Hyperbaric oxygen (HBO) therapy is the administration of 100% oxygen at more than
one atmosphere. It greatly improves tissue oxygenation and facilitates mechanisms of
wound healing, which in turn benefits some patients with chronic wounds. A prominent
fact in therapeutic HBO is the acceleration of neoangiogenesis during granulation tissue
formation. Angiogenesis is a highly orchestrated event, a diverse range of cells and
angiogenesis factors are involved in the process. The formation of reactive oxidative
species (ROS) during HBO has been controversially considered as signalling regulator for
angiogenic factors, as well as harmful originator for oxidative stress-induced cyto- and
geno-toxicity in cells. This thesis contributes to this interesting while challenging topic.
The project starts with investigation the direct HBO effects on blood vessel in vitro
under physiological conditions and pathological conditions. The data clearly show that a
single HBO treatment does not induce oxidative stress and cell damage under
physiological conditions. Nevertheless, under pathological conditions, HBO induces
oxidative stress with more ROS formation and cell damage. Interestingly, no evidence has
been shown that HBO alone or synergically promotes nitric oxide and vascular endothelial
growth factor production in either condition. The response of blood vessel to HBO
treatment is not explained by autocrine release of angiogenesis factors locally in the blood
vessel.
Next, HBO-induced intracellular calcium (Ca2+) changes and DNA damage were
investigated using cultured human umbilical vein endothelial cells. A single HBO
treatment significantly elevates intracellular Ca2+ level without inducing cell damage.
Furthermore, HBO treatment has small but significant effect on DNA migration when
evaluated by comet assay (e.g. 6.8 ± 0.8 % comparing to 4.6 ± 0.2 % DNA in tail of air
treatment). However, this effect is totally reversible after 24h recovery. Importantly, HBO
treatment protects endothelial cells against subsequent oxidative stress attack, and an
increased antioxidant capacity was found as reflected in higher ratio of GSH to GSSG. The
findings suggest that the beneficial effect of HBO is possibly via HBO-induced adaptation
in cellular redox status. However, the details of Ca2+ signalling and roles of antioxidants in
HBO treatment are areas for further research.
Date of Award | 2007 |
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Original language | English |
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Awarding Institution | |
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- Hyperbaric Oxygen
- Oxidative Stress
- Vascular Endothelial Growth Factor
- Nitric Oxide
- Endothelial Cells
- Calcium
- DNA Damage
Effects of hyperbaric oxygen on oxidative stress, angiogenesis factors and endothelial cell injury
Yuan, J. (Author). 2007
Student thesis: PhD