Please use this identifier to cite or link to this item: https://open.uns.ac.rs/handle/123456789/3085
Title: The Impact of Positive Acceleration (+Gz) on Antioxidant Capacity and Histopathological Alterations in Different Organs and Tissues in Rats
Authors: Ristic J.
Nikolić, Čedomir
Jeremic J.
Stojić, Ivana 
Janicijevic-Hudomal S.
Popović, Miroslav
Arsic-Komljenovic G.
Radojevic-Popovic R.
Srejovic I.
Zivkovic V.
Issue Date: 14-Jul-2017
Journal: Serbian Journal of Experimental and Clinical Research
Abstract: © 2017 Jelena Ristic et al., published by De Gruyter Open. Since the early 1940s, a significant amount of research has been conducted to describe the impact of the high-G acceleration on the cardiovascular system. The objective of the present study was to examine the role of the antioxidant enzyme system under biodynamic stress in the liver, heart and gastric mucosa in response to high-magnitude +Gz exposure in a rat model. Twenty adult male Wistar albino rats (10 rats per group; 9-11 weeks old, 200-250 g b.w.) were divided into the following two groups: control and G (exposed to a biodynamic stress model under positive (+7 Gz) acceleration for 40 s). The influence of acute biodynamic stress on pro-oxidative parameters in the rat liver (oxidase (XOD), catalase (CAT), peroxidase (Px), glutathione peroxidase (GSH-Px), total content of glutathione (GSH), lipid peroxidation (LPx)) and on histopathological alterations in the liver, cardiac muscle and gastric mucosa was examined. Biodynamic stress resulting from positive (+7 Gz) acceleration resulted in a highly statistically significant increase of CAT GSH-Px activity compared to the control group. The LPx levels were significantly decreased, but the GSH contents and the activities of other enzymes were not significantly changed. Significant microscopic changes in the liver, heart and gastric mucosa were observed in the G group. These results clearly indicate that +Gz acceleration alters biochemical systems. These alterations in cellular processes may be mediated by influences of hypoxia or ischaemia via changes in the antioxidant capacity.
URI: https://open.uns.ac.rs/handle/123456789/3085
ISSN: 18208665
DOI: 10.1515/sjecr-2016-0066
Appears in Collections:MDF Publikacije/Publications

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