Reactive oxygen species or ROS and free radicals can cause severe damage to the normal cells of the body. This damage can be to the DNA, proteins, and other macromolecules. This damage forms the basis of a wide variety of diseases, most notably heart disease and cancer.
There are numerous studies that prove that since these diseases are mediated by oxidative stress and disbalance between pro-oxidant and antioxidant factors, antioxidants may play a pivotal role in preventing or slowing the progression of these conditions.
Some of the notable diseases caused due to oxidative stress include:
Heart Disease
Heart disease is the leading cause of death worldwide. Heart disease risk is raised by several factors including high cholesterol levels, high blood pressure, cigarette smoking, and diabetes. These promote atherosclerosis. Atherosclerosis refers to formation of hardened walls of the arteries that impairs blood flow to the heart and other vital organs.
It is speculated that a critical step in development of atherosclerosis is oxidation of low-density lipoprotein (LDL) (a type of bad cholesterol in blood) within the arterial wall. Several studies show an association between low intakes of dietary antioxidants to an increased frequency of heart disease.
On the other hand, those with high blood levels of antioxidants have lower risk of heart disease. For examples, humans who took more vitamin E on a regular basis had a 41% lower incidence of heart disease than those who took less amounts as seen in a study on nurses. Dietary increases in antioxidant vitamins may reduce the risk of heart disease by 20-30%.(1)
Cancer
Cancer kills millions worldwide. Diet may be the cause for cancer in as much as 35% of all human cancers. Low antioxidant intake in diet may also be responsible. Low dietary intake of fruits and vegetables doubles the risk of most types of cancers.
Pro-oxidants, or those who generate free radicals, stimulate cell division and these form the beginnings of mutagenesis and tumor formation. When a cell with a damaged DNA strand divides, it gives rise to disturbed and deformed clusters of cells that form the cancer.
Antioxidants exert their protective effect by:
- decreasing oxidative damage to DNA and
- decreasing abnormal increases in cell division
In addition, cigarette smoking and chronic inflammation lead to strong free radical generation that seems to be the reason for many cancers. Some research has indicated that people who smoke tend to have lower antioxidant levels than non-smokers and this makes smokers more at risk of cancers.
Lung diseases
The respiratory system is a well known target for free radical insult. This comes from endogenous factors as well as exposure to air pollutants and toxins, cigarette smoke etc.
Recent studies suggest that free radicals may be involved in the development of pulmonary disorders such as asthma. Antioxidants have been seen to reduce the development of asthmatic symptoms. Vitamin C, vitamin E, and beta carotene supplementation has been associated with improved lung function.
Neural disorders
Free radicals can also damage nerves and the brain. Neural tissue may be particularly susceptible to oxidative damage. This is because the brain receives a disproportionately large percentage of oxygen and has large amounts of polyunsaturated fatty acids which are highly prone to oxidation and oxidative damage.
Diseases implicated to oxidative stress include:
- Alzheimer's disease
- Parkinson's disease
- dementia etc.
Cataracts
Formation of cataracts is believed to involve damage to lens protein by free radicals. This leads to opacity of the lens. Cataract formation may be slowed with the regular consumption of supplemental antioxidants like vitamin E, vitamin C, and the carotenoids.
Other diseases
Other diseases like Diabetes, Rheumatoid arthritis etc. are also associated with low antioxidant levels in blood.
References
- http://acudoc.com/Antioxidants.PDF
- https://publichealth.jhu.edu/
- https://www.womenfirst.net/
- https://www.osu.edu/
- http://www.medlabs.com/Downloads/Antiox_acti_.pdf
Further Reading
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