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Drug Summary: Selenium is a mineral found in small quantities that is essential to the diet. Selenium contributes to the normal functioning of the immune system and the thyroid gland. It is the central element in glutathione peroxidase (GPx), an antioxidant enzyme that protects cells against the oxidative damage caused by peroxides and free radicals. (For more information on free radicals and antioxidants, click here.)

Because of its antioxidant role, selenium has been studied for its potential to protect the body from many degenerative diseases, including Parkinson’s disease and cancer. (For a comparison between Parkinson’s and HD, click here.) Selenium is thought to protect against cancer because a form of selenium from yeast was found to have caused cancer cells in test tubes and in animals to undergo apoptosis, or programmed cell death.

Selenium can be found in a variety of foods including brazil nuts, yeast, whole grains, and seafood. Plant foods in most countries are also major dietary sources of selenium. The Recommended Dietary Allowance (RDA) is the average daily dietary intake level that is sufficient to meet the nutritional requirements of nearly all healthy individuals in each life-stage and gender group. The RDAs for selenium in adults is 55 micrograms (mcg), for pregnant women it is 60 mcg, and for lactating (breast feeding) women it is 70 mcg. While selenium can be taken as a supplement, most healthy adults get enough from the diet alone. One brazil nut alone has 100 mcg, an egg has 12 mcg, and a slice of whole wheat bread has 11 mcg of selenium.


People who eat foods grown primarily on selenium-poor soils are at risk for deficiency, but selenium deficiencies are rare in Western countries. However, studies have shown that the amount of selenium found in the blood decreases significantly with age and that decreased amounts of selenium might be a risk factor for dementia.

Research on selenium^

Santamaría, et al. (2003) recognized that in neurodegenerative diseases such as HD, oxidative stress and free radicals contribute to the degeneration of nerve cells. In order to study these effects and a possible treatment, these researchers gave rats a substance called quinolinic acid (QUIN). QUIN has traditionally been used to produce a model of HD in rats and primates because it mimics what the nerve cells of someone with HD would look like. QUIN causes damage to nerve cells by producing free radicals and causing oxidative stress. This is similar to what occurs in HD: damaged mitochondria produce free radicals, which contribute to the progression of the disease. Researchers can then study the effects of different substances on these cells.

In this study, researchers at the National Institute of Neurology in Mexico City, Mexico tested how selenium affected the QUIN rats. They did this by studying the effects of selenium both in vitro and in vivo. The in vitro studies looked at the brain cells directly (outside of the body, after death), while the in vivo studies look at the effects on the bodies of the living rats as a whole. The researchers measured the activity of the enzyme GPx in the cells because it depends on selenium for its antioxidant properties. They also looked at the physical behavior of the rats. To determine the degree of damage, the researchers examined the rat brains and counted samples for how many nerve cells were preserved and how many were damaged.

Because of its antioxidant effects, selenium was able to reduce toxicity caused by QUIN in rats. Different concentrations were found to be effective in different parts of the brain, but selenium specifically reduced the damage caused by QUIN in the and striatum and and hippocampus. The animals that were given QUIN alone had nerve cells that were very damaged; many of these nerve cells died. The animals that were given QUIN and then treated with selenium had only a few sick nerve cells and most were healthy. Selenium decreased nerve cell degeneration by 70%. As expected, the presence of selenium increased GPx activity, most likely helping to reduce the toxic effects on the nerve cells.

Rats treated with selenium did not differ in bodyweight significantly compared to rats not receiving treatment. Moreover, an equal number of rats died in the treated and non-treated groups (two in each). Because of these results, the researchers concluded that this level of selenium does not cause any harmful side effects in rats.

Since selenium was found to protect against QUIN-related damage, and QUIN causes damage similar to that present in HD, treatment with selenium could possibly slow the progression of Huntington’s disease.

Zafar, et al. (2003) studied the effects of selenium on protecting nerve cells in the brains of rat models of Parkinson’s disease. Damage to nerve cells caused by free radicals and oxidative stress contributes to the progression of both Parkinson’s and Huntington’s diseases.

The researchers gave rats selenium in the chemical form of sodium selenite for seven days before inducing Parkinson’s-like symptoms. They were then tested for a variety of things including antioxidant activity and behavioral effects.

Rats treated with selenium were found to have greater antioxidant activity compared to those not treated. In the physical tests, selenium treatment was found to significantly lessen the harmful effects of Parkinson’s on the rats. They were less prone to circling around, had better muscle coordination, and wasted less time in traveling a specific distance.

These results confirm the fact that selenium plays an important role in decreasing oxidative stress. This study and others suggest that selenium may be helpful in treating neurodegenerative diseases such as Parkinson’s and HD.

For further reading^

  1. Santamaría, et al. Protective effects of the antioxidant selenium on quinolinic acid-induced neurotoxicity in rats: in vitro and in vivo studies. 2003. Journal of Neurochemistry 86(2): 479-488. Online.
    This article presents the research findings of a study of selenium in QUIN-treated rats. It is highly technical and meant for a scientific audience.
  2. Wilkins, Joanna. Selenium. 2013. A Healthy Me. Online.
    This is a very informative web page that explains the importance of selenium and how to get enough of it.
  3. Zafar, et al. Dose-dependent protective effect of selenium in rat model of Parkinson’s disease: neurobehavioral and neurochemical evidences. 2003. Journal of Neurochemistry 84(3): 438. Online.
    This article presents the research findings of a study of selenium in a rat model of Parkinson’s disease. It is highly technical and meant for a scientific audience. While it does not directly pertain to HD the findings are important because both diseases involve nerve cell death related to oxidative damage.

-K. Taub, 11/21/04