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Selenium, an essential trace element for multiple cellular processes, was initially deemed undesirable due to its confirmed toxicity in the early 1900s.
During the late 20th century, there was a significant shift in understanding the importance of selenium for human nutrition and health. The groundbreaking research conducted by Schwarz and Foltz demonstrated that even at low concentrations, selenium is an essential nutrient vital to our well-being. This is primarily due to its ability to be incorporated into crucial enzymes and proteins like selenocysteine.
Selenium has demonstrated anticancer properties in both laboratory and clinical studies, in addition to being an essential micronutrient. At pharmacologically active dietary concentrations, selenium can act as a chemoprotector against carcinogenic compounds and prevent cancer development. However, previous studies have produced conflicting results due to variations in the types of selenium compounds (selenite vs. selenomethionine) used at differing concentrations and studying either with animal models or human subjects.
Although low concentrations of selenium can offer protection against the development of cancer, high levels may have genotoxic effects. The toxicity is likely caused by reactive oxygen species generation and consequent DNA oxidation within living organisms.
Selenium is known to possess anticarcinogenic characteristics, as well as antimetastatic effects that hinder cell migration, invasion and angiogenesis in various cancers such as breast cancer, colorectal cancer, melanoma, liver cancer lung carcinoma , prostate carcinoma and brain gliomas.
The various methods by which Selenium acts as an anticancer agent include ROS production, thiol modification, chromatin binding/modification and DNA repair. The focus of this review is on its effectiveness in inhibiting carcinogenesis through the mechanism of DNA repair.
Follow the link of the selected polymorphism to read a brief description of how the selected polymorphism affects Selenium and see a list of existing studies.
SNP polymorphisms related to the topic Selenium:
rs9637365 | Selenoprotein gene polymorphism affecting the risk of selenium deficiency. |
rs9420 | Selenoprotein gene polymorphism affecting the risk of selenium deficiency. |
rs11718498 | Selenoprotein gene polymorphism affecting the risk of selenium deficiency. |
rs3788317 | Selenoprotein gene polymorphism affecting the risk of selenium deficiency. |
rs3788314 | Selenoprotein gene polymorphism affecting the risk of selenium deficiency. |
rs756661 | Selenoprotein gene polymorphism affecting the risk of selenium deficiency. |
rs4880 | Polymorphism of antioxidant enzymes as risk factors for complications, leads to increased oxidative stress. Affects the level of selenium in serum. |
rs2769264 | Gene variants affecting copper, selenium and zinc content in blood. |
rs12151188 | |
rs4325816 | |
rs11548 | |
rs10412049 | |
rs2769265 | |
rs2264132 | |
rs3733548 | |
rs10173522 | |
rs6539137 | |
rs9606186 | |
rs11541479 | |
rs10861192 | |
rs13306278 | |
rs4630362 | |
rs147285094 | |
rs9332314 | |
Li Dali, a National Foundation for Outstanding Youth Fund recipient, is a researcher at the School of Life Sciences in East China Normal University. He earned his PhD in genetics from Hunan Normal University in 2007 and conducted collaborative research at Texas A&M University during his doctoral studies. Li Dali and his team have optimized and innovated gene editing technology, leading to the establishment of a world-class system for constructing gene editing disease models.