Potential Role of Selenoenzymes and Antioxidant Metabolism in relation to Autism Etiology and Pathology

Table 2

Selenoprotein	Functions	References
GPx1	Detoxifies peroxides in aqueous compartment of cellular cytosol	[58]
GPx2	Expressed in cytosol of liver and tissues of the digestive system	[59]
GPx3	Synthesized primarily by kidney; secreted into plasma for transport to other tissues	[60]
GPx4	Prevents and reverses oxidative damage to lipids in brain and other tissues	[61]
TRx1	Reduces T(SH)2, vitamin C, polyphenols, and other substrates to regulate intercellular redox state	[62–64]
TRx2	Located in mitochondria and controls and regulates redox state	[63, 64]
TRx3	Reduces mitochondrial glutathione disulfide, abundant in testes	[63, 64]
MsrB1	Restores oxidatively damaged methionine (R-sulfoxides) to native configuration	[64]
DIO1	Converts T4 (thyroxine) prohormone into T3 (active thyroid hormone)	[65]
DIO2	Regulates thyroid hormone status, activating as well as inactivating T3	[65]
DIO3	Activates thyroid hormone in brain, placenta, important in fetal development	[65]
SPS2	Creates the Se-phosphate precursor required for synthesis of all selenoproteins	[64]
SelM	Notably high expression levels in the brain, possible thiol-disulfide oxidoreductase	[64, 66]
SelN	Interacts with ryanodine receptor, mutations result in congenital muscular dystrophy	[64]
SelP	Transports Se in plasma (10 Sec/molecule) and delivers Se to brain and endocrine tissues	[64]
SelW	Expressed in a variety of tissues and may regulate redox state of 14-3-3 proteins	[64, 66, 67]
Sel15	Oxidoreductase that may assist in disulfide formation and protein folding	[64]