Mitochondrial injury caused by reactive oxygen species generation under high fluence low-power laser irradiation treatment

Mitochondrial injury, characterized by its depolarization, is a key to cell apoptosis. High fluence low-power laser irradiation (HF-LPLI) through endogenous photosensitive reactions can cause mitochondrial injury. However, the exact mechanisms are not fully understood. Using fluorescent image techniques, we investigated cell apoptosis caused by mitochondrial photosensitization by HF-LPLI. Our results showed that the major step of the apoptosis, decrease of mitochondrial transmembrane potential (δψm), occurred accompanying with high levels of mitochondrial reactive oxygen species (ROS) generation, indicating mitochondrial injury caused by ROS. Scavenging the photodynamical ROS completely prevented mitochondrial depolarization supported the view. Taken together, we demonstrated that HF-LPLI caused mitochondrial injury through a large amount of mitochondrial ROS generation. The specific mechanisms need to be further studied.