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Selenium Nanoparticles

Selenium Nanoparticles as a nutritional supplement

Se NPs demonstrate anticancer and antimicrobial properties that may contribute to human health, not only as dietary supplements but also as therapeutic agents.

Selenium is an essential trace element in the diet.

Selenium Nanoparticles
Product No NRE-1037
CAS No.  7782-49-2
Formula  Se
APS <100nm  (Can be Customized)
Purity 99.9%
Color  Gray
Molecular Weight  78.971 g/mol
Density   10.5 g/cm3
Melting Point      960.8 °C
Boiling Point    2212 °C

Selenium Nanoparticles as a nutritional supplement

Se NPs demonstrate anticancer and antimicrobial properties that may contribute to human health, not only as dietary supplements but also as therapeutic agents.

Selenium is an essential trace element in the diet.

Selenium nanoparticles (SeNPs) represent a novel prospect of nutrition supplements.

SeNPs also demonstrate anticancer and antimicrobial properties.

Selenium is considered the center of selenoprotein structure arrangements such as thioredoxin reductase, glutathione peroxidase (GPx), glutathione hydroxy peroxidase, and phospholipids. The protein responsible for cellular defense against oxidative collateral of the cytoplasmic structural forms is GPx. It is a selenium-dependent enzyme that has the ability to exert antioxidant properties. Because of this, selenium is involved at the nanoscale in medicine, food technology, and pharmaceutical applications.

Selenium compounds are said to be effective neuroprotective agents for the treatment of Alzheimer’s disease (AD), where low selenium was found in the hair, blood, and tissues samples of AD patients. For the diagnosis of AD, markers can be effective tools that can detect low selenium levels and GSH-Px activity. In a study, selenium nanoparticles acted as an antiviral drug against the H1N1 influenza virus, and its efficacy increased when the nanoparticles were surface decorated with the commercialized antiviral drug Zanamivir. It worked by inhibiting the activation of the caspase-3 enzyme and cleavage of PARP protein; the signaling pathways of JNK and p38 were also blocked.

 

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