#=
#################
Many people today are becoming more aware of using antioxidants
(from specific foods or supplements) to combat oxidative stress.
When asked why antioxidant strategies are taken, many say they
fear oxidative damage to their DNA (deoxyribonucleic acid), a
molecule containing genetic instructions for building cells.
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=97the 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 =96 but worsened by
exposure to added environmental pathogens such as ultraviolet
radiation, smoke or other pollutants =96 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,
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,
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.
About The Author: Dr. Paul Gross is a scientist and expert on
cardiovascular and brain physiology. Gross is founder of Berry
Health Inc, a developer of nutritional, berry-based
supplements. For more information, visit
http://www.berrywiseonline.com
Please use the HTML version of this article at:
http://www.isnare.com/html.php?aid#145307
##################