pH (examined by injection of 15There is increasing interest in lactate as an oxi dizable fuel for brain metabolism, particularly in de veloping animals. In 1971, Oldendorf demonstrated a specific carrier for transport of lactate (and other monocarboxylic acids) across the blood-brain bar rier. Vannucci and Duffy (1976) were the first to suggest that lactate might serve as a fuel for brain Preliminary data from this study were presented to the Child Neurology Society, Salt Lake City, Utah, U.S. A., 1982, and 498 mmoUkg sodium bicarbonate). Although lactate injection of hypoglycemic mice doubled levels of glucose in plasma and brain (not significant) and most of the cerebral gly colytic intermediates, values were far below normal (still in the range seen in hypoglycemic animals). By contrast, citrate and a-ketoglutarate levels returned to normal; the large increase in malate was not significant. Reduced glu tamate levels increased to normal, and elevated aspartate levels fell below normal. Thus, recovery from hypogly cemic stupor does not necessarily depend on normal levels of plasma and/or brain glucose (or glycolytic inter mediates). Near normal levels of the Krebs citric acid cycle intermediates suggest that changes in these metab olites, amino acids, or derived substrates relate to the dramatic recovery of hypoglycemic mice after lactate in jection. Key Words: Brain lactate transport-Cerebral bicarbonate metabolism-Cerebral lactate metabolism Insulin hypoglycemia-Response of hypoglycemia to lactate-Suckling-weanling mice. metabolism in immature rats. Following injection of L-[U-14 C]lactate in anoxic fetal and newborn rats they noted a progressive increase in brain radioac tivity; during recovery from anoxia, pyruvate levels increased sharply but lactate concentration re mained high and brain glucose rose above the con trol value. Based on these findings, the authors pos tulated that during recovery, lactate was oxidized to pyruvate and that there was a continued influx of lactate from the blood with sparin...

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“…Since nucleoside mono-, and diphosphates equilibrated rapidly with the nucleoside triphosphates, the energy charge could be calculated directly from the radioactivity measurements. The adenylate energy charge is defined as [ATP + 0.5 ADP] /[ATP + ADP + AMP] [6] ; the definition of the guanylate energy change is exactly analogous.…”

Section: Methodsmentioning

confidence: 99%

“…Uncharged tRNA may accumulate and cause polyribosome disaggregation [5]. Similarly, the energy charge [6] of adenine and guanine nucleotides might diminish because transport of glucose is inhibited.…”

Section: Introductionmentioning

confidence: 99%

Small changes in energy charge affect protein synthesis in reticulocyte lysates

Rupniak¹,

Quincey²

1975

FEBS Letters

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Energy charge of the adenylate pool as a regulatory parameter. Interaction with feedback modifiers

Cited by 2,318 publications

References 13 publications

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Lactate Reverses Insulin-Induced Hypoglycemic Stupor in Suckling—Weanling Mice: Biochemical Correlates in Blood, Liver, and Brain

Small changes in energy charge affect protein synthesis in reticulocyte lysates

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