Developmental aspects of experimental pulmonary oxygen toxicity

Frank, Lee

doi:10.1016/0891-5849(91)90062-8

Cited by 183 publications

(108 citation statements)

References 212 publications

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“…Previous studies carried out on this strain [1,2,25] showed a high percentage of malformations in embryos of the hyperglycemic CDs rats between gestational days 11 and 13. Other studies from our [17,26] and other [27,28] laboratories showed a gradual increase in SOD and catalase activities with embryonic age, reaching peak levels during neonatal period. Based on these studies, we chose to study 12.5-day-old embryos of CDs and CDr rats.…”

supporting

confidence: 51%

The Role of Reactive Oxygen Species in Diabetes‐Induced Anomalies in Embryos of Cohen Diabetic Rats

Zangen

Yaffe

Shechtman

et al. 2000

Journal of Diabetes Research

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The role of the antioxidant defense mechanism in diabetesinduced anomalies was studied in the Cohen diabetes-sensitive (CDs) and -resistant (CDr) rats, a genetic model of nutritionally induced type 2 diabetes mellitus. Embryos, 12.5-day-old, of CDs and CDr rats fed regular diet (RD) or a diabetogenic high-sucrose diet (HSD) were monitored for growth retardation and congenital anomalies. Activity of superoxide dismutase (SOD) and catalaselike enzymes and levels of ascorbic acid (AA), uric acid (UA), and dehydroascorbic acid (DHAA) were measured in embryonic homogenates. When fed RD, CDs rats had a decreased rate of pregnancy, and an increased embryonic resorption. CDs embryos were smaller than CDr embryos; 46% were maldeveloped and 7% exhibited neural tube defects (NTDs). When fed HSD, rate of pregnancy was reduced, resorption rate was greatly increased (56%; P < .001), 47.6% of the embryos were retrieved without heart beats, and 27% exhibited NTD. In contrast, all the CDr embryos were normal when fed RD or HSD. Activity of SOD and catalase was not different in embryos of CDs and CDr rats fed RD. When fed HSD, levels of AA were significantly reduced, the ratio DHAA/AA was significantly increased, and SOD activity was not sufficiently increased when compared to embryos of CDr. The reduced fertility of the CDs rats, the growth retardation, and NTD seem to be genetically determined. Maternal hyperglycemia seems to result in The increased rate of fetal malformations in diabetic pregnancy despite better glycemic control represents a clinical problem and a research challenge. The exact mechanism behind the elevated rate of malformations is presently unknown. It has, however, been suggested that both intrauterine (maternal) environment as well as genetic background may be important [1][2][3][4][5][6][7] in the teratogenic process. As of today, the literature describes 3 main pathways by which diabetes may affect the normal development of the embryos: disturbed inositol uptake, yielding lowered intracellular inositol concentration [8]; diminished flow in the arachidonic acid-prostaglandin pathway, yielding decreased PGE2 concentration [9]; and excess amount of reactive oxygen species, resulting in decreased amount of low-molecular-weight antioxidants, such as vitamin C, uric acid, glutathione, and vitamin E [5,6,10,11]. The reactive oxygen species pathway seems to be the most important pathway because antioxidants may protect against the disturbances of both the inositol and the arachidonic pathways. The proposed mechanisms for increased reactive oxygen species generation at higher glucose concentrations include nonenzymatic protein glycosylation [12][13][14], enhanced mitochondrial electron transport chain flow [15], autooxidation [16], and changes in the redox potential. The relative 247

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supporting

confidence: 51%

The Role of Reactive Oxygen Species in Diabetes‐Induced Anomalies in Embryos of Cohen Diabetic Rats

Zangen

Yaffe

Shechtman

et al. 2000

Journal of Diabetes Research

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“…However, oxidant defense mechanisms are induced late in gestation. 7,31 Antioxidant enzyme systems are upregulated primarily during the latter part of gestation. Non-enzymatic antioxidants cross the placenta in increasing quantities during the same timeframe, as reviewed previously.…”

Section: Discussionmentioning

confidence: 99%

Total antioxidant capacity and total oxidant status after surfactant treatment in preterm infants with respiratory distress syndrome

et al. 2011

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Background: Oxidative damage is important in the pathogenesis of respiratory distress syndrome (RDS). However, data on the effect of surfactant therapy on oxidative stress in vivo are limited. We aimed to evaluate the oxidant/antioxidant status in preterm infants with RDS via measurement of total antioxidant capacity (TAC) and total oxidant status (TOS), to determine the effect of surfactant on oxidant/antioxidant balance and to assess the association between TAC, TOS and clinical outcomes of the patients. Methods: Sixty-nine infants with RDS were included. Blood samples for determining TAC and TOS were collected before and 48 h after surfactant treatment. TAC and TOS levels were analysed in serum. Patients were followed up until discharge or death. Results: Post-surfactant TAC levels were significantly higher than pre-surfactant TAC levels (P ¼ 0.029). TAC/TOS ratio significantly increased after surfactant treatment (P ¼ 0.018). Infants ,28 weeks of gestational age had lower levels of baseline TAC than those 28 weeks of gestational age (P ¼ 0.020), whereas TOS levels were similar. Baseline TAC/TOS ratio was lower in infants who died in the study period than those who survived (P ¼ 0.023). After controlling gestational age, baseline TAC levels were significantly and inversely correlated with the duration of total respiratory support (r ¼ 20.343; P ¼ 0.009) and hospitalization (r ¼ 20.341; P ¼ 0.009). TAC or TOS levels were not associated with the development of bronchopulmonary dysplasia or other complications as determined during the investigation period. Conclusions: Oxidant-antioxidant balance shifts in favour of the antioxidant system after surfactant treatment. Lower TAC/ TOS ratio in preterm infants may be associated with increased mortality.

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“…In the neonatal period, this condition has long-lasting consequences, as alveolarization continues for many weeks postnatally (48). Nonetheless, neonatal rodents are more tolerant to hyperoxia than adults (25). Some of this may be related to NFjB signaling, because the neonatal lung readily activates NFjB in hyperoxia, which targets BCL2 gene transcription and protein expression and prevents apoptosis in lung cells (71).…”

Section: Innovationmentioning

confidence: 99%

Oxidative Stress and Inflammation Modulate Rev-erbα Signaling in the Neonatal Lung and Affect Circadian Rhythmicity

Guang

Wright

Hinson

et al. 2014

Antioxidants & Redox Signaling

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Aims: The response to oxidative stress and inflammation varies with diurnal rhythms. Nevertheless, it is not known whether circadian genes are regulated by these stimuli. We evaluated whether Rev-erba, a key circadian gene, was regulated by oxidative stress and/or inflammation in vitro and in a mouse model. Results: A unique sequence consisting of overlapping AP-1 and nuclear factor kappa B (NFjB) consensus sequences was identified on the mouse Rev-erba promoter. This sequence mediates Rev-erba promoter activity and transcription in response to oxidative stress and inflammation. This region serves as an NrF2 platform both to receive oxidative stress signals and to activate Rev-erba, as well as an NFjB-binding site to repress Rev-erba with inflammatory stimuli. The amplitude of the rhythmicity of Rev-erba was altered by pre-exposure to hyperoxia or disruption of NFjB in a cell culture model of circadian simulation. Oxidative stress overcame the inhibitory effect of NFjB binding on Rev-erba transcription. This was confirmed in neonatal mice exposed to hyperoxia, where hyperoxiainduced lung Rev-erba transcription was further increased with NFjB disruption. Interestingly, this effect was not observed in similarly exposed adult mice. Innovation: These data provide novel mechanistic insights into how key circadian genes are regulated by oxidative stress and inflammation in the neonatal lung. Conclusion: Rev-erba transcription and circadian oscillation are susceptible to oxidative stress and inflammation in the neonate. Due to Rev-erba's role in cellular metabolism, this could contribute to lung cellular function and injury from inflammation and oxidative stress. Antioxid. Redox Signal. 21, 17-32.

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Developmental aspects of experimental pulmonary oxygen toxicity

Cited by 183 publications

References 212 publications

The Role of Reactive Oxygen Species in Diabetes‐Induced Anomalies in Embryos of Cohen Diabetic Rats

The Role of Reactive Oxygen Species in Diabetes‐Induced Anomalies in Embryos of Cohen Diabetic Rats

Total antioxidant capacity and total oxidant status after surfactant treatment in preterm infants with respiratory distress syndrome

Oxidative Stress and Inflammation Modulate Rev-erbα Signaling in the Neonatal Lung and Affect Circadian Rhythmicity

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