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Related Concept Videos

Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

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Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells
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Nutrient-sensitive mitochondrial NAD+ levels dictate cell survival.

Hongying Yang1, Tianle Yang, Joseph A Baur

  • 1Department of Pathology, Paul F. Glenn Laboratories, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.

Cell
|September 25, 2007
PubMed
Summary

Mitochondrial nicotinamide adenine dinucleotide (NAD+) protects cells from genotoxic stress, even when nuclear NAD+ is depleted. Fasting increases this protective mitochondrial NAD+ via the enzyme Nampt.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolism

Background:

  • Genotoxic stress often leads to cell death due to depletion of nicotinamide adenine dinucleotide (NAD+).
  • NAD+ is crucial for cellular energy metabolism and signaling pathways.
  • Mitochondria play a vital role in cell survival and energy production.

Purpose of the Study:

  • To investigate the role of mitochondrial NAD+ in cell survival under genotoxic stress.
  • To explore the impact of fasting on NAD+ levels and cell viability.
  • To identify key enzymes and pathways involved in maintaining mitochondrial NAD+ homeostasis.

Main Methods:

  • Genotoxic stress induction in cell models.
  • Measurement of NAD+ levels in nuclear, cytoplasmic, and mitochondrial compartments.
  • Analysis of nicotinamide phosphoribosyltransferase (Nampt) enzyme activity.
  • Investigation of the mitochondrial NAD+ salvage pathway and sirtuin deacetylases (SIRT3, SIRT4).

Main Results:

  • Mitochondrial NAD+ levels remain stable during genotoxic stress, unlike nuclear and cytoplasmic pools.
  • Fasting for 48 hours increases Nampt levels and mitochondrial NAD+ in rodents.
  • Elevated Nampt confers protection against cell death, dependent on mitochondrial NAD+ salvage and SIRT3/SIRT4 activity.

Conclusions:

  • Mitochondria serve as a reservoir for NAD+ that can maintain cell viability during genotoxic stress.
  • Fasting-induced upregulation of Nampt enhances mitochondrial NAD+ and promotes cell survival.
  • These findings highlight the interplay between nutrition, NAD+ metabolism, and cell death pathways.