Selenium is an essential trace mineral that the human body requires for numerous biological processes. Since it is obtained solely through diet, intake fluctuates widely based on soil content and food choices. The body does not rely on a continuous supply, and the mineral is definitively stored. This storage mechanism maintains a steady reserve, ensuring consistent availability for critical functions even during periods of low dietary intake.
The Body’s Selenium Reserves
The body maintains its selenium supply by incorporating the mineral into various tissues, creating a reserve pool. Selenium is primarily stored as selenomethionine, a dietary organic compound found in plant-based foods. Selenomethionine is chemically similar to the amino acid methionine, allowing it to be non-specifically integrated into general body proteins. This incorporation into non-functional proteins forms the body’s main storage reservoir.
The largest repository for stored selenium is the skeletal muscle, holding approximately 28% to 46% of the body’s total content. Other significant storage sites include the liver and the kidneys, which are central to selenium metabolism. This reserve acts as a buffer, providing a source of the mineral that can be released when dietary levels drop.
Functional Role of Selenium
The stored reserves are constantly drawn upon to synthesize specialized proteins known as selenoproteins. These proteins incorporate selenium in the form of the amino acid selenocysteine. Humans synthesize around 25 distinct selenoproteins, each performing a specific biological function.
A major function of selenoproteins is their role in antioxidant defense, protecting cells from damage caused by reactive molecules. Examples include glutathione peroxidases (GPXs) and thioredoxin reductases (TrxRs), which neutralize harmful peroxides and maintain cellular redox balance. Without these, the body’s tissues would be more susceptible to oxidative stress.
Selenium is indispensable for the proper functioning of the thyroid gland, which has a higher concentration of the mineral than any other organ. Selenoproteins called iodothyronine deiodinases (DIOs) regulate thyroid hormone metabolism by converting inactive thyroxine (T4) into the active form, triiodothyronine (T3). GPXs and TrxRs also help protect the gland from the hydrogen peroxide it naturally produces during hormone synthesis.
Maintaining Optimal Levels: Selenium Homeostasis
The body employs a tight regulatory system to manage selenium status, balancing intake, storage, and elimination. Dietary selenium, particularly selenomethionine, is highly bioavailable, with the body absorbing up to 90% of what is consumed. Since absorption efficiency does not decrease significantly with high intake, robust control over the mineral is necessary once it is inside the body.
When selenium intake is low, the body implements a triage system to prioritize the allocation of the limited supply. Selenium is preferentially channeled toward the synthesis of the most functionally critical selenoproteins, such as those needed for the brain and the endocrine system. This prioritization means the general storage pool in the muscle may be depleted before functional selenoproteins are compromised.
During periods of excess intake, the body maintains homeostasis by increasing the rate of excretion. The main route for eliminating excess selenium is through the urine, where it is converted into compounds like trimethylselenonium ion and selenosugars. When intake is extremely high, selenium can also be excreted through the lungs, resulting in a characteristic garlicky odor on the breath.
Health Consequences of Imbalance
When homeostatic mechanisms fail, significant health consequences arise from both deficiency and excess. A severe selenium deficiency can lead to impaired immune function and specific cardiac issues. In extreme cases, deficiency is a necessary condition for the development of Keshan disease, a form of cardiomyopathy. Low selenium status is also associated with thyroid dysfunction due to the lack of deiodinases needed for hormone activation.
Chronic high intake can lead to a toxic condition called selenosis. The early signs of selenosis involve changes to the appendages, including hair loss (alopecia), brittle and deformed nails, and a metallic taste in the mouth. More severe toxicity can result in nervous system damage, manifesting as paresthesia and hyperreflexia.