RESUMEN
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.
RESUMEN
Freeze-lesioned regions of the forebrain cortex provide adequate environment for growth of non-differentiated neural progenitors, but do not support their neuron formation. Reduced oxygen supply, among numerous factors, was suspected to impair neuronal cell fate commitment. In the present study, proliferation and differentiation of neural stem/progenitor cells were investigated at different oxygen levels both in vitro and in vivo. Low (1% atmospheric) oxygen supply did not affect the in vitro viability and proliferation of stem cells or the transcription of "stemness" genes but impaired the viability of committed neuronal progenitors and the expression of proneural and neuronal genes. Consequently, the rate of in vitro neuron formation was markedly reduced under hypoxic conditions. In vivo, neural stem/progenitor cells survived and proliferated in freeze-lesioned adult mouse forebrains, but did not develop into neurons. Hypoperfusion-caused hypoxia in lesioned cortices was partially corrected by hyperbaric oxygen treatment (HBOT). HBOT, while reduced the rate of cell proliferation at the lesion site, resulted in sporadic neuron formation from implanted neural stem cells. The data indicate that in hypoxic brain areas, neural stem cells survive and proliferate, but neural tissue-type differentiation can not proceed. Oxygenation renders the damaged brain areas more permissive for tissue-type differentiation and may help the integration of neural stem/progenitor cells.