Effects of
selenium deficiency on testicular morphology and function in rats.
(4) While a deficiency in selenium will not lead to specific symptoms or clinical illness in most people,
selenium deficiency has been identified as a public health concern in certain populations, and coordinated efforts have been made in the past to prevent
selenium deficiency in these populations.
Selenium deficiency usually results in growth and of activity of enzyme GPx reductions (NRC, 2011).
Protein oxidation is known to be related to
selenium deficiency (Moskovitz and Stadtman, 2003).
Previous trials have reported reduction of TPOAb with selenium after six months and we know that
selenium deficiency leads to glutathione peroxidase inactivity, which may induce oxidative harm for thyroid cells leading to thyroid damage and fibrosis.
Prolonged dietary
selenium deficiency or excess does not globally affect selenoprotein gene expression and/or protein production in various tissues of pigs.
Selenium deficiency is common in ruminants, mainly due to insufficient dietary levels or the formation of insoluble compounds in the rumen that inhibit their absorption (SPEARS, 2003).
In this way,
selenium deficiency can result in both production of T3 and elimination of [H.sub.2][O.sub.2] inefficient, moreover it contributes to initiation of oxidative damage, fibrosis and impaired thyroid tissue repair.
Unfortunately, as has been stated in many countries across the world, human food ingredients can contain low levels of selenium and
selenium deficiency in human nutrition has become a global phenomenon [17-19].
(7,8) According to previous studies, zinc and
selenium deficiency is common in cirrhosis and can affect nitrogen metabolism.
Selenium deficiency has been associated with cognitive decline in the elderly (Akbaraly et al.
Effect of dietary
selenium deficiency on the in vitro fertilizing ability of mice spermatozoa.