부산대학교 도서관

The NADPH Oxidase (NOX) enzymes are key producers of reactive oxygen species (ROS) and consist of seven different isoforms, distributed across the tissues and cell types. The increasing level of ROS induces oxidative stress playing a crucial role in neuronal death and the development of epilepsy. Recently, NOX2 was reported as a primary source of ROS production, activated by NMDA receptor, a crucial marker of epilepsy development. Here, we demonstrate spatial, temporal, and cellular expression of NOX2 and NOX4 complexes in in-vitro and in-vivo seizure models. We showed that the expression of NOX2 and NOX4 was increased in the initial 24 h following a brief seizure induced by pentylenetetrazol. Interestingly, while this elevated level returns to baseline 48 h following seizure in the cortex, in the hippocampus these levels remain elevated up to one week following the seizure. Moreover, we showed that 1- and 2- weeks following status epilepticus (SE), expression of NOX2 and NOX4 remains significantly elevated both in the cortex and the hippocampus. Furthermore, in in-vitro seizure model, NOX2 and NOX4 isoforms were overexpressed in neurons and astrocytes following seizures. These results suggest that NOX2 and NOX4 in the brain have a transient response to seizures, and these responses temporally vary depending on, seizure duration, brain region (cortex or hippocampus), and cell types. [Display omitted] • NADPH oxidase (NOX) enzymes are key producers of reactive oxygen species (ROS) in cells, distributed across the tissues, having cell-type expression and various responses to stimuli. • In the cortex, NOX2 expression is first decreased (up to 6 h) and then increased at 24 h post-seizure, while in the hippocampus it was overexpressed for 1–7 days post-seizure. • NOX4 is overexpressed during the first 24 h following a seizure in the cortex and the hippocampus. • NOX2 and NOX4 expression is increased up to 2 weeks post-status epilepticus (SE), in both cortex and hippocampus. • Following seizures, NOX2 expression is increased mainly in neurons, while NOX4 expression is increased in both neurons and astrocytes. [ABSTRACT FROM AUTHOR]