Mitochondrial Reactive Oxygen Species (mtROS) are made as a by-product in redox reactions in the electron transport chain in the mitochondria. Due to the oxidant potential of mtROS it can damage cells, but it might also function as a signalling molecule in different pathways; e.g. in the regulation of cell cycle. Cell cycle is primarily regulated by cyclic variations in the intracellular levels of cyclin and cyclin dependent kinases. Experiments indicate that ROS are involved in the regulation of cell cycle and changes in the cyclin D isoform level. The cyclin D isoform level is critical in the transition from G1 to S phase in cell cycle. Some experiments demonstrate that a lowered level of the cyclin D isoforms is observable at high and low concentrations of ROS. Simultaneously, several experiments observe changed levels of different cell cycle regulating proteins respectively p21, p27, p42 and p44 as well as a changed degradation of the cyclin D isoforms. It is not possible to conclude a consistent link between ROS and the cyclin D isoforms or which factors that are involved in this correlation. The different test results do not agree and have conflicting explanations of how ROS might have an influence on the transition from G1 to S phase in cell cycle. Moreover, it is not possible to conclude whether it is mtROS in specifically that are implicated in the changes in the level of the cyclin D isoforms, because only few experiments indicate this. However, it is possible to conclude that the redox stage of the cell is important in the regulation of cell cycle because of the observed deviations in the level of ROS induce an inhibition or a blocking of cell cycle.
|Uddannelser||Basis - Naturvidenskabelig Bacheloruddannelse, (Bachelor uddannelse) Basis|
|Udgivelsesdato||19 jun. 2008|
- cyclin D
- mitokondrielt ROS