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PubMed2004

Treatment with N-acetylcysteine plus deferoxamine protects rats against oxidative stress and improves survival in sepsis.

OBJECTIVE: Oxidative stress plays an important role in the development of multiple organ failure and septic shock. Here we have evaluated the effects of a combination of antioxidants (N-acetylcysteine plus deferoxamine) in a murine model of polymicrobial sepsis induced by cecal ligation and puncture (CLP). DESIGN: Prospective, randomized, controlled experiment. SETTING: Animal basic science laboratory. SUBJECTS: Male Wistar rats, weighing 300-350 g. INTERVENTIONS: Rats subjected to CLP were treated with either N-acetylcysteine (20 mg/kg, 3 hrs, 6 hrs, 12 hrs, 18 hrs, and 24 hrs after CLP, subcutaneously) plus deferoxamine (20 mg/kg, 3 hrs and 24 hrs after CLP, subcutaneously) or vehicle with or without "basic support" (saline at 50 mL/kg immediately and 12 hrs after CLP plus ceftriaxone at 30 mg/kg and clindamycin 25 mg/kg every 6 hrs). MEASUREMENTS AND MAIN RESULTS: After 12 hrs, tissue myeloperoxidase (indicator of neutrophil infiltration), thiobarbituric acid reactive species (as a marker of oxidative stress), catalase and superoxide dismutase activities (antioxidant enzymes), and mitochondrial superoxide production (index of uncoupling of electron transfer chain) were measured in major organs involved in septic response. Rats treated with antioxidants had significantly lower myeloperoxidase activity and thiobarbituric acid reactive species formation in all organs studied. Mitochondrial superoxide production was significantly reduced by antioxidant treatment. Furthermore, antioxidants significantly improved the balance between catalase and superoxide dismutase activities. Survival in untreated septic rats was 10%. Survival increased to 40% with fluids and antibiotics. In rats treated only with N-acetylcysteine plus deferoxamine, survival was also significantly improved (47%) in a manner similar to basic support. Survival increased to 66% with basic support with N-acetylcysteine plus deferoxamine. CONCLUSIONS: Our data provide the first experimental demonstration that N-acetylcysteine plus deferoxamine reduces the consequences of septic shock induced by CLP in the rat, by decreasing oxidative stress and limiting neutrophil infiltration and mitochondrial dysfunction, thereby improving survival.

Acetylcysteine↗
PubMed1986

Inhibition of proliferation of human leukaemic cell populations by deferoxamine.

Deferoxamine is a hydroxylamine which binds ferric ions to form a highly stable complex. Since iron is thought to be required at a critical stage for cell proliferation, we investigated the effect of deferoxamine on the proliferative activity of human leukaemic cell populations in vitro by means of 3 permanent cell lines, HL60, U937 and 8402. We found deferoxamine to be a potent inhibitor of DNA synthesis and proliferation of leukaemic cells, acting by accumulating treated cells at the early S phase of the cell cycle. Suppression of leukaemic proliferation was obtained at deferoxamine concentrations in the range usually achieved in the treatment of patients for iron overload. Deferoxamine might therefore warrant further investigation as a potentially useful agent for leukaemia chemotherapy.

Cell Division↗
PubMed2002

Comparison of the effects of deferiprone versus deferoxamine on growth and virulence of Yersinia enterocolitica.

Deferoxamine, a drug used to treat patients with iron overload, has the capacity to promote systemic Y. enterocolitica infections in humans. The aim of this study was to determine whether deferiprone, the only orally active alternative treatment, has the same potential. When Y. enterocolitica IP864 was grown in an iron-poor chemically defined medium, addition of deferoxamine promoted its growth, while various concentrations of deferiprone did not display this activity. Similarly, on iron-poor agar plates, various Y. enterocolitica strains were able to grow around paper disks impregnated with deferoxamine in a dose-dependent manner, while no growth was observed around the deferiprone disks. In a mouse experimental model of infection, the 50% lethal dose (LD(50)) of strain IP864 was decreased by more than 5 log units in mice pretreated with deferoxamine, while a deferiprone pretreatment did not affect it. Therefore, in contrast to deferoxamine, deferiprone does not enhance growth of pathogenic Y. enterocolitica in vitro and does not have the potential to promote Y. enterocolitica septicemia in a mouse model of infection. Deferiprone may thus represent a useful alternative iron-chelation therapy during invasive Y. enterocolitica infections.

2,2'-Dipyridyl↗
PubMed2003

Attenuation of glycerol-induced acute renal failure in rats by trimetazidine and deferoxamine.

The pathogenesis of glycerol-induced myoglobinuric acute renal failure involves, among other causes, ischaemia, vascular congestion, and reactive oxygen metabolites. The aim of this study was to investigate the roles of ischaemia and iron-induced oxidative stress by employing trimetazidine, an anti-ischemic drug with an additional antioxidant effect, and deferoxamine, an iron chelator, in glycerol-induced acute renal failure in rats. Five groups of rats were employed in this study: group 1 served as control group, group 2 was given 50% glycerol alone (8 ml/kg i.m.), group 3 was given glycerol plus trimetazidine (3 mg/kg), and groups 4 and 5 were given glycerol plus deferoxamine (50 and 100 mg/kg, respectively). Renal injury was assessed by measuring plasma creatinine and blood urea nitrogen levels and creatinine and urea clearances. The oxidative stress was measured on the basis of the renal malondialdehyde and reduced glutathione levels and the activities of catalase, glutathione reductase, and superoxide dismutase. Glycerol treatment resulted in marked renal oxidative stress and deranged renal functions which significantly improved by trimetazidine and deferoxamine treatments. Deferoxamine, by interacting with Fenton reaction chemistry, and trimetazidine, by its anti-ischaemic and antioxidative properties, protected the kidney against the oxidative stress and the resultant renal dysfunction produced by glycerol. Based on these results, this study points towards renal ischaemia and iron as potential mediators and demonstrates the potential beneficial effects of deferoxamine and trimetazidine in glycerol-induced acute renal failure in rats.

Acute Kidney Injury↗
PubMed1987

Improvement of postischemic myocardial function and metabolism induced by administration of deferoxamine at the time of reflow: the role of iron in the pathogenesis of reperfusion injury.

Reperfusion of ischemic myocardium has been postulated to result in a specific oxygen radical-mediated component of tissue injury. In a previous study we demonstrated improved recovery of ventricular function and metabolism when the superoxide radical scavenger superoxide dismutase was administered at the time of postischemic reflow. Studies in vitro, have suggested that superoxide toxicity might be mediated via the generation of more reactive hydroxyl radicals in an iron-catalyzed reaction. The present study was designed to test the hypothesis that myocardial reperfusion injury might be reduced by administration of the iron chelator deferoxamine at the time of reflow, most likely by preventing hydroxyl radical formation. Sixteen isolated Langendorff rabbit hearts, perfused within the bore of a superconducting magnet, were subjected to 30 min of normothermic (37 degrees C) total global ischemia followed by 45 min of reperfusion. At reflow eight treated hearts received a 10 ml bolus containing 50 mumol of deferoxamine followed by an infusion of 11 mumol/min for the first 15 min of reflow. The hearts were then perfused with standard perfusate for an additional 30 min. Eight untreated control hearts received a similar bolus of perfusate followed by 45 min of standard reperfusion. Serial 5 min 31P nuclear magnetic resonance spectra were recorded. Myocardial phosphocreatine (PCr) content fell to 5% to 7% of control during ischemia in both groups of hearts. Deferoxamine-treated hearts recovered 99 +/- 10% of control PCr content, while untreated hearts recovered 60 +/- 16% (p less than .05). Intracellular pH fell to 5.9 during ischemia in both groups, before showing more rapid and complete recovery in treated hearts (p less than .01). Recovery of developed pressure reached 70 +/- 6% of control in treated hearts compared with 35 +/- 10% in untreated hearts (p less than .05). Iron content of the perfusate was 7 microM, and by electron paramagnetic resonance spectroscopy was in the form of Fe3+-EDTA complexes. In the effluent of treated hearts iron was in the form of Fe3+-deferoxamine chelates. In summary, administration of the iron chelator deferoxamine at the time of postischemic reflow results in greater recovery of myocardial function and energy metabolism, which supports the hypothesis that iron plays an important role in the pathogenesis of reperfusion injury.

Adenosine Triphosphate↗
PubMed1992

Protection from cold injury by deferoxamine, an iron chelator.

The presence of hydroxyl radical (OH) has been implicated in the pathogenesis of cold injury. Since iron is known to catalyze the OH formation responsible for cellular injury, this study was designed to examine whether an iron chelator such as deferoxamine can salvage a tissue from cold injury. Cold injury was induced in the hind limbs of rabbits. The experimental group received 0.6 mM of deferoxamine through the femoral vein prior to cooling of the limbs. Deferoxamine reduced the tissue injury, as evidenced by the decreased release of lactate dehydrogenase, a nonspecific marker for cellular injury. In addition, this drug inhibited OH formation and lipid peroxidation when examined by monitoring the formation of conjugated dienes and malonaldehyde, presumptive markers for lipid peroxidation. Rewarming of the cooled limbs was also associated with the loss of membrane phospholipids, with the corresponding accumulation of lysophosphoglycerides and free fatty acids, especially linoleic and arachidonic acids. Deferoxamine prevented the loss of phospholipids and inhibited the accumulation of amphipathic lipid products. These results indicates that deferoxamine salvaged the tissue from cold injury, possibly by preventing the formation of OH presumably by chelating iron, thus protecting the phospholipids from free radical attack.

Animals↗
PubMed2003

Effects of allopurinol and deferoxamine on reperfusion injury of the brain in newborn piglets after neonatal hypoxia-ischemia.

The hypothesis was tested that treatment with allopurinol, a xanthine oxidase inhibitor, or deferoxamine, a chelator of nonprotein-bound iron, preserved cerebral energy metabolism, attenuated development of edema, and improved histologic outcome in the newborn piglet at 24 h after hypoxia-ischemia. Thirty-two newborn piglets were subjected to 1 h of hypoxia-ischemia by occluding both carotid arteries and reducing the fraction of inspired oxygen; five newborn piglets served as sham-operated controls. The depth of hypoxia-ischemia was controlled by phosphorous magnetic resonance spectroscopy. Upon reperfusion and reoxygenation, piglets received vehicle (n= 12), allopurinol (30 mg/kg/d, n = 10), or deferoxamine (12.5 mg/kg/d, n = 10). The cerebral energy status was determined with phosphorous magnetic resonance spectroscopy. The presence of vasogenic edema was assessed by T2-weighted magnetic resonance imaging. Brain cell injury was assessed with caspase-3 activity, histology, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end (TUNEL)-labeling. At 24 h after hypoxia-ischemia, the phosphocreatine/inorganic phosphate ratios were significantly decreased in vehicle-treated, but not in allopurinol- or deferoxamine-treated piglets. Water T2 values were significantly increased at 24 h after hypoxia-ischemia in cerebral cortex, thalamus, and striatum of vehicle-treated piglets, but not in allopurinol- and deferoxamine-treated piglets. No differences in caspase-3 activity, histologic outcome, or TUNEL-labeling were demonstrated between the three treatment groups. We suggest that allopurinol and deferoxamine may have an additional value in the treatment of perinatal hypoxia-ischemia with other neuroprotective agents or in combination with hypothermia.

Allopurinol↗
PubMed2006

Deferoxamine reduces tissue damage during endotoxin-induced mastitis in dairy cows.

The protective effects of 3 antioxidants on polymorphonuclear neutrophil-induced damage to mammary cells were evaluated in vivo using an endotoxin-induced mastitis model. Fifteen healthy, midlactation cows with no history of clinical Escherichia coli mastitis were randomly assigned to 1 of the 3 treatment groups corresponding to each modulator to be evaluated, that is, deferoxamine, catechin, and glutathione ethyl ester. Each cow had 1 quarter infused with saline and 1 quarter infused with the selected modulator; a third quarter was infused with lipopolysaccharides (LPS), whereas the fourth quarter received a combination of LPS and the modulator. Infusion of LPS caused acute mastitis as determined by visual observations and by large increases in milk somatic cell count, BSA, and proteolytic activity. These parameters were not affected by antioxidant administration. The extent of cell damage was evaluated by measuring milk levels of lactate dehydrogenase and N-acetyl-beta-D-glucosaminidase activity. Levels of these parameters were several times higher after LPS administration. Intramammary infusions of catechin or glutathione ethyl ester did not exert any protective effect, whereas infusion of deferoxamine, a chelator of iron, decreased milk lactate dehydrogenase and NA-Gase activity, suggesting a protective effect against neutrophil-induced damage. The protective effect of deferoxamine was also evidenced by a lower milk level of haptoglobin. The proteolytic activity of mastitic milk was not influenced by the presence of deferoxamine. Overall, our results suggest that local infusion of deferoxamine may be an effective tool to protect mammary tissue against neutrophil-induced oxidative stress during bovine mastitis.

Animals↗
PubMed1987

Fatal Rhizopus infections in hemodialysis patients receiving deferoxamine.

Four hemodialysis patients receiving deferoxamine for metal overload had fatal rhinocerebral rhizopus infections. Serious fungal infections are not commonly seen in patients on dialysis, and none of these patients had the usual risk factors for rhizopus infection. Deferoxamine is being used with increased frequency in dialysis patients for aluminum and iron overload states. We propose that there is a link between the deferoxamine therapy and this unusual infection. Deferoxamine may serve as a specific growth factor for Rhizopus species or may alter host immune function. We suggest searching for fungal organisms in patients with unexplained illnesses receiving deferoxamine.

Adult↗
PubMed2000

[Development of arterial thrombus of Mucorales hyphae during deferoxamine therapy in a patient with aplastic anemia in transformation to myelodysplastic syndrome].

A 58-year-old woman with a diagnosis of aplastic anemia had been treated with anabolic steroid for mild anemia in 1984. In May 1995, pancytopenia progressed and the patient became dependent on red blood cell transfusions. Chromosome analysis of bone marrow cells revealed trisomy 8 and the patient was thought to have aplastic anemia in transformation to myelodysplastic syndrome. In July 1996, deferoxamine was administered for iron overload. The patient was admitted because of pneumonia on July 31, 1998. Chest computed tomograms showed arteriothrombus of the right pulmonary artery and pulmonary mycosis. Although an antifungal agent was administered, the patient experienced respiratory failure and eventually died of hypovolemic shock due to gastric bleeding from a Dieulafoy ulcer. Autopsy revealed arteriothrombus of hyphae of Mucorales in the right pulmonary artery and right renal artery branch. Cases of mucormycosis occurring in dialysis patients receiving deferoxamine have recently appeared in the literature. Deferoxamine may be a risk factor for mucormycosis. Deferoxamine has been also used in the treatment of iron overload patients with aplastic anemia. Four cases of mucormycosis developing in such patients have been reported in Japan including this case. There may be a relationship between mucormycosis and deferoxamine in patients with aplastic anemia.

Anemia, Aplastic↗
PubMed1990

Deferoxamine fails to improve postischemic cardiac function in hypertrophied hearts.

Myocardial hypertrophy is a well-recognized risk factor in congenital cardiac surgery. Hypertrophied hearts have been demonstrated to have an increased vulnerability to ischemia/reperfusion injury. We studied the effects of the iron chelator and hydroxyl radical scavenger deferoxamine given during early reperfusion in a model of isolated retroperfused rabbit hearts made hypertrophic by aortic banding early in life (1 week of age). The rabbits were studied at 6-8 weeks of age, and the hearts were subjected to 30 minutes of 37 degrees C ischemia followed by 30 minutes of reperfusion. Postischemic recovery of isovolumic developed pressure was measured by using an intracavitary balloon in both the untreated (n = 6) and the deferoxamine-treated (n = 6) groups and compared with normal age-matched controls. Deferoxamine (50 mumol/kg) was given to one group with the hypertrophied hearts during the first 10 minutes of reperfusion. The left ventricular weight/body weight ratio in the hypertrophied hearts was 2.9 +/- 0.4 x 10(-3) (n = 14) versus 2.0 +/- 0.1 x 10(-3) in the age-matched controls (p less than 0.05). Postischemic peak developed pressure recovered to 102 +/- 6% of the preischemic value in the normal hearts after 30 minutes of reperfusion compared with 75 +/- 5% for the untreated and 71 +/- 4% for the deferoxamine-treated hearts (p less than 0.05 vs. control). We conclude that chronic hypertrophy from early in life leads to increased susceptibility to ischemia and that the iron chelator deferoxamine is not effective in preventing the injury of reperfusion in hypertrophied hearts.

Animals↗
PubMed1990

A promising approach for improving the recovery of heart transplants. Prevention of free radical injury through iron chelation by deferoxamine.

Iron catalysis is involved in the generation of the highly cytotoxic hydroxyl radical and in the chain reactions of subsequent lipid peroxidation that lead to irreversible membrane damage. Assuming that ischemically stored heart transplants may incur free radical injury at the time of reoxygenation, we assessed the effects of the iron chelator deferoxamine in 70 isolated isovolumic buffer-perfused rat hearts subjected to the following protocol: cardioplegic arrest; cold (2 degrees C) storage for 5 hours; global ischemia at 15 degrees C for 1 hour, intended to simulate the implantation procedure; and normothermic reperfusion for 1 additional hour. During poststorage ischemic arrest, the following techniques of myocardial protection were evaluated: hypothermia alone; high-pressure (60 cm H2O) cardioplegia given at 0, 30, and 55 minutes of arrest; low-pressure (30 cm H2O) cardioplegia given at 0 and 55 minutes of arrest; and low-pressure (30 cm H2O) cardioplegia only given at 55 minutes of arrest. Treated hearts had deferoxamine (6 mumol) added to the cardioplegic solution used throughout the experimental time course. Further, in the treated group subjected to the protocol of single cardioplegic delivery at end ischemia, deferoxamine was given both in the cardioplegic reperfusate and in the Krebs buffer over the 15 initial minutes of reflow. Based on comparisons of postreperfusion ventricular pressure development, maximal rate of rise of ventricular pressure, left ventricular compliance, and coronary flow, the best myocardial protection was afforded by deferoxamine given as an additive to single-dose cardioplegic solution at the end of arrest and to the reperfusate during the initial phase of reoxygenation. As the drug has no inotropic effect, its protective action is most likely related to a decrease in catalytic iron available for free radical production and lipid peroxidation. These results support the hypothesis that oxidative damage may contribute to donor heart failure and demonstrate that this form of damage can be efficiently acted upon by iron chelation. The clinical relevance of these data stems from the fact that deferoxamine is available for human use and might become an effective means of improving donor heart preservation in the setting of clinical heart transplantation.

Animals↗
PubMed1987

Antimicrobial alternatives for calf diarrhea: enteric responses to Escherichia coli, deferoxamine, or gallium in neonatal calves.

Intestinal malabsorption or transferable resistance in enteric bacteria are potentially serious complications of routine oral administrations of antibiotics. On the basis of reports on antimicrobial effects of host iron sequestration and on synthetic iron chelators or competitors in vitro, 2 iron antagonists were studied for their potential as alternative antimicrobials for Escherichia coli diarrhea. Deferoxamine, a fungal iron chelator used to treat acute iron intoxication, and elemental gallium, a competitive inhibitor of iron activity in metabolic enzyme systems, were examined for their effects on enteric morphology and function in neonatal calves. Twelve male calves were allotted to 4 groups: (1) given nonpathogenic E coli (control); (2) given enterotoxigenic B44 E coli; (3) given deferoxamine (50 mg/kg, twice a day); and (4) given gallium (4 mg/kg, twice a day). Calves were studied for 8 days, including the conduct of oral glucose and lactose tolerance tests on days 1, 3, and 7. By day 7, according to oral glucose and lactose tolerance tests, peak plasma glucose concentrations in all calves of groups 2, 3, and 4 were lower than those values in controls. The frequency of diarrhea was significant in all treated calves, and disease was most severe in the deferoxamine-treated calves. Quantitative cultural examination on day 8 showed significant numerical increases of jejunal and ileal E coli and ileal lactobacilli in deferoxamine-treated calves (group 3) and of ileal streptococci in gallium-treated calves (group 4) and showed jejunal and ileal overgrowths of Saccharomyces yeast in deferoxamine-treated calves.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

Deferoxamine-chelatable iron in hemochromatosis and other disorders of iron overload.

Deferoxamine-chelatable iron was measured in 103 patients with known or suspected iron overload. All of 34 patients with untreated hemochromatosis had distinctly elevated values for deferoxamine-chelatable iron. The mean value in these cases was significantly greater than that in patients with cirrhosis, who had little or no stainable hepatic iron. In 15 patients with hemochromatosis who were tested sequentially during the course of phlebotomy therapy, deferoxamine-chelatable iron proved a reliable index of the degree of reduction of storage iron. In 22 additional patients with partially treated hemochromatosis and 14 with iron overload accompanying chronic anemia, this test correlated well with the magnitude of iron deposits in liver or bone marrow. In patients with unexplained elevations of serum iron, normal or only slightly elevated deferoxamine-chelatable iron correctly indicated that storage (hepatic) iron was not excessive. The test was more reliable than determination of serum iron or transferrin saturation as an indicator of increased storage iron. Elevated values could not be attributed to disturbed liver function. Determination of deferoxamine-chelatable iron is a safe, practical, and useful procedure for identifying persons with increased iron stores and for assessing the effect of phlebotomy therapy.

Adult↗
PubMed1993

[Successful treatment with deferoxamine in a case of refractory anemia].

A 60-year-old female was admitted to our hospital because of macrocytic anemia with anisopoikilocytosis and thrombocytopenia. A bone marrow aspiration revealed hypolasia with nuclear deformity of neutrophils and decrease of megakaryocytic numbers. Karyotype analysis showed 47, XX, +8. A diagnosis of refractory anemia was made. The patient was treated with metenolone acetate without clinical response. Deferoxamine (2g/day) was given intravenously by continuous infusion. Ten days after deferoxamine treatment, the levels of RBC and platelet increased and the effect lasted 100 days after discontinuance of deferoxamine. Bone marrow aspiration showed normoplasia with normal megakaryocytes numbers. However, anisopoikilocytosis, abnormality of MCH and MCHC, and karyotype abnormality similar to the first medical examination remained. These data might suggest that deferoxamine induced differentiation of abnormal hemopoietic cells in refractory anemia. Retrobulbar neuritis which developed 30 days after initiation of treatment disappeared after halting deferoxamine treatment.

Anemia, Refractory↗
PubMed1996

Iron complexation with oral deferoxamine in a swine model.

A controversial therapy in the management of acute iron poisoning is the oral administration of deferoxamine which purportedly complexes unabsorbed iron, exerts protection at the cellular level, and/or enhances the renal elimination of ingested iron. To study the effects of oral deferoxamine on iron absorption, fasted male pigs weighing an average of 10 kg simulated potentially toxic iron overdoses in 12 to 24-mo-old children. A control group of 13 pigs received 60 mg elemental iron/kg via oral gavage followed by 50 ml of distilled water. Serum iron (SI) levels were obtained at 0, 1 2, 4, 6 and 8 h post-iron dosing. The study group of 10 pigs received 60 mg elemental iron/kg po followed by 10 g deferoxamine (1 g/kg). SI levels were obtained at the same intervals. There was no mortality in either group. Statistical differences in SI were noted at 6 and 8 h. Characteristic urine discoloration secondary to deferoxamine was noted at 4 h in the study group. Deferoxamine reduced some peak 51 levels but did not diminish the total absorption of iron.

Administration, Oral↗
PubMed2002

The expanded clinical spectrum of deferoxamine retinopathy.

OBJECTIVE: To describe early and unusual features in 16 patients with deferoxamine-induced retinal toxicity and to assess the role of diagnostic tests in the diagnosis and management of patients with the disorder. DESIGN: Retrospective, observational case series. PARTICIPANTS: Sixteen patients with deferoxamine retinopathy identified from members of the Vitreous, Retina, and Macula societies of the United States. INTERVENTION/TESTING: The patients underwent complete ophthalmologic examination. Most patients were also evaluated by fluorescein angiography and electrophysiologic testing. The diagnosis was based on the medical history, systemic and ocular findings, and the results of electrophysiologic tests. MAIN OUTCOME MEASURES: Ocular symptoms, ophthalmoscopic, fluoroangiographic, and electrophysiologic findings. RESULTS: We confirmed previously reported findings in patients with established disease, including macular and/or peripheral pigmentary changes, reduced electroretinographic (ERG) amplitudes, and reduced electrooculographic (EOG) light-peak to dark-trough ratios. Peripapillary, papillomacular, and paramacular patterns of retinal pigment epithelial (RPE) degeneration were each observed in one patient. Diffuse RPE or outer retinal fluorescence by fluorescein angiography was a marker for active retinopathy both at the onset of disease and during recurrence and preceded the development of RPE pigment mottling. CONCLUSIONS: Unusual patterns of deferoxamine retinopathy may occur in addition to the foveomacular and/or peripheral patterns previously described. Fluorescein angiography is particularly useful for determining whether there is ongoing retinal/RPE injury. ERG and EOG testing may indicate earlier or more widespread injury than is suggested by fundus examination alone. Patients who do not discontinue deferoxamine after the development of retinopathy risk further retinal/RPE injury and visual deterioration.

Adolescent↗
PubMed1999

Cataractous changes in rat lens following cigarette smoke exposure is prevented by parenteral deferoxamine therapy.

OBJECTIVES: To test whether iron accumulation in the lens following cigarette smoke exposure is the principal mechanism in smoke-related cataractogenesis and to assess the possible protective effect of deferoxamine mesylate treatment against lenticular degeneration with in vivo exposure to cigarette smoke. METHODS: Thirty-two male Wistar rats were randomly divided into 4 equal groups. Groups 3 and 4 rats were exposed to cigarette smoke for 1 hour each day for 90 consecutive days, and groups 1 and 2 rats were treated in a similar manner but exposed only to room air. In addition, deferoxamine was given subcutaneously to groups 2 and 4 rats. Both eyes of all the animals were then enucleated and 1 eye prepared for histopathological examination. The fellow eye was used to measure iron, calcium, zinc, and copper levels. RESULTS: Significantly higher iron and calcium and lower zinc levels were observed in the lenses of group 3 rats compared with those in the other groups. Similar comparisons performed between groups 1 and 2, 1 and 4, and 2 and 4 did not show any significant difference. Copper concentrations did not differ between groups. Distinct histopathological changes in the anterior lens epithelium, such as hyperplasia, hypertrophy, and epithelial multilayering, and the presence of swollen epithelial cells overlying the posterior lens capsule, observed in group 3 rats, were not present in the other groups. CONCLUSIONS: Cataractogenesis following cigarette smoke exposure in rats was associated with the accumulation of iron, and concurrent deferoxamine therapy prevented such cataract formation. CLINICAL RELEVANCE: Our results may apply to human cataract formation associated with cigarette smoking, so such pathogenesis may be prevented by concurrent parenteral deferoxamine treatment. Clinical studies are needed, however, to determine the value of this suggestion.

Animals↗