Nitroso-Oxidative Stress, Acute Phase Response, and Cytogenetic Damage in Wistar Rats Treated with Adrenaline

Abstract

This study is aimed at analysing biochemical and genetic endpoints of toxic effects after administration of adrenaline. For this purpose, the study was carried out on Wistar rats and three doses of adrenaline were used: 0.75 mg/kg, 1.5 mg/kg, and 3 mg/kg body weight. To achieve these aims, we investigated the effects of adrenaline on catalase (CAT), Cu, Zn-superoxide dismutase (SOD), malondialdehyde (MDA), nitrite (NO2−), carbonyl groups (PCC), and nitrotyrosine (3-NT). Total activity of lactate dehydrogenase (LDH), its relative distribution (LDH1–LDH5) activity, level of acute phase proteins (APPs), and genotoxic effect were also evaluated. The obtained results revealed that all doses of adrenaline induced a significant rise in CAT activity, MDA level, PCC, NO2−, and 3-NT and a significant decrease in SOD activity compared to control. Adrenaline exerted an increase in total activity of LDH, LDH1, and LDH2 isoenzymes. Further study showed that adrenaline significantly decreased serum albumin level and albumin-globulin ratio, while the level of APPs (α1-acid glycoprotein and haptoglobulin) is increased. The micronucleus test revealed a genotoxic effect of adrenaline at higher concentrations (1.5 mg/kg and 3 mg/kg body weight) compared to untreated rats. It can be concluded that adrenaline exerts oxidative and nitrative stress in rats, increased damage to lipids and proteins, and damage of cardiomyocytes and cytogenetic damage. Obtained results may contribute to better understanding of the toxicity of adrenaline with aims to preventing its harmful effects.

A Case of Acute Kidney Injury in a Patient with Renal Hypouricemia without Intense Exercise

“…Bellomo et al [13] reported that activation of type α1 adrenaline receptors could cause excessive renal vasoconstriction and decreased renal blood flow in models of healthy renal hemodynamics. Radaković et al [14] described that adrenaline induction increased ROS and caused a disruption in oxidant/antioxidant balance. Considering these results and the developmental mechanism of EIAKI (i.e., ROS and renal ischemia), we suspect that the vasopressors may have affected the onset or worsening of EIAKI by increasing ROS, exacerbating vasoconstriction, and forming a vicious cycle of diminished renal hemodynamics.…”

Changes in saliva proteins in two conditions of compromised welfare in pigs: An experimental induced stress by nose snaring and lameness

“…During stress condition, a high amount of catecholamines is released to prepare the body for "fight or flight" response (Ranabir and Reetu, 2011). Radaković et al (2018) showed that adrenaline caused an increase in total activity of LDH, LDH1 and LDH2 isoenzymes in rats. Drouet et al (2015) showed significant increases (1.9 fold-increases) in plasma levels of LDH in rats after a model of acute restraint stress in relation to control group.…”

Cardioprotective effect of thymol against adrenaline-induced myocardial injury in rats

“…Adrenaline was found to induce MI by causing lipid peroxidation leading to depletion of cellular antioxidants ( Andreadou et al., 2009 ). In cardiomyocytes, adrenaline was shown to increase lipid, protein, and DNA damage with overproduction of nitrosative derivatives ( Radaković et al., 2018 ). Since ROS play a crucial role in the pathogenesis of MI, efforts have been directed towards the use of natural products possessing anti-oxidant activity as adjuvants with few side effects and great safety in treatment of MI ( Li et al., 2012 ).…”