What Is NADH?
NADH, often called reduced Nicotinamide Adenine Dinucleotide is made in our bodies from Niacin (Vitamin B3).
It is also increased when we indulge in food and eat more than we should as our bodies have to metabolise the carbohydrates + fats into energy (ATP).
Just like NAD+, NADH is considered a molecule containing the atoms of:、CarbonHydrogen
Nitrogen
Oxygen
Phosphorous
The bond between NAD+ and -H is what creates NADH which is considered the activated carrier molecule.
NADH acts as the transfer of the extra electrons to the inner membrane of the mitochondria and are considered the activated carrier molecule.
Once the electrons are in the inner membrane of the mitochondria, they are donated to a structure called the electron transport chain - NADH acts as an electron donor.
Inside the mitochondrial membrane, the electron transporters shuttle electrons from NADH to molecular oxygen which is an electron acceptor also.
NADH converts back to NAD+ in a reverse reaction and the process of electron transfer is carried out with the movement of protons as H+ ions.
The generation of positive charges from one side of the membrane to the other side activates a protein responsible for generating ATP which is the fuel your cells use.
There will be NAD+ left over which can be used as an electron acceptor when more food enters the system.
How NADH works?
NADH enters the human body and is directly decomposed into NAD+ and hydrogen (H), while releasing a certain amount of energy (ATP). Under the synergistic effect of the three, it not only has a comprehensive effect of delaying aging, but also performs well in improving immunity.
NADH Production Process
Fermentation
Fermentation is another anaerobic (non-oxygen-requiring) pathway for breaking down glucose, one that's performed by many types of organisms and cells. In fermentation, the only energy extraction pathway is glycolysis, with one or two extra reactions tacked on at the end.
Fermentation and cellular respiration begin the same way, with glycolysis. In fermentation, however, the pyruvate made in glycolysis does not continue through oxidation and the citric acid cycle, and the electron transport chain does not run. Because the electron transport chain isn't functional, the NADH made in glycolysis cannot drop its electrons off there to turn back into NAD+
The purpose of the extra reactions in fermentation, then, is to regenerate the electron carrier NAD+from the NADH produced in glycolysis. The extract reactions accomplish this by letting NADH drop its electrons off with anorganic molecule (such as pyruvate, the end product of glycolysis). This drop-off allows glycolysis to keep running by ensuring a steady supply of NAD+.
NADH functional benefits
THE NAD TO NADH PATHWAY EXPLAINED
Here’s the science...
NAD+ and NADH are really the same molecule but undergone a transformation.
In the body, it starts as NAD. NAD is a key component in the energy-making process by the mitochondria of our cells, each living cell’s powerhouse.
A low NAD to NADH ratio has been linked to mitochondrial dysfunction and accelerated aging.
NAD is first introduced in this energy cycle as NAD+.
This acts like a car ready to pick up a passenger. It comes along and picks up a hydrogen molecule with two charged electrons … making it NADH.
NADH’s primary purpose is to bring these charged electrons to the mitochondrial enzymes needed for the energy-making process (the plus sign is removed because negatively charged hydrogen molecule cancels the positively charged NAD+ molecule).
Once NADH gets to the enzyme, it drops off the electrons (expels the hydrogen atom) and becomes NAD+ again.
Now NAD+ is back to being that car ready to pick up a new passenger.
KEY LEARNING: Generating more NAD+ will generate more NADH. However, NAD+ is really what your cells are building when you use an NAD+ Booster, and now you can see why that specific molecule is what your body needs.
NADH Experimental Data
Results：
NAD+/NADH ratios were decreased in C2C12 myoblasts cultured at high density
The concentrations of NAD+ and NADH and the size of the total NAD (NAD+ + NADH) pool in C2C12 myoblasts increased over time in culture (72 h compared to 24 h) (Figure 1A). Comparison of 72 h cultures at two different seeding densities showed that NAD+, NADH, and total NAD were also increased with cell density (Figure 1A). In addition, NAD+/NADH ratio of C2C12 myoblasts decreased with the extension of culture time or high seeding density (Figure 1B, 1C). A decrease in NAD+/NADH ratio was recapitulated by culturing C2C12 myoblasts under low pH, high lactate, or in conditioned medium from cells plated at high density for 48 h (Figure 1D). Thus, lactic acid buildup in the medium likely contributed to the redox shift observed over time in cell cultures.
Quality Standard:
Rapamycin restored NAD+/NADH ratio in long-term cultured C2C12 myoblasts
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Rapamycin restored NAD+/NADH ratio in long-term cultured C2C12 myoblasts
We cultured C2C12 myoblasts for 24-72 h and then subjected them to 24 h rapamycin treatment. Although the NAD+/NADH ratio of freshly plated C2C12 myoblasts (2×105 cells/well, cultured for 24 h) was not significantly changed by 24 h rapamycin treatment (data not shown), rapamycin significantly increased the NAD+/NADH ratio and decreased NADH concentration of C2C12 myoblasts cultured for either 48 h or 72 h (Figure 2A, 2B). Similarly, rapamycin significantly increased the NAD+/NADH ratio (Figure 2C) and decreased NADH concentration (Figure 2D) in C2C12 myoblasts that had been cultured longer and differentiated into myotubes (P < 0.05). Therefore, rapamycin significantly affected NADH and NAD+/NADH ratio but not NAD+ (despite an uptrend in the differentiated myotubes) in C2C12 myoblasts cultured longer than 24 h.
EFFECT:
NADH is mainly involved in material and energy metabolism in cells. NADH plays an important role in maintaining cell growth, differentiation, energy metabolism and cell protection.
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