Aging and Mitochondria!

Why do we age?
The average human life expectancy has increased, and so has the impact of aging and age-related diseases on the population. Research on aging is now the focus of hundreds of laboratories pioneering in the areas of molecular and cellular biology, biochemistry, and genetics. However, understanding aging completely is still a big challenge. Interestingly, more often than not, mitochondrial dysfunction is related to cellular aging, leading to the question, what are mitochondria and are they making us old?
Mitochondria are one of the most important cell organelles and are commonly known as the powerhouse of the cell since they generate energy by converting glucose into ATP (oxidative phosphorylation process). Although, the factors that contribute towards mitochondrial dysfunction are often debated, there is enough evidence to suggest that mitochondrial health impacts everything from aging to heart failure to Alzheimer’s disease.
Image from Northwestern Medicine Magazine
It is believed that mitochondria have their own DNA pool because they were once small, free-living creatures, like bacteria. Long ago in the distant past, our eukaryotic single-celled ancestors engulfed them, and now mitochondria make energy for the cell. However, it turns out that mtDNA gets mutations more frequently than the DNA in the nucleus. The prominent reason for this is the presence of ROS or “reactive oxygen species” (also termed “free radicals”) in the mitochondria. When mitochondria generate energy from food, they also create ROS that damage the mtDNA. Often, this is considered to be the reason why eating less leads to longevity in animals: less food means fewer ROS1.
ROS causes cellular damages at various levels that increase the susceptibility to mitochondrial dysfunction, leading towards accelerated aging and decreased lifespan. Interestingly, enzymes encoded by the SIRTUIN gene family, called Sirtuins, can modulate cellular response to ROS by regulating the redox system. Recent research has shown that the activity of the Sirtuin enzymes can be modulated with dietary supplements like NAD (Nicotinamide Adenine Dinucleotide)2. Sirtuins regulate the cellular NAD:NADH ratio and are responsible for feeding NAD into the energy generation pathway and restoring mitochondrial function.
Why is NAD important?
Our body is made up of more than 200 different cell types, each one containing many important coenzymes, and one of those is NAD. Discovered in 1906, NAD plays a vital role in energy generation process and maintaining mitochondrial health. Our cellular supply of NAD declines with age, resulting in cellular decay. NAD is actively studied for its potential use in the therapy of neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
Recent research suggests a possible reversal of mitochondrial decay with dietary supplements that cause an increase in the NAD levels in the cell. NAD precursors have shown promising prospects in the reversal of mitochondrial decay too. Nicotinamide mononucleotide (NMN), a precursor of NAD, when administered into elderly mice, showed a strong reversal in age-related mitochondrial deterioration3. Another readily available precursor of NAD, Nicotinamide riboside (NR), is now gaining attention. NR is also called the hidden vitamin and is commonly found in cow’s milk.
Cheers to aging
Although resveratrol is not easy to assimilate for the body and is not an essential nutrient, recent findings have suggested that resveratrol does prevent obesity, diabetes, and heart diseases5. However, as much as 500 mg of resveratrol may be necessary to provide any health benefits to humans and to get that, a person would have to drink more than 1,000 liters of red wine every day!
The Basis of getting younger: The might-o-chondrial way!
Recent advances towards understanding the mechanisms which control cellular aging, differentiation and survival are providing new insight into the regulation of human aging. From telomerase to mitochondrial health, and from stem cells to energy metabolism, this is an exciting new age in the multidisciplinary area of aging research. New research has addressed the limitation of resveratrol assimilation and optimal sirtuin activation with the development of Basis which is a dietary supplement developed by Elysium Health6. Interestingly, there are half a dozen Nobel Prize winners standing behind this Basis! Improving mitochondrial health is one of the main strategies behind the development of Basis. It is formulated from NR (NAD precursor) and a powerful antioxidant, pterostilbene (Taro-STILL-bene), an analog of resveratrol. Pterostilbene is more bioavailable, or easier for the body to incorporate, than resveratrol. Research has shown that pterostilbene also improves mitochondrial function7. Basis replenishes the NAD decline and improves mitochondrial health along with targeting other cellular detoxification and DNA repair.

Image from Natural News
We also care about monitoring mitochondrial health at BioLegend. You can check out our mitochondrial probes here on our webpage. MitoSpy™ Orange CMTMRos localizes to the mitochondria based on its membrane potential and is useful to indicate mitochondrial health as well as for localization. If you have any comments about this or want more information, please contact us at tech@biolegend.com.
HeLa cells stained MitoSpy™ Orange CMTMRos (top left), stained with anti-Cytochrome C Alexa Fluor® 647 (top right) and counterstained with DAPI (lower left). All three images were merged in the bottom right panel.
References:
  1. Cellular Repair and Reversal of Aging: the Role of NAD
  2. Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase
  3. Declining NAD(+)induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging
  4. Resveratrol Improves Mitochondrial Function and Protects against Metabolic Disease by Activating SIRT1 and PGC-1α
  5. Resveratrol in cardiovascular health and disease.
  6. Elysium
  7. SIRT1 activation by pterostilbene attenuates the skeletal muscle oxidative stress injury and mitochondrial dysfunction induced by ischemia reperfusion injury.
Contributed by Nidhi Vashistha, PhD.
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