Differential Effect of γ-radiation-induced Heme Oxygenase-1 Activity in Female and Male C57BL/6 Mice

Abstract

Ionizing radiation produces reactive oxygen species, which exert diverse biological effects on cells and animals. We investigated alterations of heme oxygenase (HO) and non-protein thiols (NPSH), which are known as two major anti-oxidant enzymes, in female and male C57BL/6 mice in the lung, liver, and brain after whole-body γ-irradiation with 10 Gy (1-7 days) as well as in the lung after whole-thorax γ-irradiation (WTI) with 12.5 Gy (1-26 weeks). Most significant alteration of HO activity was observed in the liver, which elevated 250% in males. NPSH level in female liver was increased on the 5th-7th days but decreased in males on the 3rd day. In the lung, the elevation of HO activity in both sexes and the pattern of NPSH change were similar to that of the liver. On the other hand, the increase of HO activity on the 16th week and the decrease of NPSH level on the 2nd week were observed only in male lung after WTI. This study shows that the liver is the most sensitive tissue to γ-irradiation-induced alterations of HO activity in both female and male mice. In addition, there exists significant differential effect of γ-irradiation on anti-oxidant system in female and male mice.

Ferroptosis, radiotherapy, and combination therapeutic strategies

“…This raises the possibility that GCH1 might also be involved in regulating IR-induced ferroptosis. Furthermore, IR promotes iron release from heme by inducing heme oxygenase-1 (HO-1) or from ferritin (Han et al, 2005 ; Wolszczak and Gajda, 2010 ; Hassannia et al, 2018 ) (Fig. 1 ).…”

Caffeic acid phenethyl ester attenuates ionize radiation-induced intestinal injury through modulation of oxidative stress, apoptosis and p38MAPK in rats

“…Radiation produces reactive oxygen species (ROS), which can lead to the damage of lipids, proteins, nucleic acids, and therefore destroy cancer cells in the treated area. Unfortunately, normal cells in the surrounded area also can be injured (Han et al, 2005). ROS is thought to play a key role in the promotion of apoptosis by affecting mitochondrial permeability, release of cytochrome c, activation of p53 and caspases (Kobashigawa et al, 2015;Yazlovitskaya et al, 2013).…”