Al-Said A. Haffor is the Professor of Physiology, College of Medicine, Dar Aluloom University, Riyadh, Saudi Arabia. He completed his Ph.D., Applied Physiology, The Ohio State University, Columbus, Ohio, USA, 1985. He has served as the Professor of Physiology, College Science, and College of Applied Medical Science, King Saud University in the year 2013. He worked as a Principal Investigator and main research area is focused on Differentiation of Different Stages of Bronchial Responsiveness in Asthma Patients using X-Ray in Relation to Blood Cells Changes, and also – Effects of Selenium on the Activities of Glutathione Peroxidase and Lactate Dehydrogenase and their Relations to Free Radical Production in the Lungs.


Emphysema is characterized by destruction of lungs units and increased load on the diaphragm. The purpose of the present study was to examine the effects of O2 breathing (OB) on ultrastructural pathological alterations in the diaphragm and the lungs in relation to free radicals (FR) accumulation. Twenty adult male rats were randomly assigned to two groups; control (C); and OB. Animals of the OB were breathing 100%O2 for 72 hr continuously. Serum, lungs and diaphragm tissue supernatant analysis showed significantly higher (p<0.05) FR in HP group, as compared with control group. Ultrastructure examinations showed that OB 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 myofilaments from Z plates and tearing of the endothelial cell of the interstitial blood capillaries. Ultrastructure examination of lungs showed that OB breathing resulted in desquamated pneumocyte Type II with degenerated surfactant materials, thickened alveolar wall and thickening of alveolar septum due to proliferation of endothelial cells lining the pulmonary capillaries as a result of an active transmigration. Based on the results of the present study, it can be concluded that OB inducted acceleration ROS formation, damaged the lungs' parenchyma and damaged the contractile apparatuses of the diaphragm and related endomembrane proteins that could involve intracellular calcium channels proteins.

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