Deferoxamine promotes recovery of traumatic spinal cord injury by inhibiting ferroptosis

Ferroptosis is an iron-dependent novel cell death pathway. Deferoxamine, a ferroptosis inhibitor, has been reported to promote spinal cord injury repair. It has yet to be clarified whether ferroptosis inhibition represents the mechanism of action of Deferoxamine on spinal cord injury recovery. A rat model of Deferoxamine at thoracic 10 segment was established using a modified Allen's method. Ninety 8-week-old female Wistar rats were used. Rats in the Deferoxamine group were intraperitoneally injected with 100 mg/kg Deferoxamine 30 minutes before injury. Simultaneously, the Sham and Deferoxamine groups served as controls. Drug administration was conducted for 7 consecutive days. The results were as follows:(1) Electron microscopy revealed shrunken mitochondria in the spinal cord injury group.(2) The Basso, Beattie and Bresnahan locomotor rating score showed that recovery of the hindlimb was remarkably better in the Deferoxamine group than in the spinal cord injury group.(3) The iron concentration was lower in the Deferoxamine group than in the spinal cord injury group after injury.(4) Western blot assay revealed that, compared with the spinal cord injury group, GPX4, xCT, and glutathione expression was markedly increased in the Deferoxamine group.(5) Real-time polymerase chain reaction revealed that, compared with the Deferoxamine group, mRNA levels of ferroptosis-related genes Acyl-CoA synthetase family member 2(ACSF2) and iron-responsive element-binding protein 2(IREB2) were up-regulated in the Deferoxamine group.(6) Deferoxamine increased survival of neurons and inhibited gliosis. These findings confirm that Deferoxamine can repair spinal cord injury by inhibiting ferroptosis. Targeting ferroptosis is therefore a promising therapeutic approach for spinal cord injury.

Neuroprotective effect of deferoxamine on erastin-induced ferroptosis in primary cortical neurons

The iron chelator deferoxamine has been shown to inhibit ferroptosis in spinal cord injury.However,it is unclear whether deferoxamine directly protects neurons from ferroptotic cell death.By comparing the survival rate and morphology of primary neurons and SH-SY5Y cells exposed to erastin,it was found that these cell types respond differentially to the duration and concentration of erastin treatment.Therefore,we studied the mechanisms of ferroptosis using primary cortical neurons from E16 mouse embryos.After treatment with 50μM erastin for 48 hours,reactive oxygen species levels increased,and the expression of the cystine/glutamate antiporter system light chain and glutathione peroxidase 4 decreased.Pretreatment with deferoxamine for 12 hours inhibited these changes,reduced cell death,and ameliorated cellular morphology.Pretreatment with the apoptosis inhibitor Z-DEVD-FMK or the necroptosis inhibitor necrostain-1 for 12 hours did not protect against erastin-induced ferroptosis.Only deferoxamine protected the primary cortical neurons from ferroptosis induced by erastin,confirming the specificity of the in vitro ferroptosis model.This study was approved by the Animal Ethics Committee at the Institute of Radiation Medicine of the Chinese Academy of Medical Sciences,China(approval No.DWLL-20180913)on September 13,2018.

Baicalin and deferoxamine alleviate iron accumulation in different brain regions of Parkinson's disease rats

Previous studies found that iron accumulates in the substantia nigra of Parkinson＇s disease patients However, it is still unclear whether other brain regions have iron accumulation as well. In this experiment, rats with rotenone-induced Parkinson＇s disease were treated by gastric perfusion of baicalin or intraperitoneal injection of deferoxamine. Immunohistochemical staining demonstrated that iron accumulated not only in the substantia nigra pars compacta, but also significantly in the striatum globus pallidus, the dentate gyrus granular layer of the hippocampus, the dentate-interpositus and the facial nucleus of the cerebellum. Both baicalin and deferoxamine, which are iron chelating agents, significantly inhibited iron deposition in these brain areas, and substantially reduced the loss of tyrosine hydroxylase-positive cells. These chelators also reduced iron content in the substantia nigra. In addition to the substantia nigra, iron deposition was observed in other brain regions as well. Both baicalin and deferoxamine significantly inhibited iron accumulation in different brain regions, and had a protective effect on dopaminergic neurons.

Deferoxamine improves neurological function in a rat model of experimental spinal cord injury

A rat model of spinal cord injury was established using modified Allen＇s method and treated with the ferric iron-chelating agent, deferoxamine. Hematoxylin-eosin, Nissl and Perl＇s Prussian blue staining, at 7 14 days following spinal cord injury, showed that following deferoxamine treatment, glial cells proliferation increased significantly, nerve cell morphology was improved and hemosiderin was significantly reduced in the injury region. At 1 56 days following injury, Basso, Beattie, and Bresnahan Locomotor Rating Scale scores were increased, while latencies of somatosensory-evoked potentials and motor-evoked potentials were decreased. Results demonstrate that deferoxamine can promote neurological functional recovery after experimental spinal cord injury in rats.

Therapeutic Drug Monitoring of Chelating Agent Deferoxamine for <i>β</i>-Thalassemia Major Patients

Therapeutic drug monitoring is used to prevent or decrease the risk associated with the toxic effects of medication. This study aims to evaluate the potential advantages of Therapeutic Drug Monitoring (TDM) of subcutaneous Deferoxamine injection and prevention of clinical problems in β-thalassaemia major patients. Patients & Methods: Fifty-four thalassemia patients were allocated into two groups;missing, and not missing deferoxamine dose. TDM of Deferoxamine injection and it clinical outcomes was critically studied under the following subheadings: assessment of the adequacy of Deferoxamine usage, serum peak and trough concentrations of Deferoxamine and ferroxamine with needed pharmacokinetics, cardiac parameters and biomarkers, biochemical and hematological indices, adverse effects/toxicity, urinary assessment of Fe, Zn, selenium, and copper levels, compliance to treatment, dose adjustment in correlation to therapeutic index and life style. Results: Demographic data showed no significant difference. Peak plasma concentrations were 144.83±69 and 43.54±39.16 μg/L, while trough concentrations were 33±26.32 and 31.13±21.58 μg/L of Deferoxamine and ferroxamine, respectively. The elimination rate constant was 0.0237±0.00029 min-1, half-life was 34 min, and distribution volume was 0.93±0.078. Although cardiac parameters showed no significant differences, there were significant differences in CK-MB, and hsCRP levels;troponin I value could not be detected. Biochemical and hematological studies showed significant differences in Ferritin B, urea, SGPT, SGOT, alkaline phosphatase, serum albumin and serum calcium. Assessment of adverse effects/toxicity showed significant differences. The correlation of serum ferritin to therapeutic index, and the life style including Vitamin C and/or E administration were assessed for the compliance to treatment. Conclusion: Therapeutic monitoring of chelation therapy by Deferoxamine in β-thalassemia patients is necessary to ensure effective treatment, compliance, and to avoid adverse side effects and toxicity.

Neutrophilia-Inducing Deferoxamine in Mice Infected with <i>Staphylococcus aureus</i>

The ability to sequester iron is a primary defense mechanism against bacterial infection. Iron chelation therapy has been considered as a possible treatment for various infectious diseases. S. aureus isolated from neonatal septicemia were used to study the effect of deferoxamine and sub-minimal inhibitory concentration of gentamicine on some virulence factors of this isolates. Also an experimental sepsis was inducted in mice and treated with gentamicin and deferoxamine. The expression of virulence factor (alpha-hemolysin, beta-hemolysin, delta-hemolysin, coagulase, and DNase) by Staphylococcus?aureus isolates was significantly decreased (p < 0.05) after exposure to DFO and/or gentamicin. The data of the present study showed that using of DFO led to significant decrease (p < 0.05) in the mortality rate of mice infected with S. aureus. In a murine model of S. aureus sepsis, deferoxamine treatment had an additional effect on survival and bacterial eradication from the organs of septicemic mice. In vitro exposure of S. aureus isolated to gentamicin and deferoxamine led to a decrease in the production of some virulence factors by these isolates.

The Effect of Hemin and Deferoxamine on Selenium, Zinc, and Iron Levels of K562 Cells

This study investigated contents of trace elements selenium, zinc and iron both in control K562 cells, human leukemia cell line, and cells treated with hemin or the iron chelator deferoxamine cells. K562 cell line was grown in RPMI medium supplemented with 10% fetal calf serum, 100 IU/mL penicillin, 100 μg/mL streptomycin, 25 μg/mL amphotericin B and 2 mM L-glutamine at 37?C in humidified air containing 5% CO2. K562 cells were treated with hemin and deferoxamine from the first day to the fifth day. The trace element levels were measured by inductively coupled plasma optical emission spectrometry. Treatment of K562 cells with hemin resulted in an increase in the levels of selenium on fifth day compared with first day. No differences were observed in selenium levels of the control group compared with the hemin-induced group. Also there were no significant differences observed in the zinc levels of control cells compared with deferoxamine- and hemin-induced cells. Iron levels of hemin-induced cells were decreased on the fourth day com-pared with the third day. On the third day, iron levels of hemin-induced cells were significantly increased compared to the control group. Our observations suggest that alterations of selenium and zinc levels may play a role in hemin-induction and deferoxamine-inhibition, respectively. On the other hand, iron levels may influence both in hemin-induction and deferoxamine-inhibition of K562 human leukemia cell

Influence of deferoxamine on hydrocephalus after intraventricular hemorrhage and expressions of Wnt1 and Wnt3a in rat

Objective To observe the effect of deferoxamine on chronic hydrocephalus after intraventricular hemorrhage (IVH) and the role of Wnt (Wnt1 and Wnt3a) . Methods A total of 130 Sprague Dawley male rats were randomly assigned into 4 groups: normal control group, sham IVH group,IVH group and deferoxamine-treated group.

An injectable bioactive dressing based on platelet-rich plasma and nanoclay:Sustained release of deferoxamine to accelerate chronic wound healing

Delayed diabetic wound healing has placed an enormous burden on society.The key factors limiting wound healing include unresolved inflammation and impaired angiogenesis.Platelet-rich plasma(PRP)gel,a popular biomaterial in the field of regeneration,has limited applications due to its non-injectable properties and rapid release and degradation of growth factors.Here,we prepared an injectable hydrogel(DPLG)based on PRP and laponite by a simple one-step mixing method.Taking advantages of the non-covalent interactions,DPLG could overcome the limitations of PRP gels,which is injectable to fill irregular injures and could serve as a local drug reservoir to achieve the sustained release of growth factors in PRP and deferoxamine(an angiogenesis promoter).DPLG has an excellent ability in accelerating wound healing by promoting macrophage polarization and angiogenesis in a full-thickness skin defect model in typeⅠdiabetic rats and normal rats.Taken together,this study may provide the ingenious and simple bioactive wound dressing with a superior ability to promote wound healing.

Carrier-Free Deferoxamine Nanoparticles against Iron Overload in Brain

Although considerable progress has been achieved in treating iron-overload diseases with deferoxamine(DFO)-based biomaterials,high DFO loading and multifunctional integration in one system are still grand challenges.Herein,a series of carrier-free,high DFO-loading(∼80%),uniform spherical nanoparticles(NPs)assisted by polyphenols have been facilely developed with both efficient iron and reactive oxygen species-scavenging properties.Interestingly,those DFO-based NPs have demonstrated excellent scavenging performance in iron-overloaded cell model and energetically exhibited brain cell protection in vivo in intracerebral hemorrhage animal models.This study could provide a promising strategy to significantly improve the curative effect of DFO delivery systems for iron-overload diseases.

Quenching effect of deferoxamine on free radical-mediated photon production in luminol and ortho-phenanthroline-dependent chemiluminescence

Removing excessive free radicals （FRs） by a synthetic chemical might give a clue for treatment of many iron-mediated diseases. Deferoxamine （DFO） can be one of the chemicals of choice for the clue. To investigate photoredox properties of DFO, its quenching effect on superoxide radical （O2°）, hydrogen peroxide （H202） and hydroxyl radical （OH~） was examined using luminol and ortho-phenanthroline （o- phen） chemiluminescence （CL） systems and UV-vis spectrophotometry. Stern-Volmer equation was also used for the CL kinetics. The observed quenching effect of DFO on CL]photon production in luminol and o-phen CL systems strongly confirmed the static arm of quenching properties of DFO on OH° and H2O2, but much less pronounced on O2^-°; the quenching property was maximal when iron was involved in the reaction systems. The Stern-Volmer plots in the designed photochemical reaction systems also confirmed a potent quenching effect of DFO on FR-mediated CL. Our study highlights strong photoreducing and antioxidant properties of DFO with huge quenching capacity on excessive FRs, and thus implies its promising prospects for therapeutic applications.

Myocardial reperfusion injury and oxidative stress: Therapeutic opportunities

Acute myocardial infarction(AMI) is the leading cause of death worldwide. Its associated mortality, morbidity and complications have significantly decreased with the development of interventional cardiology and percutaneous coronary angioplasty(PCA) treatment, which quick-ly and effectively restore the blood flow to the area previously subjected to ischemia. Paradoxi-cally, the restoration of blood flow to the ischemic zone leads to a massive production of reactive oxygen species(ROS) which generate rapid and severe damage to biomolecules, generating a phenomenon called myocardial reperfusion injury(MRI). In the clinical setting, MRI is associated with multiple complications such as lethal reperfusion, no-reflow, myocardial stunning, and reperfusion arrhythmias. Despite significant advances in the understanding of the mechanisms accounting for the myocardial ischemia reperfusion injury, it remains an unsolved problem. Although promising results have been obtained in experimental studies(mainly in animal models), these benefits have not been translated into clinical settings. Thus, clinical trials have failed to find benefits from any therapy to prevent MRI. There is major evidence with respect to the contribution of oxidative stress to MRI in cardiovascular diseases. The lack- of consistency between basic studies and clinical trials is not solely based on the diversity inherent in epidemiology but is also a result of the methodological weak-nesses of some studies. It is quite possible that pharmacological issues, such as doses, active ingredients, bioavailability, routes of administration, co-therapies, startup time of the drug intervention,and its continuity may also have some responsibility for the lack- of consistency between different studies. Furthermore, the administration of high ascorbate doses prior to reperfusion appears to be a safe and rational therapy against the development of oxidative damage associated with myocardial reperfusion. In addition, the association with N-acetylcysteine(a glutathione donor) and deferoxamine(an iron chelator) could improve the antioxidant cardioprotection by ascorbate, mak-ing it even more effective in preventing myocardial reperfusion damage associated with PCA following AMI.

Baicalin suppresses iron accumulation after substantia nigra injury: relationship between iron concentration and transferrin expression

Previous studies have shown that baicalin prevented iron accumulation after substantia nigra injury, reduced divalent metal transporter 1 expression, and increased ferroportin 1 expression in the substantia nigra of rotenone-induced Parkinson＇s disease rats. In the current study, we investigated the relationship between iron accumulation and transferrin expression in C6 cells, to explore the mechanisms of the inhibitory effect of baicalin on iron accumulation observed in Parkinson＇s disease rats. Iron content was detected using inductively coupled plasma-atomic emission spectroscopy. Results showed that iron content decreased 41% after blocking divalent metal transporter 1 and ferroportin 1 proteins. After treatment with ferric ammonium citrate of differing concentrations （10, 50, 100, 400 ktg/mL） in C6 glioma cells, cell survival rate and ferroportin 1 expression were negatively correlated with ferric ammonium citrate concentration, but divalent metal transporter 1 expression positively correlated with ferric ammonium citrate concentration. Baicalin or deferoxamine reduced divalent metal transporter 1 expression, but increased ferroportin 1 expression in the 100 μg/mL ferric ammonium citrate-loaded C6 cells. These results indicate that baicalin down-regulated iron concentration, which positively regulat- ed divalent metal transporter 1 expression and negatively regulated ferroportin 1 expression, and decreased iron accumulation in the substantia nigra.

Iron increases HMOX1 and decreases hepatitis C viral expression in HCV-expressing cells

AIM： To investigate effects of iron on oxidative stress, heme oxygenase-1 （HMOX1） and hepatitis C viral （HCV） expression in human hepatoma ceils stably expressing HCV proteins. METHODS： Effects of iron on oxidative stress, HMOX1, and HCV expression were assessed in CON1 cells. Measurements included mRNA by quantitative reverse transcription-polymerase chain reaction, and protein levels by Western blots. RESULTS： Iron, in the form of ferric nitrilotriacetate,increased oxidative stress and upegulated HMOX1 gene expression. Iron did not affect mRNA or protein levels of Bach1, a repressor of HMOXl. Silencing the up-regulation of HMOXl nuclear factor-erythroid 2-related factor 2 （Nrf2） by Nrf2-siRNA decreased FeNTA-mediated up-regulation of HMOXl mRNA levels. These iron effects were completely blocked by deferoxamine （DFO）. Iron also significantly decreased levels of HCV core mRNA and protein by 80%-90%, nonstructural 5A mRNA by 90% and protein by about 50% in the Con1 full length HCV replicon cells, whereas DFO increased them. CONCLUSION： Excess iron up-regulates HMOXl and down-regulates HCV gene expression in hepatoma cells. This probably mitigates liver injury caused by combined iron overload and HCV infection.

New developments and controversies in iron metabolism and iron chelation therapy

Iron is essential for all organisms including microbial,cancer and human cells. More than a quarter of the human population is affected by abnormalities of iron metabolism, mainly from iron deficiency and iron overload. Iron also plays an important role in free radical pathology and oxidative damage which is observed in almost all major diseases, cancer and ageing. New developments include the complete treatment of iron overload and reduction of morbidity and mortality in thalassaemia using deferiprone and selected deferiprone/deferoxamine combinations and also the use of the maltol iron complex in the treatment of iron deficiency anaemia. There is also a prospect of using deferiprone as a universal antioxidant in non iron overloaded diseases such as neurodegenerative, cardiovascular, renal, infectious diseases and cancer. New regulatory molecules of iron metabolism such as endogenous and dietary chelating molecules, hepcidin, mitochondrial ferritin and their role in health and disease is under evaluation. Similarly, new mechanisms of iron deposition, removal, distribution and toxicity have been identified using new techniques such as magnetic resonance imaging increasing our understanding of iron metabolic processes and the targeted treatment of related diseases. The uniform distribution of iron in iron overload between organs and within each organ is no longer valid. Several other controversies such as the toxicity impact of non transferrin bound iron vs injected iron, the excess levels of iron in tissues causing toxicity and the role of chelation on iron absorption need further investigation. Commercial interests of pharmaceutical companies and connections to leading journals are playing a crucial role in shaping worldwide medical opinion on drug sales and use but also patients' therapeutic outcome and safety. Major controversies include the selection criteria and risk/benefit assessment in the use of deferasirox in thalassaemia and more so in idiopathic haemochromatosis, thalassaemia intermedia and ex-thalassaemia transplanted patients who are safely treated with venesection. Iron chelating drugs can override normal regulatory pathways, correct iron imbalance and minimise iron toxicity. The use of iron chelating drugs as main, alternative or adjuvant therapy is in progress in many conditions, especially those with non established or effective therapies.

Transition of Thalassaemia and Friedreich ataxia from fatal to chronic diseases

Thalassaemia major(TM) and Friedreich's ataxia(FA) are autosomal recessive inherited diseases related to the proteins haemoglobin and frataxin respectively. In both diseases abnormalities in iron metabolism is the main cause of iron toxicity leading to increased morbidity and mortality. Major efforts are directed towards the prevention of these diseases and also in their treatment using iron chelation therapy. Both TM and FA are endemic in Cyprus, where the frequency per total population of asymptomatic heterozygote carriers and patients is the highest worldwide. Cyprus has been a pioneering nation in preventing and nearly eliminating the birth of TM and FA patients by introducing an organized health structure, including prenatal and antenatal diagnosis. Effective iron chelation therapy, improved diagnostic methods and transfusion techniques as well as supportive therapy from other clinical specializations have improved the survival and quality of life of TM patients.Despite the tiresome clinical management regimes many TM patients are successful in their professional lives, have families with children and some are now living well into their fifties. The introduction of deferiprone led to the elimination of cardiac failure induced by iron overload toxicity, which was the major cause of mortality in TM. Effective combinations of deferiprone with deferoxamine in TM patients caused the fall of body iron to normal physiological ranges. In FA different mechanisms of iron metabolism and toxicity apply to that of TM, which can be targeted with specific iron chelation protocols. Preliminary findings from the introduction of deferiprone in FA patients have increased the hopes for improved and effective therapy in this untreatable condition. New and personalised treatments are proposed in TM and FA. Overall, advances in treatments and in particular of chelation therapy using deferiprone are transforming TM and FA from fatal to chronic conditions. The paradigm of Cyprus in the prevention and treatment of TM can be used for application worldwide.

Chelation therapy in liver diseases of childhood: Current status and response

Chelation is the mainstay of therapy in certain pediatric liver diseases.Copper and iron related disorders require chelation.Wilson’s disease(WD),one of the common causes of cirrhosis in children is treated primarily with copper chelating agents like D-penicillamine and trientine.D-Penicillamine though widely used due its high efficacy in hepatic WD is fraught with frequent adverse effects resulting discontinuation.Trientine,an alternative drug has comparable efficacy in hepatic WD but has lower frequency of adverse effects.The role of ammonium tetra-thiomolybdate is presently experimental in hepatic WD.Indian childhood cirrhosis is related to excessive copper ingestion,rarely seen in present era.DPenicillamine is effective in the early part of this disease with reversal of clinical status.Iron chelators are commonly used in secondary hemochromatosis of liver in hemolytic anemias.There are strict chelation protocols during bone marrow transplant.The role of iron chelation in neonatal hemochromatosis is presently not in vogue due to its poor efficacy and availability of other modalities of therapy.Hereditary hemochromatosis is rare in children and the use of iron chelators in this condition is limited.

World health dilemmas: Orphan and rare diseases, orphan drugs and orphan patients

According to global annual estimates hunger/malnutrition is the major cause of death(36 of 62 million). Cardiovascular diseases and cancer(5.44 of 13.43 million) are the major causes of death in developed countries, while lower respiratory tract infections, human immunodeficiency virus infection/acquired immunodeficiency syndrome, diarrhoeal disease, malaria and tuberculosis(10.88 of 27.12 million) are the major causes of death in developing countries with more than 70% of deaths occurring in children. The majority of approximately 800 million people with other rare diseases, including 100000 children born with thalassaemia annually receive no treatment. There are major ethical dilemmas in dealing with global health issues such as poverty and the treatment of orphan and rare diseases. Of approximately 50000 drugs about 10% are orphan drugs, with annual sales of the latter approaching 100 billion USD. In comparison, the annual revenue in 2009 from the top 12 pharmaceutical companies in Western countrieswas 445 billion USD and the top drug, atorvastatin, reached 100 billion USD. In the same year, the total government expenditure for health in the developing countries was 410 billion USD with only 6%-7% having been received as aid from developed countries. Drugs cost the National Health Service in the United Kingdom more than 20 billion USD or 10% of the annual health budget. Uncontrollable drug prices and marketing policies affect global health budgets, clinical practice, patient safety and survival. Fines of 5.3 billion USD were imposed on two pharmaceutical companies in the United States, the regulatory authority in France was replaced and clinicians were charged with bribery in order to overcome recent illegal practises affecting patient care. High expenditure for drug development is mainly related to marketing costs. However, only 2 million USD was spent developing the drug deferiprone(L1) for thalassaemia up to the stage of multicentre clinical trials. The criteria for drug development, price levels and use needs to be readdressed to improve drug safety and minimise costs. New global health policies based on cheaper drugs can help the treatment of many categories of orphan and rare diseases and millions of orphan patients in developing and developed countries.

Near-fatal ferrous sulfate poisoning:A case report of successful conservative management

Rationale:Acute iron poisoning is commonly seen in a pediatric population caused by accidental ingestion of iron syrups.We describe a case of iron poisoning who presented to the hospital following intentional near-fatal ingestion of ferrous sulfate.Patient’s Concern:A 14-years-old previously healthy female patient presented to the emergency department with a history of an intentional overdose of 80 ferrous sulfate tablets.Diagnosis:Ferrous sulfate poisoning.Interventions:The patient developed acute fulminant liver failure 24 h after of the overdose.She was managed conservatively,mainly with deferoxamine and N-acetylcysteine while awaiting transfer to a liver transplant facility.Outcomes:The patient responded well to medical therapy and was discharged on the 9th day of intensive care unit admission.Lessons:This case highlights the patient’s successful recovery with prompt conservative therapy.Severe iron toxicity can be treated with early use of deferoxamine and N-acetylcysteine where a liver transplant facility is not available.

Iron Overdose during Pregnancy: Case and Treatment Review

A 22-year-old pregnant female was transferred to the emergency department having ingested a bottle of iron-containing prenatal vitamins, ondansetron (Zofran?) tablets and alcohol. The patient was hemodynamically stable but suffered from intense bouts of brown, sandy emesis for the first few hours. Investigation revealed the patient ingested 13.57 mg/kg of elemental iron. Due to the initial iron level, history and presentation time whole bowel irrigation was initiated with polyethylene glycol solution. Acute iron toxicity in pregnancy is a medical emergency that can result in multisystem organ failure leading to maternal death and potential fetal demise. High maternal serum iron loads do not affect the developing fetus and are not associated with fetal malformations;however advanced poisoning can lead to maternal death, spontaneous abortions or preterm emergency deliveries. Initial treatment strategies may include whole bowel irrigation using polyethylene glycol electrolyte lavage solution and deferoxamine treatment along with necessary supportive care management. Despite concerns of teratogenicity deferoxamine does not cross the placenta and is regarded as safe for use during pregnancy. Maternal resuscitation must always be the primary objective in acute iron overdoses and, therefore such concern should not delay clinically indicated maternal treatment.