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Hindi Research Article
Effects of Hyperoxia Exposure on Free Radicals Accumulation in Relation to Ultrastructural Pathological Changes of Diaphragm
Khaldoon Aljerian1,2 and Al-Said Haffor2*1Department of Pathology, College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia
2College of Medicine, Dar Aluloom University, Riyadh, Kingdom of Saudi Arabia
- *Corresponding Author:
- Al-Said Haffor
Ph.D., Professor, College of Medicine
Dar Aluloom University, Riyadh
Kingdom of Saudi Arabia115112
Tel: 9660507201601
E-mail: saidhaffor @yahoo.com
Received date: July 17, 2015; Accepted date: August 13, 2015; Published date: August 15, 2015
Citation: Aljerian K, Haffor A (2015) Effects of Hyperoxia Exposure on Free Radicals Accumulation in Relation to Ultrastructural Pathological Changes of Diaphragm. J Clin Exp Pathol 5:247. doi: 10.4172/2161-0681.1000247
Copyright: © 2015 Aljerian K et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
COPD are associated with an increased load on the diaphragm leading to accumulation of reactive oxygen species (ROS) and the subsequent cellular damages and death. The pathological alterations inducted by ROS in the diaphragm during oxygen breathing are not known. The purpose of the present study was to examine the effects of hyperoxia exposure (HP) on free radicals (FR) accumulation in relation to the ultrastructural pathological alterations in the diaphragm. Twenty adult male rats were randomly assigned to two groups; control (C); and hyperoxia (HP). Animals of the HP were breathing 100% O2 for 72 hr continuously. Both serum and diaphragm tissue supernatant analysis showed significantly higher (p<0.05) FR in HP group, as compared with control group. Ultrastructure examinations showed that HP resulted in variety of pathological alterations in the mitochondria and endoplasmic reticulum that were associated with disarrangement of myofibrils, loss of I-banding for myosin, focal myolysis of the myofilaments, complete fragmentation of myosin, tearing of myofilamments from Z plates and tearing of the endothelial cell of the interstitial blood capillaries. Based on the results of the present study, it can be concluded that hyperoxia-induced acceleration ROS formation damaged the contractile apparatuses of the diaphragm and related endomembrane proteins that could involve intracellular calcium channels proteins.
