Many people today are becoming more aware of the use of antioxidants (from specific foods or supplements) to combat oxidative stress. When asked why they take antioxidant strategies, many say they fear oxidative damage to their DNA (deoxyribonucleic acid), a molecule that contains the genetic instructions for building cells.

These fears may be justified. The fact is that the resulting mutation of oxidized DNA can trigger pathological outcomes, such as cancer, neurological degeneration, and organ failure. Other oxidation targets include proteins, cell membranes, lysosomes, mitochondria, blood and tissue lipids, polyunsaturated fatty acids, and vitamins or antioxidant molecules themselves.

So how does oxidative stress start and what attacks DNA?

Oxidative stress in our DNA

Our bodies use oxygen to create energy as fuel for our cells, forming byproducts in the process. Carbon dioxide and water are two of these byproducts, but others include reactive oxygen species (ROS), which have both beneficial and potentially dangerous roles in human physiology.

ROS are reactive species because they lack an electron. This electron deficiency forces reactive species to aggressively seek out a new one from any source, including cell membranes and DNA. ROS are typically neutralized by antioxidants that make up our bodies (endogenous antioxidants, eg glutathione) and by antioxidants provided by food (dietary antioxidants, eg phenolics).

Reactive Oxygen Species: The Good Side, The Bad Side

The beneficial functions of ROS include antibacterial and antiviral actions, cell-to-cell signaling (such as nitric oxide and hydrogen peroxide), the stimulation of enzymatic functions, and the regulation of cells that control the release of hormones. That’s the good thing. However, when your body produces more ROS than is needed to perform these useful functions, and when your body does not have sufficient stores of antioxidants, this creates a ROS-positive state, or oxidative stress.

How to possibly prevent an oxidative attack

Even during normal, healthy metabolism, but worsened by exposure to additional environmental pathogens, such as ultraviolet radiation, smoke, or other pollutants, ROS (which are continually being formed) attack every cell in our bodies thousands of times per minute or more. out of a million times a day!

When counterbalancing antioxidant mechanisms are insufficient, DNA damage occurs, including loss or oxidation of parent material and DNA strand breaks. The good news is that not all DNA damage becomes pathogenic, as our cells (very hard workers, in fact) also contain repair functions to correct the DNA damage, called base excision repair (BER).

While it works to repair most of the time, BER may not fully correct all DNA lesions, leading to DNA mutation, as found in carcinogenesis, aging, or cancer-related diseases. age.

Give your body a “metabolic tune-up”

For 20 years, Dr. Bruce N. Ames of the University of California-Berkeley has analyzed ROS-initiated DNA damage, the onset of aging, and disease progression, and has advocated nutritional remedies for protection, including dietary supplementation with lipoic acid, acetylcarnitine, folic acid, biotin, vitamins C, E, B6 (pyridoxine) and -12 (cyanocobalamin), iron and zinc. Together, these nutrients provide what Dr. Ames has called “metabolic trim.”

An excerpt from a 2002 publication in the Annals of the NY Academy of Science (partially edited)

In feeding studies in aged rats, these antioxidant and mitochondrial metabolites provide several benefits including 1) halting the age-associated decline in ambulatory activity and memory, 2) partially restoring mitochondrial structure and function, 3) inhibiting the increase of age-associated oxidative damage to lipids, proteins, and nucleic acids, 4) raising antioxidant levels, and 5) restoring the activity and substrate-binding affinity of a key mitochondrial enzyme, carnitine acetyltransferase. These mitochondrial metabolites and antioxidants 1) protect neuronal cells from neurotoxin and oxidant-induced toxicity and oxidative damage; 2) retard normal aging of human fibroblast cells, and 3) inhibit oxidant-induced acceleration of aging. These results suggest a plausible mechanism: with age, increased oxidative damage to proteins and lipid membranes, particularly in mitochondria, causes a) a deformation of the enzyme structure, with b) a consequent decrease in enzyme activity, as well as c) the binding affinity of the substrate for its substrates. A higher level of substrate restores the rate of the reaction and restores mitochondrial function, which delays mitochondrial deterioration and aging.

So if you want to combat reactive oxygen radicals, eat the right antioxidant foods.

References and Reading

* Liu J, Atamna H, Kuratsune H, Ames BN. Delay brain mitochondrial deterioration and aging with antioxidants and mitochondrial metabolites. Ann NY Acad Sci. 2002 April; 959: 133-66.

* Ames BN. A role of supplements in optimizing health: metabolic tuning. Arch Biochem Biophys. 2004 March 1; 423(1):227-34.

* PubMed, US National Library of Medicine online database, http://pubmed.org

* Wikipedia, the free encyclopedia, Oxidative Stress, http://en.wikipedia.org/wiki/Oxidative_stress

Reading and References

* Nutrient Data Laboratory, Agricultural Research Service, US Department of Agriculture, http://www.nal.usda.gov/fnic/foodcomp/contact.html

* USDA Phytochemical Database, Agricultural Research Service, http://www.pl.barc.usda.gov/usda_chem/achem_home.cfm

* Wikipedia, the free encyclopedia, http://www.wikipedia.com

Copyright 2006 Berry Health Inc.