The NAD+/NADH redox state in astrocytes: Independent control of the NAD+ and NADH content

2011 ◽  
Vol 89 (12) ◽  
pp. 1956-1964 ◽  
Author(s):  
Franziska Wilhelm ◽  
Johannes Hirrlinger
Keyword(s):  
Redox State ◽  
Independent Control ◽  
Nadh Redox State

scholarly journals Circadian Oscillations of NADH Redox State Using a Heterologous Metabolic Sensor in Mammalian Cells

2016 ◽  
Vol 291 (46) ◽  
pp. 23906-23914 ◽  
Author(s):  
Guocun Huang ◽  
Yunfeng Zhang ◽  
Yongli Shan ◽  
Shuzhang Yang ◽  
Yogarany Chelliah ◽  
...  
Keyword(s):  
Mammalian Cells ◽  
Redox State ◽  
Metabolic Sensor ◽  
Nadh Redox State

In vivo monitoring of cellular energy metabolism using SoNar, a highly responsive sensor for NAD+/NADH redox state

2016 ◽  
Vol 11 (8) ◽  
pp. 1345-1359 ◽  
Author(s):  
Yuzheng Zhao ◽  
Aoxue Wang ◽  
Yejun Zou ◽  
Ni Su ◽  
Joseph Loscalzo ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Redox State ◽  
Cellular Energy ◽  
In Vivo Monitoring ◽  
Cellular Energy Metabolism ◽  
Nadh Redox State

scholarly journals Mitochondrial NAD+/NADH Redox State and Diabetic Cardiomyopathy

2019 ◽  
Vol 30 (3) ◽  
pp. 375-398 ◽  
Author(s):  
Jessica M. Berthiaume ◽  
Jacob G. Kurdys ◽  
Danina M. Muntean ◽  
Mariana G. Rosca
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Redox State ◽  
Nadh Redox State

Multiparametric monitoring of the awake brain exposed to carbon monoxide

1995 ◽  
Vol 78 (3) ◽  
pp. 1188-1196 ◽  
Author(s):  
A. Mayevsky ◽  
S. Meilin ◽  
G. G. Rogatsky ◽  
N. Zarchin ◽  
S. R. Thom
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Redox State ◽  
Ionic Homeostasis ◽  
Awake Rat ◽  
Brain Oxidative Stress ◽  
The Brain ◽  
Measurable Change ◽  
Nadh Redox State

We have applied in vivo real-time techniques to monitor the physiological changes associated with exposure to a pattern of carbon monoxide (CO) known to cause brain oxidative stress. Using a multiparametric monitoring device connected to the brain, we exposed unanesthetized rats to two levels of CO, 0.1 and 0.3% in air. Energy metabolism was evaluated by the optical monitoring of relative cerebral blood flow (CBF) and intramitochondrial redox state. Ionic homeostasis was assessed by measurements of K+,Ca2+, and H+ or Na+ levels in the extracellular space. The electrical parameters monitored were the electrocorticogram and direct current steady potential. Under 1,000 ppm of CO, the CBF was increased significantly without any measurable change in the NADH redox state, suggesting that the cause for the increased CBF was not hypoxia. Exposing the awake rat to 1,000 ppm of CO (40 min) followed by 3,000 ppm of CO (20 min) led to an increase in CBF followed by episodes of spontaneous brain depolarizations characterized by changes in ionic homeostasis and blood flow. These changes were similar to those recorded under cortical spreading depression. In most animals exposed to 3,000 ppm of CO, spontaneous oscillations in CBF and NADH redox state that were negatively correlated were recorded. The results indicate that an inspired CO level of 0.1% had effects largely restricted to blood flow, whereas at a higher CO level an additional impairment in energy supply resulted in a complex pattern of effects similar to that caused by brain ischemia.

NAD/NADH: redox state changes on cat brain cortex during stimulation and hypercapnia

1982 ◽  
Vol 243 (6) ◽  
pp. H1032-r-H1032-r
Author(s):  
Laszlo Gyulai ◽  
Eörs Dora ◽  
Arisztid G. B. Kovach
Keyword(s):  
Experimental Research ◽  
Redox State ◽  
Brain Cortex ◽  
University Of Pennsylvania ◽  
Research Department ◽  
Cat Brain ◽  
State Changes ◽  
Medical University ◽  
Nadh Redox State

Page H619: Laszlo Gyulai, Eörs Dora, and Arisztid G. B. Kovach. “NAD/NADH: redox state changes on cat brain cortex during stimulation and hypercapnia.” Authors' affiliation line should read: Experimental Research Department and Second Institute of Physiology, Semmelweis Medical University, Budapest, Üllöi ut 78/a, Hungary. Address for reprint requests: L. Gyulai, Johnson Research Foundation, University of Pennsylvania, 37th and Hamilton Walk, Richards Bldg.Ü5th Floor, Philadelphia, PA 19104.

scholarly journals Effect of Acute Arterial Hypo- and Hypertension on Cerebrocortical NAD/NADH Redox State and Vascular Volume

1982 ◽  
Vol 2 (2) ◽  
pp. 209-219 ◽  
Author(s):  
Eörs Dóra ◽  
Arisztid G. B. Kovách
Keyword(s):  
Redox State ◽  
Arterial Hypotension ◽  
Minor Role ◽  
Vascular Volume ◽  
Fluorescence Measurements ◽  
Arterial Blood ◽  
Nadh Fluorescence ◽  
Alpha Receptors ◽  
A Minor ◽  
Nadh Redox State

The effects of stepwise arterial hypotension (MABP: 80, 60, 40 mm Hg) and moderate arterial hypo- and hypertension (MABP: 80, 150–160 mm Hg) on cerebrocortical vascular volume and NAD/NADH redox state were studied in anaesthetized cats, The vascular volume and NADH fluorescence measurements were performed on closed skull preparations using a microscope fluororeflectometer. To determine the possible role of adrenergic alpha-receptors in the autoregulatory adjustment of cerebrocortical vascular volume, some of the animals were pretreated with intra-arterially infused phenoxybenzamine (1 mg/kg), It was found that longlasting stepwise arterial hypotension leads to a gradual increase in cerebrocortical vascular volume and NADH fluorescence, Though the cerebrocortical arteries dilatated considerably at 80 mm Hg, sustained for 30 min, the NAD/NADH redox state failed to be reoxidized but was shifted to a more reduced state. This finding suggests that some factor other than tissue hypoxia is responsible for the dilatation of cerebrocortical vessels during moderate arterial hypotension. When the arterial blood pressure was restored following stepwise arterial hypotension, the cerebrocortical vascular volume did not decrease and the NAD/NADH redox state remained reduced, showing that the autoregulatory capability of the vessels was lost and the tissue metabolism was irreversibly altered. During a 5-min duration of moderate arterial hypo- and hypertension, biphasic changes were obtained in cerebrocortical vascular volume while the NAD/NADH redox state was shifted to a more reduced and oxidized state. Since the dilatation and the constriction of the cerebrocortical vessels during arterial hypo- and hypertension lagged by 40–80 s behind the redox state alterations, it is suggested that the myogenic mechanism has a minor role in CBF autoregulation. Phenoxybenzamine (PBZ) dilatated the cerebrocortical vessels, indicating the existence of an active alpha-receptor-mediated vasoconstrictory tone. Since the extent of autoregulatory vascular volume changes was not affected by PBZ pretreatment, the involvement of adrenergic alpha-receptors in the autoregulation of CBF can be excluded, at least for cats.

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