Lipid hydroperoxide formation regulates postnatal rat lung cell apoptosis and alveologenesis

Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

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“…Tert butyl hydroperoxide is a strong free radical source and has been utilized to induce lipid peroxidation in vivo mammalian model [386–392]. …”

Section: The Use Of Mammalian Model In Lipid Peroxidation Researchmentioning

confidence: 99%

Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

Ayala

Muñoz

Argüelles

2014

Oxidative Medicine and Cellular Longevity

4,306

3,003

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“…Peripheral pulmonary vessels per unit area were counted from within these fields. Only vessels with both inner and outer elastin bands, to identify arterioles, and outer diameters of 20–65 µm, as assessed by superimposed concentric rings, were counted as previously described …”

Section: Methodsmentioning

confidence: 99%

“…Only vessels with both inner and outer elastin bands, to identify arterioles, and outer diameters of 20-65 mm, as assessed by superimposed concentric rings, were counted as previously described. 22,23,35 Western Analyses…”

Section: Hart's Elastin Stainingmentioning

confidence: 99%

Cyclooxygenase‐2 inhibition partially protects against 60% O₂‐mediated lung injury in neonatal rats

Masood

Man

Lau

et al. 2013

Pediatric Pulmonology

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“…Taken together, lipid metabolism not only plays an important role in maintaining the normal physiological function of the human body but also acts as an important factor in maintaining the normal development of a fetus (29). Experimental and clinical evidence showed that the lipid nutrition and lipid metabolism of fetus and newborn could significantly affect the growth, development and function of the lungs, as well as long-term pulmonary health and disease risk (32)(33)(34). Pediatricians consider that abnormal lipid metabolism caused by unknown reasons is closely related to NRDS.…”

Section: Raw Datamentioning

confidence: 99%

Decrease in lipid metabolic indexes in infants with neonatal respiratory distress syndrome

Zheng,

et al. 2023

Exp Ther Med

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Incomplete pulmonary function and insufficient production of pulmonary surfactant in premature infants may affect alveolar relaxation, inducing neonatal respiratory distress syndrome (NRDS). The present study was a retrospective comparison of lipid metabolism indexes and clinic information between NRDS and non-NRDS infants. Data on general information, pregnancy, clinical symptoms, family history as well as plasma biochemical and lipid metabolic indexes were retrospectively collected and statistically analyzed from 79 patients with NRDS and 44 non-NRDS infants. Infants in the NRDS group showed lower body weight (2,055 vs. 3,225 g) and gestation age (33.39 vs. 38.53 weeks) than those in the non-NRDS group (P<0.05). Baseline information was corrected by the inverse probability of treatment weighting (IPTW) analysis. The weighted adjusted median age was the same in both groups and there was no significant difference between two groups in birth weight. The IPTW analysis revealed that the levels of plasma triglyceride (TG), total cholesterol, low-density lipoprotein, free triiodothyronine, free thyroxine, glucose, calcium (Ca 2+ ) and phosphorus in the NRDS infants were significantly lower compared with those in the non-NRDS infants. Additionally, NRDS infants had significantly higher incidence rates of pneumonia, sepsis, brain injury infection, preterm birth, patent foramen ovale, patent ductus arteriosus and premature rupture of membranes compared with the non-NRDS infants (P<0.05). Multivariate logistic analysis showed that TG and Ca 2+ were risk factors associated with NRDS (P<0.05). Infants with NRDS have significantly lower levels of plasma lipid indexes. The results of the present study provide data to guide the clinical management of NRDS.

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Lipid hydroperoxide formation regulates postnatal rat lung cell apoptosis and alveologenesis

Cited by 4 publications

References 41 publications

Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

Cyclooxygenase‐2 inhibition partially protects against 60% O₂‐mediated lung injury in neonatal rats

Decrease in lipid metabolic indexes in infants with neonatal respiratory distress syndrome

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Lipid hydroperoxide formation regulates postnatal rat lung cell apoptosis and alveologenesis

Cited by 4 publications

References 41 publications

Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

Cyclooxygenase‐2 inhibition partially protects against 60% O2‐mediated lung injury in neonatal rats

Decrease in lipid metabolic indexes in infants with neonatal respiratory distress syndrome

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Resources

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Cyclooxygenase‐2 inhibition partially protects against 60% O₂‐mediated lung injury in neonatal rats