鐵在人體細胞中的作用

鐵通過控制的穩(wěn)定性和翻譯來調(diào)節(jié)調(diào)節(jié)轉鐵蛋白和鐵蛋白的水平。研究證明由于鐵缺乏導致的轉鐵蛋白基因表達的增加是通過提高轉錄水平來實現(xiàn)的。鐵對鐵蛋白基因表達的調(diào)控與轉鐵蛋白基因表達控制不同當鐵存在時它能與鐵反應要素結合導致暴露翻譯起始位點?使得細胞很快合成鐵蛋白而且鐵含量越高鐵蛋白基因表達就越快；當鐵的供給不足時，起始位點被鐵反應要素覆蓋鐵蛋白合成快速停止。缺鐵或者鐵的利用不良將導致氧的運輸、貯存、二氧化碳的運輸以及氧化還原等代謝過程紊亂影響生長發(fā)育甚至發(fā)生貧血等各種疾病。

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抗壞血酸亞鐵Ferrous Ascorbate、賴氨酸甘氨酸鎂Magnesium Lysinate Glycinate、甘氨酸谷氨酰胺鎂Magnesium Glycinate Glutamine、檸檬酸蘋果酸鎂Magnesium Citrate Malate、檸檬酸鍶Strontium Citrate、檸檬酸錳Manganese Citrate、檸檬酸銅Copper Citrate、天門冬氨酸鋰Lithium Aspartate、抗壞血酸錳Manganese Ascorbate、?；撬嵛?/span>Selenium Taurate。

The role of iron in human cells

Iron regulates the levels of regulatory transferrin and ferritin through controlled stability and translation. The study demonstrated that the increased expression of the transferrin gene due to iron deficiency is achieved by increasing the level of transcription. The regulation of ferritin gene expression by iron is different from the control of transferrin gene expression. In the presence of iron, it can bind to the iron-reactive elements, resulting in exposure to the translation initiation site ?, which enables cells to synthesize ferritin quickly and the higher the iron content, the faster the ferritin gene expression; When the supply of iron is insufficient, the initiation site is coated with iron reactive elements and ferritin synthesis stops rapidly. Iron deficiency or poor use of iron will lead to oxygen transport, storage, carbon dioxide transport and REDOX and other metabolic processes disorders affect growth and development and even anemia and other diseases.

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Ferrous Ascorbate, Magnesium Lysinate Glycinate, Magnesium lysinate Glycinate Glutamine, Magnesium citrate malate Citrate Malate, Strontium Citrate, Manganese Citrate, Copper Citrate, Lithium Aspartate, Manganese ascorbate Ascorbate, Selenium Taurate.