Iron overload: Effects on cellular biochemistry

Nogueira, Leilismara Sousa; Oliveira, Marina Mendes; Pessôa, Marco Túlio C.; Barbosa, Leandro A.

doi:10.1016/j.cca.2019.11.029

Cited by 74 publications

(49 citation statements)

References 195 publications

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“…Iron is also a pro‐oxidant agent, which can react with the hydrogen peroxide to produce reactive oxygen species (ROS) (Sousa et al , 2020). When the antioxidant system is saturated, excess of lipid ROS causes cellular changes, eventually leading to ferroptosis, a non‐apoptotic cell death (Torti et al , 2018; Friedmann Angeli et al , 2019; Hassannia et al , 2019).…”

Section: Introductionmentioning

confidence: 99%

The deubiquitinase OTUD1 enhances iron transport and potentiates host antitumor immunity

et al. 2021

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Section: Introductionmentioning

confidence: 99%

The deubiquitinase OTUD1 enhances iron transport and potentiates host antitumor immunity

et al. 2021

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“…This causes DNA, protein, and lipid oxidation, resulting in the loss of function in critical organs, such as the liver, heart, pancreas, and kidneys. [ 3–5 ] Furthermore, ROS generated by intracellular iron accumulation via the Fenton reaction leads to ferroptosis, a newly described form of regulated cell death that is characterized by iron‐dependent lipid peroxidation. [ 6 ]…”

Section: Introductionmentioning

confidence: 99%

Coaction of hepatic thioredoxin and glutathione systems in iron overload‐induced oxidative stress

Aydın

Hukkamlı

Budak

2021

J Biochem & Molecular Tox

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In the present study, we demonstrate the coaction of thioredoxin and glutathione (GSH) systems in mouse liver against iron overload‐induced oxidative stress (OS). Mice were injected intraperitoneally with an iron dextran solution twice a week for 3 weeks. Iron accumulation in mouse liver was demonstrated spectroscopically. To confirm the iron overload model in the liver, the increased gene expression levels of hepcidin (Hamp), ferroportin (Fpn1), and ferritin (Fth1), which regulate iron trafficking, were observed by a quantitative polymerase chain reaction. In the case of iron overload, the GSH level and the reduced glutathione/oxidized glutathione ratio, which represents a marker of OS, decreased significantly. An increase in the malondialdehyde level, one of the final products of the lipid peroxidation process, was observed. The gene expression of the thioredoxin system, including thioredoxin (Trx1) and thioredoxin reductase (TrxR1), was examined. Though TrxR1 expression decreased, no changes were observed in Trx1. The enzyme activity and semiquantitative protein expression of TRXR1 increased. The activity of GSH reductase and GSH peroxidase increased in the iron overload group. The gene and protein expressions of thioredoxininteracting protein, which is an indicator of the commitment of the cell to apoptosis, were elevated significantly. The increased protein expression of Bcl‐2‐related X protein and CASPASE‐3, which is an indicator of apoptosis, increased significantly. In conclusion, excess iron accumulation in mouse liver tissue causes OS, which affects the redox state of the thioredoxin and GSH systems, inducing cell apoptosis and also ferroptosis due to increased lipid peroxidation and the depletion of GSH level.

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“…Iron participates in oxygen transport, DNA synthesis, and electron transport associated with cellular respiration (Crichton 1991). Iron overload can damage organs, tissues, and cells, cause histopathological changes and decrease the number of relevant cells to the immune system (Sousa et al 2020).…”

Section: Introductionmentioning

confidence: 99%

Biochemical and Genotoxic Effects of Iron and Manganese in Oreochromis Niloticus (Teleostei: Cichlidae)

Passos

Coppo

Pereira

et al. 2021

Preprint

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The Doce River, southeastern Brazil, in 2015 received iron mining tailings after the Fundão (MG) dam burst, which resulted in the leakage of about 50 million cubic meters of tailings mud, which have iron (Fe) and manganese (Mn) as main components, causing much damage to health to aquatic organisms, including death. Since exposure of aquatic organisms to metals can cause genotoxic damage and induce the generation of reactive oxygen species, causing oxidative damage to biomolecules, the present study aimed to evaluate the toxicity of the association between Fe and Mn in Oreochromis niloticus through genotoxic (micronucleus test and comet assay), and biochemical (CAT and GST enzymes) assays. The tested treatments were T1 = control group, T2 = 3.81 mg/L of Fe + 0.5 mg/L of Mn, and T3 = 7.62 mg/L of Fe + 5.23 mg/L of Mn, during 96-h bioassays. All animals exposed to the metals showed a significant increase in erythrocyte micronucleus frequency and DNA damage. The hepatic GST activity increased two times in animals exposed to T3 compared to control group. The results indicate that Fe + Mn caused genotoxic and biochemical changes in exposed fish. Therefore, excess metals in ecosystems, even those essential for organisms, can be dangerous for the local biota due to the risk associated with high concentrations of these metals.

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Iron overload: Effects on cellular biochemistry

Cited by 74 publications

References 195 publications

The deubiquitinase OTUD1 enhances iron transport and potentiates host antitumor immunity

The deubiquitinase OTUD1 enhances iron transport and potentiates host antitumor immunity

Coaction of hepatic thioredoxin and glutathione systems in iron overload‐induced oxidative stress

Biochemical and Genotoxic Effects of Iron and Manganese in Oreochromis Niloticus (Teleostei: Cichlidae)

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