Mitochondria as Potential Targets and Initiators of the Blue Light Hazard to the Retina

Figure 2

Possible mechanisms of blue light-induced ROS generation in mitochondria. On the one hand, absorption of blue light by the endogenous chromophores in the respiratory chain excites the chromophore (for example, porphyrin) from its ground state (¹S) to a transient singlet state (¹S) and then to the triplet state (³S) via intersystem crossing (ISC). Porphyrin in the triplet state can transfer an electron to an oxygen molecule present in the mitochondria; as a result, the oxygen molecule is activated from its ground state (³O₂) to become a superoxide anion (O₂^•-), and a photosensitizer radical cation (S^•+) is produced at the same time. In addition, the excited triplet state of porphyrin (³S) can return to its ground state (¹S) by energy transfer to an oxygen molecule (³O₂), which leads to the generation of singlet oxygen (¹O₂). On the other hand, blue light disrupts electron transport and increases the leakage of electrons; these electrons interact with O₂, which leads to the production of O₂^•- as well. The O₂^•- produced by either method can be subsequently converted into other forms of ROS by receiving more electrons in the mitochondria. In addition, O₂^•- and H₂O₂ can be, respectively, detoxified by Mn-SOD and GPx, the major antioxidases in the mitochondria. However, the hydroxyl radical (^•OH) cannot be eliminated through an enzymatic reaction, even though, among the ROS, it is characterized as having the greatest toxic effect on the tissue; it has a very short half-life in vivo. A wide range of mitochondrial oxidative damage is realized when the antioxidant system cannot counteract ROS generation.