The Effectiveness of Radiation Damage Reduction in Mice by Laser Light in Dependence of the Time Interval between Exposures

A research was carried out to determine the period of time during which it is possible to reduce the radiation damage in mice by means of laser radiation （650 nm） after gamma irradiation. First, the mice were exposed to γ- radiation （whole body irradiation）, then after 2 h or 24 h they were irradiated with laser radiation. The results of these studies have shown that the use of laser irradiation to reduce radiation damage in mice is effective 24 h after the exposure to 5 Gy ionizing radiation which leads to the bone-marrow clinical form of the ARS （Acute radiation sickness）. In case of the lethal dose of ionizing radiation 7 Gy （the transitional clinical form of the ARS）, the increase in life expectancy of mice is observed using laser radiation both 2 and 24 h after the exposure to γ- radiation, but the effectiveness of the laser used 2 h after the ionizing radiation is significantly more efficient.

Reductive damage induced autophagy inhibition for tumor therapy

Numerous therapeutic anti-tumor strategies have been developed in recent decades.However,their therapeutic efficacy is reduced by the intrinsic protective autophagy of tumors.Autophagy plays a key role in tumorigenesis and tumor treatment,in which the overproduction of reactive oxygen species(ROS)is recognized as the direct cause of protective autophagy.Only a few molecules have been employed as autophagy inhibitors in tumor therapy to reduce protective autophagy.Among them,hydroxychloroquine is the most commonly used autophagy inhibitor in clinics,but it is severely limited by its high therapeutic dose,significant toxicity,poor reversal efficacy,and nonspecific action.Herein,we demonstrate a reductive-damage strategy to enable tumor therapy by the inhibition of protective autophagy via the catalytic scavenging of ROS using porous nanorods of ceria(PN-CeO_(2))nanozymes as autophagy inhibitor.The antineoplastic effects of PN-CeO_(2)were mediated by its high reductive activity for intratumoral ROS degradation,thereby inhibiting protective autophagy and activating apoptosis by suppressing the activities of phosphatidylinositide 3-kinase/protein kinase B and p38 mitogen-activated protein kinase pathways in human cutaneous squamous cell carcinoma.Further investigation highlighted PN-CeO_(2)as a safe and efficient anti-tumor autophagy inhibitor.Overall,this study presents a reductive-damage strategy as a promising anti-tumor approach that catalytically inhibits autophagy and activates the intrinsic antioxidant pathways of tumor cells and also shows its potential for the therapy of other autophagy-related diseases.