Bradykinin and noradrenaline preconditioning influences level of antioxidant enzymes SOD, CuZn-SOD, Mn-SOD and catalase in the white matter of spinal cord in rabbits after ischemia/reperfusion

Abstract

The aim of present work is to assess the effects of bradykinin (Br) or noradrenaline (Nor) preconditioning to the levels of antioxidant enzymes: superoxide dismutase (SOD), copper, zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (Mn-SOD) and catalase in ischemia/reperfusion (I/R) model in the rabbit spinal cord white matter as well as effect on glial fibrillary acidic protein (GFAP) and ubiquitin immunoreaction in glial cells. Rabbits were preconditioned by intraperitoneal single dose of Br or Nor 48 h prior to 20 min of ischemia followed by 24 or 48 h of reperfusion. White matter of L3-L6 spinal cord segments was used for comparison of antioxidant enzyme levels in sham control, ischemic groups and four preconditioned groups. The total SOD level in the Br or Nor preconditioned groups after 48 h of reperfusion was increased vs Br or Nor preconditioned groups after 24 h of reperfusion. The comparison among the ischemic group vs Br preconditioned (P<0.05), and Nor preconditioned (P<0.001) groups after 48 h of reperfusion, showed statistically significant decrease of Mn-SOD activity. Tissue catalase level activity was significantly decreased in the Br preconditioned group after 48 h of reperfusion (P<0.05) and Nor preconditioned groups after 24 h of reperfusion (P<0.001) and also after 48 h of reperfusion (P<0.001), in comparison to ischemic group after 48 h of reperfusion. Significantly decreased tissue catalase activity (P<0.05) in both Nor preconditioned groups after 24 or 48 h of reperfusion was measured vs Br preconditioned group after 48 h of reperfusion. According to our results, in the white matter, activation of stress proteins in glial cells, as well as antioxidant enzymes levels, were influenced by pharmacological preconditioning followed by 20 min of ischemia and 24 or 48 h of reperfusion. These changes contribute to ischemic tolerance acquisition and tissue protection from oxidative stress during reperfusion period.

Effects of Nrf1 in Hypothalamic Paraventricular Nucleus on Regulating the Blood Pressure During Hypertension

“…Studies have found that central oxidative stress is closely related to peripheral sympathetic overactivity ( Zhang et al, 2019 ). Superoxide dismutase (SOD) converts superoxide anion to hydrogen peroxide, which is then converted into water under the catalysis of peroxidase and other antioxidant enzymes ( Danková et al, 2019 ). Nrf1 has been reported to modulate the transcription of several genes related to antioxidant expression such as SOD1 and cytochrome c oxidase subunits ( Venugopal and Jaiswal, 1996 ; Ohtsuji et al, 2008 ; Dhar et al, 2009 ; Zhao et al, 2011 ), and thus may be involved in ROS regulation during the pathophysiology of hypertension.…”

Antioxidant activity of Lactobacillus plantarum NJAU-01 in an animal model of aging

“…SOD can convert superoxide radicals to hydrogen peroxide, which is still cytotoxic and can generate hydroxyl radicals by Fenton reaction [ 34 ]. Hydroxyl radical is one of the most active ROS, which can react with organic matter in the cell with the fast reaction rate and destructive effect [ 35 ]. Moreover, CAT can decompose hydroxyl radicals to participate in cell antioxidant defense [ 36 ].…”