Is Oxidative Stress Affecting your DNA?
These fears may be justified. The fact is, the resulting mutation from oxidized DNA may trigger pathological outcomes, including 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 begin and what attacks the DNA?
Oxidative Stress on our DNA
Our bodies use oxygen to create energy as fuel for our cells, forming by-products in the process. Carbon dioxide and water are two such by-products, 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 then forces the reactive species to aggressively seek a new one from any source, including cell membranes and DNA. Usually, the ROS are neutralized by antioxidants our bodies form (endogenous antioxidants, e.g., glutathione) and by antioxidants provided from food (dietary antioxidants, e.g., phenolics).
Reactive Oxygen Species-the good side, the bad side
The beneficial roles of ROS include antibacterial and antiviral actions, cell-to-cell signaling (such as by nitric oxide and hydrogen peroxide), stimulation of enzyme functions, and regulation of cells controlling release of hormones. That's the good. However, when your body produces more ROS than needed to perform these useful functions, and when you body doesn't have enough antioxidant reserves, this creates a positive-ROS state, or oxidative stress.
How to possibly prevent an oxidative attack
Even during healthy and normal metabolism - but worsened by exposure to added environmental pathogens such as ultraviolet radiation, smoke or other pollutants - the ROS (which are formed continuously) are attacking each cell in our bodies thousands of times per minute or more than a million times per day!
When counterbalancing antioxidant mechanisms are insufficient, DNA lesions occur, including loss or oxidation of base material and breaks of DNA strands. The good news is that not all DNA lesions become pathogenic, as our cells (hard-workers, indeed) also contain mending functions for correcting the DNA injury, called base excision repair (BER).
While it works to repair most of the time, BER may not fully correct all injuries to DNA, leading to mutated DNA, as found in carcinogenesis, aging or age-related diseases.
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 lesions, aging onset and disease progression, and has advocated nutritional remedies as 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 coined a "metabolic tune-up."
An excerpt from a 2002 publication in the Annals of the NY Academy of Science (partly edited)
In feeding studies in old rats, these mitochondrial metabolites and antioxidants furnish several benefits that include 1) arresting the age-associated decline of ambulatory activity and memory, 2) partially restoring mitochondrial structure and function, 3) inhibiting age-associated increase of oxidative damage to lipids, proteins, and nucleic acids, 4) elevating levels of antioxidants, and 5) restoring 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) delay the 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 enzyme structure, with b) a consequent decrease of enzyme activity as well as c) substrate binding affinity for their substrates. An increased level of substrate restores the velocity of the reaction and restores mitochondrial function, thus delaying mitochondrial decay and aging.
So, if you want fight reactive oxygen radicals, eat the right antioxidant foods. References and Reading
* Liu J, Atamna H, Kuratsune H, Ames BN. Delaying brain mitochondrial decay and aging with mitochondrial antioxidants and metabolites. Ann N Y Acad Sci. 2002 Apr;959:133-66.
* Ames BN. A role for supplements in optimizing health: the metabolic tune-up. Arch Biochem Biophys. 2004 Mar 1;423(1):227-34.
* PubMed, online database of the US National Library of Medicine, 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
* Phytochemical database of the USDA, 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.
Related Tags: stress, oxidative stress, antioxidant, orac, dna, berry
Dr. Paul Gross is a scientist and expert on cardiovascular and brain physiology. A published researcher, Gross recently completed a book on the Chinese wolfberry and has begun another on antioxidant berries. Gross is founder of Berry Health Inc, a developer of nutritional, berry-based supplements. For more information, visit http://www.berrywiseonline.comYour Article Search Directory : Find in Articles
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