Iron supplementation at high altitudes induces inflammation and oxidative injury to lung tissues in rats

Salama, Samir A.; Omar, Hany A.; Maghrabi, Ibrahim A.; AlSaeed, Mohammed S.; El-Tarras, Adel E.

doi:10.1016/j.taap.2013.10.034

Cited by 27 publications

(18 citation statements)

References 42 publications

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“…Our results showed that the levels of the proinflammatory cytokines TNF-a, IL-6 and IL1-b were significantly elevated in iron overload group compared to the normal control and the glutamyl cysteine control groups (Fig. 5) which is consistent with previous studies [45,55]. Glutamyl cysteine administration reduced the level of the proinflammatory cytokines to the normal control levels (Fig.…”

Section: Discussionsupporting

confidence: 91%

“…Determination of total antioxidant capacity The commercially available kit (Cayman total antioxidant assay kit) was used to determine the total antioxidant capacity (TAC) in liver tissue homogenates according to the manufacturer's instructions as described previously [38]. The method based on the ability of antioxidants in liver tissue homogenates to compete with 2,2-azino-di-[3-ethylbenzthiazoline sulphonate] (ABTS) for an oxidant, inhibiting ABTS oxidation.…”

Section: Measurement Of Protein Carbonyl Contentmentioning

confidence: 99%

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Glutamyl cysteine dipeptide suppresses ferritin expression and alleviates liver injury in iron-overload rat model

et al. 2015

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Section: Discussionsupporting

confidence: 91%

Section: Measurement Of Protein Carbonyl Contentmentioning

confidence: 99%

Glutamyl cysteine dipeptide suppresses ferritin expression and alleviates liver injury in iron-overload rat model

et al. 2015

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“…phages also produce multiple pro-inflammatory mediators in response to pathogens and foreign substances [30,31] . In vitro and in vivo studies have demonstrated alterations in iron-loaded macrophages, including alterations in the production of pro-inflammatory cytokines [32][33][34][35][36] , which may explain the impaired immune function observed in thalassemia patients [37] . Furthermore, activated alveolar macrophages produce free radicals, including nitric oxide and the superoxide anion, which has been suggested as an additional source of pulmonary damage apart from metal catalysis pathways [38] .…”

Section: Discussionmentioning

confidence: 99%

Effects of Iron Chelators on Pulmonary Iron Overload and Oxidative Stress in β-Thalassemic Mice

et al. 2015

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Aim: To evaluate the effect of iron chelators on iron-related pulmonary pathology and oxidative stress in an animal model of β-thalassemia. Methods: Pulmonary iron overload was induced in heterozygous β-globin knockout mice (^muβ^th-3/+, BKO). Over a period of 2 weeks, 180 mg of iron/mouse was loaded by intraperitoneal injection of iron dextran, and subsequently treated daily via intraperitoneal with either deferoxamine (DF) or deferiprone (L1) at an equimolar concentration of iron binding (0.2 and 0.6 μmol/g body weight, respectively) for 7 days. Results: Iron loading resulted in iron deposition in peribronchial regions, septa and also in alveolar macrophages with a grading score of 3. This iron burden resulted in lung epithelial injuries, fibrosis and corresponded with increased lipid peroxidation and decreased tissue catalase activity. Treatment with DF or L1 resulted in a reduction of iron-laden alveolar macrophages and decreased oxidative stress and tissue damage, showing the iron mobilizing ability of both compounds. Conclusion: Iron chelation therapy, with DF and L1, may protect against pulmonary damage by sequestering catalytic iron and improving oxidative status. It may be beneficial in the prevention of pulmonary complications in thalassemia.

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“…Redox active transition metals have ability to induce and initiate lipid peroxidation through the production of oxygen radicals, mainly hydroxyl radical, via Fenton's/Haber-Weiss reactions [63, 406]. Transition metal, including copper [407–410], chromium [411, 412], cadmium [413–416], nickel [417, 418], vanadium [419–421], manganese [59, 422–424], and iron [59, 407, 425–434] has been utilized to induce lipid peroxidation in vivo mammalian model.…”

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

4,498

3,003

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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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Iron supplementation at high altitudes induces inflammation and oxidative injury to lung tissues in rats

Cited by 27 publications

References 42 publications

Glutamyl cysteine dipeptide suppresses ferritin expression and alleviates liver injury in iron-overload rat model

Glutamyl cysteine dipeptide suppresses ferritin expression and alleviates liver injury in iron-overload rat model

Effects of Iron Chelators on Pulmonary Iron Overload and Oxidative Stress in β-Thalassemic Mice

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

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