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Free Radicals, Antioxidants, and Oxidative Stress

Friday, March 01, 2019


A recent in-depth discussion with an ophthalmologist / biochemist friend on the vast number of oxidative stress articles published by the National Library of Medicine spurred today's Friday Pearl on oxidative stress, environmental pollution, and nutrient intake.


Air pollutants have and continue to be major factors impacting public health. These pollutants include ozone, sulfur oxides, carbon monoxide, carbon dioxide, nitrogen oxides and particulate matter. Interaction between unchecked oxidative stress byproducts is now suggested to be interfering with gene expression and cell signaling pathway activation linked to increased mortality. 


As carbon dioxide (CO2) levels climb, millions of folks are at risk of nutritional deficiencies since food crops lose nutrients when grown in elevated carbon dioxide levels. 


Oxidative stress is the biochemical end point of the imbalance between reactive oxygen species production and the ability of nutrient-based antioxidants to fight against free radical oxidative injury, including in the eye, heart, and brain.


Reactive oxygen species are chemically reactive species containing oxygen. Examples include peroxides, superoxide, hydroxyl radicals, and singlet oxygen. 


Free radicals are toxic byproducts of oxygen metabolism that can cause significant damage to living cells and tissues in the process called oxidative stress. 


Clinical, biochemical, and molecular data from anterior and posterior ocular structure and function, point to oxidative stress as a common pathogenic mechanism in ocular and full body health issues associated with loss of quality of life.


All biomolecules can be attacked by reactive oxygen species including lipids, proteins, and nucleic acids; with lipids, including essential fatty acids, being the most susceptible to oxidation, particularly those ingested without protective antioxidants such as vitamins C and E, as part of dietary intake.


Our cells maintain a healthy environment through the production of metabolizing enzymes and a consistent supply of metabolic energy. The amount of oxidative stress is dependent on the quality of interior and exterior environments, optimal production of energy, and the supply of macro and micronutrients necessary to produce energy.


When cells and their membranes do not have enough ongoing antioxidant protection they are too frequently unable to overcome excessive oxidative stress or to recover optimal cellular function. The introduction of antioxidant defenses, after the fact, frequently cannot counter the effects of reactive oxygen species (think of closing the barn door after the horse escapes).


Antioxidants are nutrient substances that help control damaging oxidation in living organisms, as well as inhibit oxidation in packaged food products. 


Understanding something about metabolic pathways that regulate reactive oxygen homeostasis is important for relieving the damaging effects of reactive oxygen in cells and tissues, the continuous, complex, and dynamic processes beginning with birth and ending with death.


For busy physicians, biochemistry geeks, and others 


One of the best known antioxidant defense systems is the mineral-based molecular enzyme superoxide dismutase copper- zinc SOD (CuZnSOD) discovered in 1969 to participate in intracellular pathogenic mechanisms.


Molecular manganese superoxide dismutase enzyme (MnSOD) is also required to support cellular mitochondrial antioxidant activity in the human, particularly in the heart, eye, and brain. It has unfortunately been overlooked in many clinical studies on optimal health.


Ellen Troyer, with Spencer Thornton, MD, David Amess and the Biosyntrx staff


PEARL: Free-radical, nutrient-based scavengers are proven to slow the reactions of oxidation, transforming them into less aggressive compounds. 


FYI: PubMed is a free search engine accessing primarily the MEDLINE database of references and abstracts on life sciences and biomedical topics. The United States National Library of Medicine at the National Institutes of Health maintains the database for public education use. As of this week, www.Pubmed.com includes 205,540 matching clinical study abstracts that address oxidative stress. 


The public service science information above is not meant to diagnose, treat, cure, or prevent any disease.