![]() ![]() In secondary active transport, there is no direct ATP coupling. This leads to the generation of proton gradients such as during photosynthesis. Photon energy can also drive primary active transport such as when the protons are moved across the thylakoid membrane. Another example is the active transport driven by the redox energy of NADH when it moves protons across the inner mitochondrial membrane against the concentration gradient. It is a transport system in a biological membrane where three Na + ions are taken out while two K + ions are taken into the cell against their respective concentration gradients. Substances moved in primary active transport are Na +, K +, Mg 2+, and Ca2 +.Īn example is an active transport involving the sodium-potassium pump. In primary active transport, there is a direct coupling of energy such as ATP. A primary active transport is one that uses chemical energy in the form of ATP whereas a secondary active transport uses potential energy often from an electrochemical potential difference. Two types of transporters are employed: symporter (left), when the directions of movement of two substrates are the same, and antiporter (right) when the movement of two substrates are in the opposite directions.Īctive transport may be primary or secondary. These data indicate that cellular transport of T 4 is different from that of T 3 in rat hepatic cells.Secondary active transport: where one substrate moves down its concentration gradient while the other moves against the concentration gradient. For both T 3 and T 4, the enhanced cellular uptake was due to the increased V max without changes in the Michaelis–Menten constant. Despite the increase in cellular T 4 uptake, nuclear T 4 uptake was decreased after treatment with sodium butyrate. ![]() The maximal increase in cellular T 4 uptake (two- to threefold increase) was attained 20 h after treatment. Although cellular T 4 uptake was also increased after treatment with sodium butyrate, the degree and time-course of the increase were different from those of T 3. When cells were incubated for 48 h with various concentrations of sodium butyrate, T 3 uptake was enhanced by 1 mm sodium butyrate, reaching a maximal level with 5 mm. After treatment with 5 mm sodium butyrate, cellular and nuclear uptake of T 3 was increased, reaching a maximal level (four- to sevenfold increase) after 48 h. Next we examined the effect of sodium butyrate on the cellular transport of thyroid hormones. On the other hand, cellular and nuclear T 4 uptake was unchanged throughout the cell cycle, suggesting the T 3 specificity of the cell cycle-dependent alteration of cellular hormone transport. Alterations in nuclear T 3 uptake were in accordance with the changes in cellular T 3 uptake. Cellular T 3 uptake was minimal in the early G1 phase and increased in the late G1 phase, reaching a maximal level in the S phase. First we examined the cell cycle-dependent alteration of thyroid hormone uptake. The saturable cellular uptake of T 3 and T 4 was demonstrated in these cells. Cellular and nuclear uptake of tri-iodothyronine (T 3) and thyroxine (T 4) was examined using the cultured cell line derived from rat liver, clone 9, and rat hepatoma, dRLH-84. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |