scholarly journals In vivo31P MRS assessment of intracellular NAD metabolites and NAD+/NADH redox state in human brain at 4 T

2016 ◽  
Vol 29 (7) ◽  
pp. 1010-1017 ◽  
Author(s):  
Ming Lu ◽  
Xiao-Hong Zhu ◽  
Wei Chen
Keyword(s):  
Human Brain ◽  
Redox State ◽  
Nadh Redox State

scholarly journals In vivo NAD assay reveals the intracellular NAD contents and redox state in healthy human brain and their age dependences

2015 ◽  
Vol 112 (9) ◽  
pp. 2876-2881 ◽  
Author(s):  
Xiao-Hong Zhu ◽  
Ming Lu ◽  
Byeong-Yeul Lee ◽  
Kamil Ugurbil ◽  
Wei Chen
Keyword(s):  
Human Brain ◽  
Redox State ◽  
Ex Vivo ◽  
Healthy Human ◽  
Nad Metabolism ◽  
Mitochondrial Functions ◽  
Age Dependent ◽  
Nadh Redox State

NAD is an essential metabolite that exists in NAD+or NADH form in all living cells. Despite its critical roles in regulating mitochondrial energy production through the NAD+/NADH redox state and modulating cellular signaling processes through the activity of the NAD+-dependent enzymes, the method for quantifying intracellular NAD contents and redox state is limited to a few in vitro or ex vivo assays, which are not suitable for studying a living brain or organ. Here, we present a magnetic resonance (MR) -based in vivo NAD assay that uses the high-field MR scanner and is capable of noninvasively assessing NAD+and NADH contents and the NAD+/NADH redox state in intact human brain. The results of this study provide the first insight, to our knowledge, into the cellular NAD concentrations and redox state in the brains of healthy volunteers. Furthermore, an age-dependent increase of intracellular NADH and age-dependent reductions in NAD+, total NAD contents, and NAD+/NADH redox potential of the healthy human brain were revealed in this study. The overall findings not only provide direct evidence of declined mitochondrial functions and altered NAD homeostasis that accompany the normal aging process but also, elucidate the merits and potentials of this new NAD assay for noninvasively studying the intracellular NAD metabolism and redox state in normal and diseased human brain or other organs in situ.

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

scholarly journals Redox Imbalance and Biochemical Changes in Cancer by probing redox-sensitive mitochondrial cytochromes in label-free visible resonance Raman imaging

2020 ◽  
Author(s):  
H. Abramczyk ◽  
B. Brozek-Pluska ◽  
M. Kopec ◽  
M. Błaszczyk ◽  
M. Radek
Keyword(s):  
Raman Spectroscopy ◽  
Brain Tumors ◽  
Human Brain ◽  
Redox State ◽  
Ductal Carcinoma ◽  
Redox Status ◽  
Raman Imaging ◽  
Breast Cancers ◽  
Human Brain Tumors ◽  
Mitochondrial Cytochromes

AbstractBackgroundTo monitoring redox state changes and biological mechanisms occurring in mitochondrial cytochromes in cancers improving novel methods are required.MethodsWe used Raman spectroscopy and Raman imaging to monitor changes in the redox state of the mitochondrial cytochromes in ex vivo human brain and breast tissues at 532 nm, 633 nm, 785 nm.ResultsWe identified the oncogenic processes that characterize human infiltrating ductal carcinoma (IDC) and human brain tumors: gliomas; astrocytoma and medulloblastoma based on the quantification of cytochrome redox status by exploiting the resonance-enhancement effect of Raman scattering. We visualized localization of cytochromes by Raman imaging in the breast and brain tissues and analyzed cytochrome c vibrations at 750, 1126, 1337 and 1584 cm-1 as a function of malignancy grade. We found that the concentration of reduced cytochrome c becomes abnormally high in human brain tumors and breast cancers and correlates with the grade of cancer aggressiveness.ConclusionsWe showed that Raman imaging provides additional insight into the biology of astrocytomas and breast ductal invasive cancer, which can be used for noninvasive grading, differential diagnosis, delineation of tumor extent, planning of surgery, and radiotherapy and post-treatment monitoring.Simple SummaryGliomas comprise around 30% of human brain tumors, while invasive ductal carcinoma (IDC) comprises around 80% of human breast cancers. The aim of our study was to show that cancerogenesis affects the redox status of mitochondrial cytochromes, which can be tracked by using Raman spectroscopy and imaging. We have shown the correlation between the intensity of cytochromes Raman bands at 750, 1126, 1337 and 1584 cm-1 and malignancy grade for brain and breast cancers.Graphical Abstract

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.

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