The effect of hyperoxia on embryonic and organ mass in the developing chick embryo

Golde, J.M.C.G. van; Borm, Paul J. A.; Wolfs, Marion C; Gerver, W. J. M.; Blanco, Carlos E.

doi:10.1016/s0034-5687(98)00048-6

Cited by 15 publications

(6 citation statements)

References 19 publications

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“…Additionally, the masses of the liver and pectoral muscle tended to be lower in the HBOT group compared to the control group when mass was corrected by egg size. These results contrast with several studies of the effect of normobaric hyperoxia, where embryo development and/or organ growth has been found to be accelerated by incubation (e.g., Smith et al, 1969 ; Bartels et al, 1973 ; Metcalfe et al, 1981 ; Baumann et al, 1983 ; Stock et al, 1983 ; van Golde et al, 1998 ). Additionally, some studies have shown that hyperoxia has minimal significant effects on pulmonary morphometry.…”

Section: Discussioncontrasting

confidence: 98%

Hyperbaric Oxygen Increases Stem Cell Proliferation, Angiogenesis and Wound-Healing Ability of WJ-MSCs in Diabetic Mice

et al. 2018

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Hyperbaric oxygen therapy (HBOT) is effective for the medical treatment of diverse diseases, infections, and tissue injury. In fact, in recent years there is growing evidence on the beneficial effect of HBOT on non-healing ischemic wounds. However, there is still yet discussion on how this treatment could benefit from combination with regenerative medicine strategies. Here we analyzed the effects of HBOT on three specific aspects of tissue growth, maintenance, and regeneration: (i) modulation of adult rodent (Mus musculus) intestinal stem cell turnover rates; (ii) angiogenesis dynamics during the development of the chorio-allantoic membrane (CAM) in Gallus gallus embryos; (iii) and wound-healing in a spontaneous type II diabetic mouse model with a low capacity to regenerate skin. To analyze these aspects of tissue growth, maintenance, and regeneration, we used HBOT alone or in combination with cellular therapy. Specifically, Wharton Jelly Mesenchymal Stem cells (WJ-MSC) were embedded in a commercial collagen-scaffold. HBOT did not affect the metabolic rate of adult mice nor of chicken embryos. Notwithstanding, HBOT modified the proliferation rate of stem cells in the mice small intestinal crypts, increased angiogenesis in the CAM, and improved wound-healing and tissue repair in diabetic mice. Moreover, our study demonstrates that combining stem cell therapy and HBOT has a collaborative effect on wound-healing. In summary, our data underscore the importance of oxygen tension as a regulator of stem cell biology and support the potential use of oxygenation in clinical treatments.

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Section: Discussioncontrasting

confidence: 98%

Hyperbaric Oxygen Increases Stem Cell Proliferation, Angiogenesis and Wound-Healing Ability of WJ-MSCs in Diabetic Mice

et al. 2018

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“…Careful measurements, however, revealed a slight but significant increase in the size of the lens relative to normoxic controls. This is consistent with earlier observations that established that the overall growth of chicken embryos was accelerated under hyperoxic conditions (van Golde et al, 1998) and that the mass of various organs systems, including the eye, was significantly greater than those in age-matched normoxic controls (McCutcheon et al, 1982;Stock et al, 1983). Furthermore, the degree of growth enhancement was shown to be proportional to the ambient oxygen concentration.…”

Section: Oxygen and Lens Organelle Degradationsupporting

confidence: 92%

The effect of elevated intraocular oxygen on organelle degradation in the embryonic chicken lens

Bassnett

McNulty

2003

Journal of Experimental Biology

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SUMMARY In the vertebrate lens, nuclei and other cytoplasmic organelles are degraded in fiber cells situated in the center of the tissue. This is believed to ensure the transparency of the tissue. The mechanism that triggers this process is unknown. We hypothesized that standing gradients of oxygen generated within the tissue may serve as a spatial cue for organelle degradation. To examine this possibility, we incubated fertilized chicken eggs under hyperoxic (50% O2) or normoxic (21% O2)conditions. Hyperoxic treatment was initiated on the seventh day of embryonic development (E7), five days before organelle degradation normally commences in the lens core. Hyperoxia was maintained until E17. Under normoxic conditions,the partial pressure of oxygen (PO) within the vitreous compartment was low. Direct measurement of PO using an optode oxygen sensor indicated values of 1.3 kPa and 0.4 kPa for the mid- and anterior vitreous, respectively. Similarly, treatment with pimonidazole, a bio-reductive hypoxia marker, led to the formation of immuno-positive protein adducts within the lens, suggesting that the embryonic lens is chronically hypoxic in situ. Following hyperoxic treatment, vitreous PO significantly increased, although pimonidazole staining in the lens was not markedly affected. Confocal microscopy of slices prepared from hyperoxic lenses revealed a significant increase in the size of the lens relative to age-matched normoxic controls. By E13, an organelle-free zone(OFZ) was present in the center of normoxic and hyperoxic lenses. However, in hyperoxic lenses, the OFZ was consistently smaller, and the distance from the lens surface to the border of the OFZ significantly larger, than in normoxic controls. These observations suggest that hyperoxia delays organelle breakdown and are consistent with a model in which hypoxia in the deep cortical layers of the normal lens serves as a trigger for the organelle loss process.

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“…4-day-old embryonic chick heart were of the same order as in newborn (6,32,78) and adult (17,67,95) cardiac tissue. SOD activity, although comparable with that in cardiomyocytes isolated from 10-day-old chick embryos (91), was about fivefold lower than in newborn (6,78) or adult (8,16,23,72,88,90) hearts, whereas CAT activity appeared to be slightly lower than in the newborn or adult myocardium.…”

Section: Endogenous Antioxidant Systemsmentioning

confidence: 55%

Differential contribution of mitochondria, NADPH oxidases, and glycolysis to region-specific oxidant stress in the anoxic-reoxygenated embryonic heart

Raddatz¹,

Thomas²,

Sarre

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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The ability of the developing myocardium to tolerate oxidative stress during early gestation is an important issue with regard to possible detrimental consequences for the fetus. In the embryonic heart, antioxidant defences are low, whereas glycolytic flux is high. The pro- and antioxidant mechanisms and their dependency on glucose metabolism remain to be explored. Isolated hearts of 4-day-old chick embryos were exposed to normoxia (30 min), anoxia (30 min), and hyperoxic reoxygenation (60 min). The time course of ROS production in the whole heart and in the atria, ventricle, and outflow tract was established using lucigenin-enhanced chemiluminescence. Cardiac rhythm, conduction, and arrhythmias were determined. The activity of superoxide dismutase, catalase, gutathione reductase, and glutathione peroxidase as well as the content of reduced and oxidized glutathione were measured. The relative contribution of the ROS-generating systems was assessed by inhibition of mitochondrial complexes I and III (rotenone and myxothiazol), NADPH oxidases (diphenylene iodonium and apocynine), and nitric oxide synthases (N-monomethyl-L-arginine and N-iminoethyl-L-ornithine). The effects of glycolysis inhibition (iodoacetate), glucose deprivation, glycogen depletion, and lactate accumulation were also investigated. In untreated hearts, ROS production peaked at 10.8 ± 3.3, 9 ± 0.8, and 4.8 ± 0.4 min (means ± SD; n = 4) of reoxygenation in the atria, ventricle, and outflow tract, respectively, and was associated with arrhythmias. Functional recovery was complete after 30-40 min. At reoxygenation, 1) the respiratory chain and NADPH oxidases were the main sources of ROS in the atria and outflow tract, respectively; 2) glucose deprivation decreased, whereas glycogen depletion increased, oxidative stress; 3) lactate worsened oxidant stress via NADPH oxidase activation; 4) glycolysis blockade enhanced ROS production; 5) no nitrosative stress was detectable; and 6) the glutathione redox cycle appeared to be a major antioxidant system. Thus, the glycolytic pathway plays a predominant role in reoxygenation-induced oxidative stress during early cardiogenesis. The relative contribution of mitochondria and extramitochondrial systems to ROS generation varies from one region to another and throughout reoxygenation.

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The effect of hyperoxia on embryonic and organ mass in the developing chick embryo

Cited by 15 publications

References 19 publications

Hyperbaric Oxygen Increases Stem Cell Proliferation, Angiogenesis and Wound-Healing Ability of WJ-MSCs in Diabetic Mice

Hyperbaric Oxygen Increases Stem Cell Proliferation, Angiogenesis and Wound-Healing Ability of WJ-MSCs in Diabetic Mice

The effect of elevated intraocular oxygen on organelle degradation in the embryonic chicken lens

Differential contribution of mitochondria, NADPH oxidases, and glycolysis to region-specific oxidant stress in the anoxic-reoxygenated embryonic heart

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