Hyperbaric oxygen preconditioning protects skin from UV-A damage

Fuller, Ashley M.; Giardina, Charles; Hightower, Lawrence E.; Perdrizet, George A.; Tierney, Cassandra A.

doi:10.1007/s12192-012-0362-2

Cited by 18 publications

(16 citation statements)

References 81 publications

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“…These findings extend our previous work on HBOT in which we demonstrated protection of human microvascular endothelial cells (HMEC-1) grown in culture from oxidants (Godman et al 2010a, b) and protection of mouse skin from UV-A damage (Fuller et al 2013). Whether these observations can be reproduced in patients is not known, although antioxidant genes can be activated in human tissue by HBOT (Ferrer et al 2007).…”

Section: Discussionsupporting

confidence: 86%

“…The exposures we employed were based on our previous studies (Godman et al 2010a, b;Fuller et al 2013) and approximated an extended clinical HBOT treatment course. We tested a number of the urinary biomarkers (Bonventre et al 2010;Waring and Moonie 2011;Deverajan 2011), and the data revealed evidence of a protective function of HBOT.…”

Section: Discussionmentioning

confidence: 99%

“…Expression of these genes can provide insights into the metabolic state of the tissue under different physiological conditions (Hooper and Hooper 2009;Hooper et al 2014). Evidence that HBOT can condition tissues to promote function and survival comes from the study of rat models of myocardial infarction (Han et al 2008;Sun et al 2011) and cerebral ischemia reperfusion injury (Li et al 2008(Li et al , 2009Cheng et al 2011), as well as a mouse model of repeated UV-A skin exposure (Fuller et al 2013). Whether or not HBOT can be used therapeutically in selected patient populations to alleviate tissue damage arising from chronic inflammation and oxidative stress remains to be determined.…”

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confidence: 99%

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Hyperbaric oxygen therapy (HBOT) suppresses biomarkers of cell stress and kidney injury in diabetic mice

Verma

Chopra

Giardina

et al. 2015

Cell Stress and Chaperones

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The disease burden from diabetic kidney disease is large and growing. Effective therapies are lacking, despite an urgent need. Hyperbaric oxygen therapy (HBOT) activates Nrf2 and cellular antioxidant defenses; therefore, it may be generally useful for treating conditions that feature chronic oxidative tissue damage. Herein, we determined how periodic exposure to oxygen at elevated pressure affected type 2 diabetes mellitus-related changes in the kidneys of db/db mice. Two groups of db/db mice, designated 2.4 ATA and 1.5 ATA, were treated four times per week with 100 % oxygen at either 1.5 or 2.4 ATA (atmospheres absolute) followed by tests to assess kidney damage and function. The sham group of db/db mice and the Hets group of db/+ mice were handled but did not receive HBOT. Several markers of kidney damage were reduced significantly in the HBOT groups including urinary biomarkers neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C (CyC) along with significantly lower levels of caspase-3 activity in kidney tissue extracts. Other stress biomarkers also showed trends to improvement in the HBOT groups, including urinary albumin levels. Expressions of the stress response genes NRF2, HMOX1, MT1, and HSPA1A were reduced in the HBOT groups at the end of the experiment, consistent with reduced kidney damage in treated mice. Urinary albumin/creatinine ratio (ACR), a measure of albuminuria, was significantly reduced in the db/db mice receiving HBOT. All of the db/db mouse groups had qualitatively similar changes in renal histopathology. Glycogenated nuclei, not previously reported in db/db mice, were observed in these three experimental groups but not in the control group of nondiabetic mice. Overall, our findings are consistent with therapeutic HBOT alleviating stress and damage in the diabetic kidney through cytoprotective responses. These findings support an emerging paradigm in which tissue oxygenation and cellular defenses effectively limit damage from chronic oxidative stress more effectively than chemical antioxidants.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Hyperbaric oxygen therapy (HBOT) suppresses biomarkers of cell stress and kidney injury in diabetic mice

Verma

Chopra

Giardina

et al. 2015

Cell Stress and Chaperones

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“…As a result of HBOT, plasma oxygen content and tissue oxygenation get into the normal range even in the depth of ulcerated wounds. HBOT also mobilizes stem cells, such as endothelial progenitor cells, therefore, may represent a therapeutic aid for revascularization [3]. However, as available oxygen content increases in the core of the body, cardiovascular oxidative damage may emerge as a possible consequence of HBOT [4,5].…”

Section: Introductionmentioning

confidence: 99%

Hyperbaric Oxygen Therapy Dampens Inflammatory Cytokine Production and Does Not Worsen the Cardiac Function and Oxidative State of Diabetic Rats

et al. 2019

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Hyperbaric oxygen therapy (HBOT) is frequently used after soft tissue injuries and in diabetic patients with ulcerated wounds; however, its ability to increase oxidative stress casts doubts. Diabetes (DM) in male Wistar rats (N = 20) weighing 300 g were induced by a single dose of streptozotocin. Ten diabetics (DMHBOT) and 10 controls (CHBOT) underwent a one-hour long hyperbaric oxygen treatment protocol (2.5 bar) 12 times after the 3rd week of diabetes. Ten animals remained untreated. Eight weeks after diabetes induction, we measured the 24-hour blood glucose profile and cardiovascular function (sonocardiography and the relaxation ability of aortae). Malonyl-dialdehyde (MDA) and cytokine levels were measured in blood plasma. Poly(ADP-ribose) polymerase (PARP) activity was estimated in cardiac and aortic tissue. HBOT did not alter most of the cardiovascular parameters. PARylation in cardiac and aortic tissues, plasma MDA levels were elevated in diabetic rats. HBOT prevented the increase of MDA in diabetic animals. In addition, levels of the pro-inflammatory cytokine-induced neutrophil chemoattractant-1 (CINC-1) the levels of anti-inflammatory tissue inhibitor of metalloproteases-1 were not altered in diabetes or in hyperoxia. Our results suggest that HBOT does not increase long-term oxidative stress, and, similar to training, the TBARS products, nitrotyrosine formation and poly(ADP-ribosyl)ation may be eased as a result of hyperoxia.

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“…Most recently, a study by Fuller et al from the University of Connecticut showed that HBO preconditioning could exert protective effect on a direct oxidative challenge of UV-A to skin tissue (Fuller et al 2012). The hairless SKH1-E mice were divided into three groups and exposed to UV-A (3 days per week) for 22 weeks.…”

mentioning

confidence: 99%