Direct inhibition of MTX on NADPH (NADPH is a cofactor for enzyme GSH reductase to make reduced GSH) together with overproduction of ROS, will cause a reduction in GSH cellular availability.[ , , , ] Furthermore, the influence of MTX on Nrf2 expression might also reduce GSH tissue level.[] SOD is an essential endogenous antioxidant enzyme, induces the conversion of mitochondrial generated ROS, mainly superoxide (O2), into less toxic hydrogen peroxide (H2O2) or molecular oxygen (O2).[] On the other hand, MTX causes mitochondrial membrane damage, and more superoxide (O2) free radical production will lower SOD activity.[] Overproduction of ROS and loss of endogenous antioxidants will shift the oxidative balance toward oxidative stress
Agnieszka Adamska, [email protected] Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers
While the aforementioned complex formation has been confirmed in several models and by different techniques, direct binding of M27 to DDB1 and/or STAT2 in absence of other proteins has to our knowledge not been documented yet
*Cutera
MS1 and MS2 mass tolerances, along with the scan window size, were automatically set by the software
