scholarly journals P056. Evaluation of oxidative stress in experimental model of Chron’s disease under hyperbaric oxygen treatment

2016 ◽  
Vol 10 (suppl 1) ◽  
pp. S116.2-S116
Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1827
Author(s):  
Nofar Schottlender ◽  
Irit Gottfried ◽  
Uri Ashery

Hyperbaric oxygen treatment (HBOT)—the administration of 100% oxygen at atmospheric pressure (ATA) greater than 1 ATA—increases the proportion of dissolved oxygen in the blood five- to twenty-fold. This increase in accessible oxygen places the mitochondrion—the organelle that consumes most of the oxygen that we breathe—at the epicenter of HBOT’s effects. As the mitochondrion is also a major site for the production of reactive oxygen species (ROS), it is possible that HBOT will increase also oxidative stress. Depending on the conditions of the HBO treatment (duration, pressure, umber of treatments), short-term treatments have been shown to have deleterious effects on both mitochondrial activity and production of ROS. Long-term treatment, on the other hand, improves mitochondrial activity and leads to a decrease in ROS levels, partially due to the effects of HBOT, which increases antioxidant defense mechanisms. Many diseases and conditions are characterized by mitochondrial dysfunction and imbalance between ROS and antioxidant scavengers, suggesting potential therapeutic intervention for HBOT. In the present review, we will present current views on the effects of HBOT on mitochondrial function and oxidative stress, the interplay between them and the implications for several diseases.


2011 ◽  
Vol 11 ◽  
pp. 2124-2135 ◽  
Author(s):  
Koichi Tsuneyama ◽  
Yen-Chen Chen ◽  
Makoto Fujimoto ◽  
Yoshiyuki Sasaki ◽  
Wataru Suzuki ◽  
...  

The effect of hyperbaric oxygen treatment (HBOT) was examined using MSG mice, which are an animal model of obesity, hyperlipidemia, diabetes, and nonalcoholic fatty liver disease. Nineteen MSG male mice were divided into HBOT treated and control groups at 12 weeks of ages. The HBOT group was treated with hyperbaric oxygen from 12 to 14 weeks (first phase) and then from 16 to 18 weeks (second phase). Interestingly, the body weight of the HBOT group was significantly lower (P<0.01) than that of the control group. In contrast, the serum lipid level did not show significant changes between the two groups. As for the effects of increasing oxidative stress, the liver histology of the HBOT group showed severer cellular damage and aberrant TNF-α expression. HBOT has the advantage of improving obesity in patients with metabolic syndrome, but the fault of causing organ damage by increasing oxidative stress.


2008 ◽  
pp. 41-47
Author(s):  
F Gürdöl ◽  
M Cimşit ◽  
YZ Öner-İyidoğan ◽  
Ş Körpinar ◽  
S Yalçinkaya ◽  
...  

Exposure to hyperbaric oxygen leads to increased amount of reactive oxygen species (ROS) that are derived from various sources. After the discovery that ROS can function as signaling molecules, the idea of ROS being hazardous to biological tissues has been challenged. The aim of this study was to examine the changes in oxidative stress parameters in diabetics undergoing hyperbaric oxygen therapy (HBOT) due to foot ulcers. Twenty patients, who received HBOT for diabetic foot ulcers, were included in the study. Blood samples were taken before HBOT and 30 min after exit from the chamber, on the day of the first and the 15th HBOT sessions. They were used for the determinations of malondialdehyde (MDA), 8-isoprostane and advanced oxidation protein products (AOPPs). 8-Isoprostane and AOPP levels were not altered significantly after the first HBOT session, while both were increased on the fifteenth day (p<0.05). MDA was significantly increased only after the first HBOT session, and remained unchanged on the fifteenth day (within-day variations). Plasma AOPP levels were lowered significantly after fifteen consecutive HBOT sessions (between-day variations). Decreased AOPP levels suggest that increased oxygenation of tissues due to HBO therapy may activate some endogenous factors that prevent hazardous effects of the disease itself.


2005 ◽  
Vol 38 (12) ◽  
pp. 1133-1137 ◽  
Author(s):  
Ayşe Eken ◽  
Ahmet Aydın ◽  
Ahmet Sayal ◽  
Aylin Üstündağ ◽  
Yalçın Duydu ◽  
...  

2020 ◽  
pp. 261-265
Author(s):  
Jonathan W. Brügger ◽  
Glenn A. Rauscher ◽  
John P. Florian ◽  

Hyperoxic myopia is a phenomenon reported in individuals who have prolonged exposure to an increased partial pressure of oxygen (PO2) and subsequently have a myopic (nearsighted) change in their vision. To date, there are numerous accounts of hyperoxic myopia in dry hyperbaric oxygen treatment patients; however, there have been only three confirmed cases reported in wet divers. This case series adds four confirmed cases of hyperoxic myopia in wet divers using 1.35 atmospheres (ATM) PO2 at the Navy Experimental Diving Unit (NEDU). The four divers involved were the first author’s patients at NEDU. Conditions for two divers were confirmed via record review, whereas the other two divers were diagnosed by the first author. All subjects were interviewed to correlate subjective data with objective findings. Each subject completed five consecutive six-hour hyperoxic (PO2 of 1.35 ATM) dives with 18-hour surface intervals. Each individual was within the U. S. Navy Dive Manual’s standards for general health. Visual acuity was measured prior to diving. Within three to four days after diving, the individuals reported blurry vision with an associated myopic refraction shift. Each diver had spontaneous resolution of his myopia over the next two to three weeks, with no significant residual symptoms. The divers in this case series were exposed to an increased PO2 (1.35 ATM for 30 hours over five days), a lesser exposure than that in other reports of hyperoxic myopia in wet divers diagnosed with hyperoxic myopia (1.3-1.6 ATM for 45-85 hours in 12-18 days). Furthermore, this pulse of exposure was more concentrated than typically seen with traditional hyperbaric oxygen therapy. Hyperoxic myopia continues to be a risk for those conducting intensive diving with a PO2 between 1.3-1.6 ATM. Additional investigation is warranted to better define risk factors and PO2 limits regarding ocular oxygen toxicity.


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