The Science Behind Celltrient Cellular Protect

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The Free Radical Theory of Aging was first described back in the 1950s, and proposed that aging is caused by the accumulation of oxidative damage to cells from free radicals.¹ Since then, the theory has evolved along with advancing science on the role of oxidative stress in cellular function and aging.² Glutathione is a key factor in maintaining antioxidant balance and helps to protect cellular functions against damaging oxidative stress that can contribute to accelerated cellular aging.³

More recently, research has focused on how novel nutritional interventions can help to address Glutathione deficits in order to promote more effective management of oxidative stress within our cells. One thought leader in this area is Dr. Rajagopal Sekhar, who has pioneered research on supplementation of specific Glutathione precursors, and the important role this can play in supporting Glutathione synthesis and combating the accumulation of cellular oxidative damage.

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Glutathione is a powerful antioxidant naturally present in our cells.⁴ It helps neutralize free radicals that can contribute to oxidative damage and is important for mitochondrial health and immune function.⁵ Known as a “master antioxidant,” Glutathione also helps other antioxidants like vitamins C & E do their jobs.⁵


Glutathione must be made inside our cells. This unique molecule is comprised of three amino acids — cysteine, glycine, and glutamic acid. Each of these amino acids must be available in sufficient amounts for cells to produce Glutathione in response to our changing cellular needs.⁴


Oxidative stress can be the result of multiple cellular processes. The constant creation of ATP, which is the fuel that energizes our cells, involves a series of chemical reactions within our mitochondria — the “powerhouses” of the cell.² These reactions generate reactive oxygen species (ROS), including free radicals, and other toxic by products.² Accumulation of ROS can be further aggravated by environmental sources of oxidative stress, including a poor diet, sedentary lifestyle, and pollutants.³

The powerful antioxidant glutathione helps to neutralize free radicals, but cellular levels of glutathione have been shown to decrease with age.⁶⁻⁷ This decrease can create an imbalance between free radicals and glutathione which contributes to oxidative damage within cells.³

While our cells will not produce excess levels of glutathione, it is possible to have too little to meet our changing needs. Research has shown that aging cells often have lower amounts of the precursor amino acids, cysteine and glycine, which may limit their ability to meet the cellular demand for glutathione.⁶


Declining levels of glutathione during aging are associated with:⁵⁻⁶

  • Increased susceptibility to cellular damage from internal oxidative stress
  • Reduced cellular protection against free radicals and other threats
  • Impaired mitochondrial function

Research over the past ten years has shown that daily supplementation which provides enough of the precursor aminoacids or “building blocks” for Glutathione needed to addressshortfalls can help to manage oxidative stress within cells.⁶⁻⁷


A patented combination of Glycine and N-Acetyl Cysteine (NAC), or GlyNAC for short, helps replenish key amino acids needed to support Glutathione production. Having the right levels of Glutathione to match your changing needs is important for cellular protection and normal immune function.

Celltrient Cellular Protect

Helps replenish amino acids important for Glutathione. Glutathione is a powerful antioxidant that acts as a natural cell defender against toxins and free radicals.

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  • 1. Harman D. J Gerontol. 1956;11(3):298-300.
  • 2. Lopez-Otin C et al. Cell. 2013;153(6);1194-1217.
  • 3. Sekhar RV et al. Encyclopedia of Gerontology and Population Aging. 2019.
  • 4. Gould RL and Pazdro R. Nutrients. 2019;11:1056.
  • 5. Teskey G et al. Adv Clin Chem. 2018;87:141-129.
  • 6. Sekhar RV et al. Am J Clin Nutr. 2011;94(3):847-853.
  • 7. Kumar P et al. Clin Transl Med. 2021;11(3)e372.