UV-filters and musk fragrances in seafood commercialized in Europe Union: Occurrence, risk and exposure assessment.

In the framework of the FP7 ECsafeSeafood project, 62 seafood samples commercialized in Europe Union from several representative species - mackerel, tuna, salmon, seabream, cod, monkfish, crab, shrimp, octopus, perch and plaice - were analysed for residues of 21 personal care products (PCPs), including 11 UV-filters (UV-Fs) and 10 musk fragrances (musks). PCPs analysis were performed by Quick, Easy, Cheap, Effective Rugged, Safe (QuEChERS), combined with liquid-liquid extraction (LLE) or dispersive solid-phase extraction (dSPE), followed by gas chromatography-tandem mass spectrometry (GC-MS/MS). The results showed the presence in a wide range of samples of nine out of eleven UV-Fs compounds analysed, namely 2-ethylhexyl salicylate (EHS), 2-ethylhexyl,4-methoxycinnamate (EHMC), 4-methylbenzylidenecamphor (4-MBC), benzophenone-1 (BP1), benzophenone-3 (BP3), isoamyl-4-methoxycinnamate (IMC), 2,2'-dihydroxy-4,4'-dimethoxybenzophenone (DHMB), homosalate (HS), and octocrylene (OC), whereas galaxolide (HHCB), galaxolide lactone (HHCB-lactone), and tonalide (AHTN) were the most found musks. The potential risks to human health associated with the exposure to eight of the more prevalent PCPs - EHS, EHMC, 4-MBC, BP1, BP3, IMC, HHCB, and AHTN - through seafood consumption were assessed for consumers from five European countries (Belgium, Ireland, Italy, Portugal and Spain). Results showed that the human exposure to UV-Fs and musks estimated from the concentration values found in seafood and the daily consumption of concerned seafood species, were far below toxicological reference values.

Co-occurrence of musk fragrances and UV-filters in seafood and macroalgae collected in European hotspots.

In the last decades, awareness regarding personal care products (PCP), i.e. synthetic organic chemicals frequently used in cosmetic and hygienic products, has become a forward-looking issue, due to their persistency in the environment and their potential multi-organ toxicity in both human and wildlife. Seafood is one of the most significant food commodities in the world and, certainly, one of the most prone to bioaccumulation of PCP, what can consequently lead to human exposure, especially for coastal population, where its consumption is more marked. The aim of this work was to evaluate the co-occurrence of musk fragrances and UV-filters in both seafood and macroalgae collected in different European hotspots (areas with high levels of pollution, highly populated and near wastewater treatment plants). Despite the fact that UV-filters were detected in three different kind of samples (mussel, mullet, and clam), in all cases they were below the limit of quantification. Galaxolide (HHCB) and tonalide (AHTN) were the musk fragrances most frequently detected and quantified in samples from the European hotspots. Cashmeran (DPMI) was also detected in most samples but only quantified in two of them (flounder/herring and mullet). The highest levels of HHCB and AHTN were found in mussels from Po estuary.

Bisphenol A analogues (BPS and BPF) present a greater obesogenic capacity in 3T3-L1 cell line.

This study was aimed at comparing the toxicity effects on cell viability and the obesogenic activity of Bisphenol A (BPA) and its analogues, Bisphenol S (BPS) and Bisphenol F (BPF), by in vitro assays with a preadipocytic 3T3-L1 cell line. To compare the toxic potential and select the concentrations of each chemical not showing a decrease in cell viability, MTT assay was performed. The cell phenotype was determined in differentiated 3T3-L1 adipocytes by red oil O staining. To determine the expression levels of the different adipogenic proteins the Western Blot test was performed. The results from MTT assay showed a greater toxic effect of BPA - at equal and even lower concentrations-than its analogues. However, BPS followed by BPF showed a greater neutral lipid storage capacity than BPA, which was reflected in the increase of the protein expression of CCAAT/enhancer binding protein α (C/EBPα), peroxisome proliferator-activated receptor gamma γ (PPARγ) and acid-binding protein 4 (FABP4). In summary, these BPA analogues -especially BPS- present a greater endocrine potential activity than BPA.

Concentrations of polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) in milk of women from Catalonia, Spain.

In this study, the concentrations of polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) in milk from women living in the vicinity of a new hazardous waste incinerator (HWI) in Catalonia, Spain, were determined. The study was performed after 4 years of regular operations in the facility and the present PCB levels were compared with baseline concentrations obtained in a pre-operational program. PCBs and PBDEs levels were determined by HRGC/HRMS in 15 samples. In the present study planar PCBs ranged from 1.3 to 6.3 pg WHO-TEQ/g fat with a mean value of 3.8 pg WHO-TEQ/g fat. After adding dioxin-like mono-ortho-PCBs the total PCB-TEQ concentrations ranged from 3.8 to 13.3 pg WHO-TEQ/g fat (mean value: 8.7 pg WHO-TEQ/g fat). A comparison of the current data with those obtained in the baseline study showed significant decreases for both planar and total WHO-TEQ of PCBs: 47.9% and 44.6%, respectively. PCB concentrations in milk of women living in urban zones were higher than those living near industrial areas (10.1 and 7.4 pg WHO-TEQ/g fat, respectively). Mean PBDE concentrations were 2.2 and 2.5 ng/g fat for women living in urban and industrial zones, respectively. Dietary intake of PCBs and PBDEs for a standard adult woman samples were 898 and 843 ng/day for PCBs, and 72 and 63 ng/day for PBDEs, for residents in urban and industrials areas, respectively. This study suggests that dietary intake is more relevant for human exposure to PCBs and PBDEs than living near the HWI.

Metal levels in sugar cane (Saccharum spp.) samples from an area under the influence of a municipal landfill and a medical waste treatment system in Brazil.

In July 2003, duplicated samples of roots, stems and leaves of sugar cane (Saccharum spp.) were collected in 25 points of an area under direct influence of the municipal landfill site (MLS) and medical waste treatment system (MWTS) of Ribeirao Preto, São Paulo, Brazil. Cadmium (Cd), chromium (Cr), copper (Cu), mercury (Hg), manganese (Mn), lead (Pb) and zinc (Zn) were determined by atomic absorption spectrophotometry. The following concentrations (mg/kg) were found in roots: Cd, 0.22+/-0.12; Cr, 64.3+/-48.7; Cu, 140.6+/-27.7; Hg, 0.04+/-0.02; Mn, 561.6+/-283.3; Pb, 7.9+/-2.1 and Zn, 177.4+/-64.9. For some metals, these levels are higher than the concentrations previously reported for different plants, reaching, in some cases, values that might be considered toxic for vegetables. Metal levels in stems were 80-90% of those found in roots, while the concentrations detected in leaves were significantly lower than those in roots. The present results suggest that MLS and MWTS activities might have been increasing metal concentrations in edible tissues of sugar cane grown in the area under their influence. Moreover, the traditional agricultural practices in the production of sugar cane could be also another determinant factor to reach the current metal levels. The results of this study indicate that sugar cane is a crop that is able to grow in areas where metals in soils are accumulated.

Effects of oral exposure to silver nanoparticles on the sperm of rats.

It has been demonstrated that exposure to silver nanoparticles (AgNPs) can induce toxicological effects in rodents. In this study, we investigated whether sub-chronic oral exposure to different doses of polyvinil pyrrolidone (PVP)-coated AgNPs (PVP-AgNPs) (50, 100 and 200mg/kg/day) could induce harmful effects on epididymal sperm rat parameters. Sperm motility, viability and morphology were examined. Moreover, a histological evaluation of testis and epididymis was also performed. High doses of PVP-AgNPs showed higher sperm morphology abnormalities, while a progressive, but not significant effect, was observed in other sperm parameters. The current results suggest that oral sub-chronic exposure to PVP-AgNPs induces slight toxicological effects in sperm rat parameters.

Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering factor.

The aim was to study the effects of radiofrequency (Rf) in a mice strain characterized by age-determined carcinogenesis of lymphatic tissues. Mice were treated with a 1?h/week Rf exposure for 4 months. A group submitted to sham exposure was used as control animals. The evolution of carcinogenesis was followed up to 18 months. The maximal life span of control mice was about 24 months. All dead animals were clinically and histologically examined to give an age-determined comparative quantification of the evolving carcinogenesis. A radiocalcium tracer method permitted the evaluation of Rf effects on transmembrane transport of extracellular calcium at 1 and 24 h after exposure. The determination of induced lipid peroxidation completed this second study. The findings show that Rf provoked an earlier general lymphocyte cell infiltration, formation of lymphoblastic ascites and extranodal tumours of different histological types, as well as an increased early mortality. The results suggest that in Rf-exposed mice, carcinogenesis may be induced earlier and with different pathological forms than in control animals. The modifications in cellular calcium homeostasis and the age-determined thymus involution appear to be important factors involved in this carcinogenesis process.

Health risks of dietary intake of environmental pollutants by elite sportsmen and sportswomen.

The dietary intake of arsenic (As), cadmium (Cd), mercury (Hg), lead (Pb), hexachlorobenzene (HCB), polychlorinated naphthalenes (PCNs), polycyclic aromatic hydrocarbons (PAHs), polychlorinated diphenyl ethers (PCDEs), polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), and polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) by elite sportsmen and sportswomen of Catalonia, Spain, was assessed. In 2000, food samples were randomly acquired in various cities of Catalonia. Analysis of the above pollutants were determined according to the appropriate analytical techniques (ICP-MS, HRGC/HRMS, HPLC). In general terms, elite sportsmen and sportswomen showed a higher intake of Cd, Hg, Pb, HCB, PCNs, PCDD/Fs and PAHs than the general population, while it was lower for PCDEs (both sexes), and PCBs and PBDEs (women). According to the FAO/WHO provisional tolerable weekly intake (PTWI) for metals, the WHO tolerable daily intake (TDI) for HCB, and the US EPA's reference dose (RfD) for PAHs, the dietary intakes of environmental pollutants should not mean a potential toxic hazard. However, the WHO-TDI for PCDD/Fs and "dioxin-like" PCBs is exceeded in sportsmen. The current results indicate that the consumption of those food groups showing the highest contribution to the intake of these pollutants should be diminished. In relation to this, the reduction of the consumption of dairy products and cereals would be important.

Placental effects of lead in mice.

Although a number of studies in animal models have shown embryolethal and teratogenic lead effects when this element is administered by a parenteral route, the mechanism of the embryonary changes is well not established. In this study, the embryonic effects of parenteral lead exposure on day 9 of gestation were assessed in the Swiss mouse. Lead acetate trihydrate was injected intraperitoneally at 14, 28, 56 and 112 mg/kg. There was no maternal toxicity evidenced by death, reduced body weight gain or reduced food consumption. However, absolute placental weight at 112 mg/kg and relative placental weight at 14, 56 and 112 mg/kg were diminished significantly. The number of total implants, live and dead fetuses, sex ratio and fetal body weight were unaffected by lead exposure. Most sections of placenta showed vascular congestion, an increase of intracellular spaces and deposits of hyaline material of perivascular predominance. Trophoblast hyperplasia was also observed, whereas there was a reinforcement of the fibrovascular network in the labyrinth. It is concluded that the trophoblast hyperplasia observed in the placenta of pregnant mice after parenteral lead exposure at doses that are not toxic for the dam could act as a repairing mechanism of the extraembryonary tissues.

Concurrent administration of D-penicillamine and zinc has no advantages over the use of either single agent on copper excretion in the rat.

The present study was conducted to examine in rats whether the combined use of D-penicillamine (DPA) and a zinc salt, or the administration of a DPA/Zn complex could have some advantages over the use of either single agent on the excretion of copper. In a first experiment, three groups of adult male Sprague Dawley rats were given by gavage one of the following treatments for 5 days: 0.5 mmol/kg/day of DPA, 0.046 mmol/kg/day of zinc acetate dihydrate, and 0.5 mmol/kg/day of DPA plus 0.046 mmol/kg/day of zinc acetate dihydrate. A fourth group of rats (control group) received deionized water during the same period. An increase in the urinary excretion of copper was observed following DPA treatment, which continued for at least 5 days after the administration of this compound was stopped. The amount of copper present in the feces, including that in the diet, was approximately 60 times greater than that normally present in control urines. During the period of zinc acetate administration, the amount of copper in the feces was slightly, but significantly greater than that during control, D-penicillamine, or D-penicillamine plus zinc acetate administration. No differences between the treated groups and the control group were found in brain, liver, kidney and spleen concentrations of rats 5 days after the end of the treatment period. In a second experiment, a similar comparison between D-penicillamine and sodium bis(3-mercapto-D-valinato)zinc hexahydrate (Na2[Zn(DPA)2] x 6H2O), both given by gavage, also showed no significant differences in the urinary excretion of copper in rats.

Effectiveness of sodium 4,5-dihydroxybenzene-1,3-disulfonate (Tiron) in protecting against uranium-induced developmental toxicity in mice.

The effect of Tiron (sodium 4,5-dihydroxybenzene-1,3-disulfonate), a chelating agent used in the treatment of experimental poisoning by a number of heavy metals, on uranium-induced developmental toxicity was evaluated in Swiss mice. A series of four Tiron injections was administered intraperitoneally to pregnant mice immediately after a single subcutaneous injection of 4 mg/kg of uranyl acetate dihydrate given on day 10 of gestation and at 24, 48, and 72 h thereafter. Controls received 0.9% saline with or without uranyl acetate. Tiron effectiveness was assessed at 500, 1000 and 1500 mg/kg per day. Amelioration by Tiron of uranium-induced embryolethality was not noted at the two lower doses. The percentage of dead and resorbed fetuses in the Tiron-treated groups was not statistically different from that in the positive control group. However, treatment at 1500 mg/kg per day showed isolated protective effects against uranium fetotoxicity, such as that evidenced by the lack of differences in fetal body weight between this group and the uranium-untreated group, as well as by a decrease in the number of skeletal defects. According to these results, the ability of Tiron to protect the developing mouse fetus against uranium-induced developmental toxicity offers only modest encouragement with regard to its possible therapeutic potential for pregnant women exposed to this metal.

Chelating agents in the treatment of acute vanadyl sulphate intoxication in mice.

Eighteen chelating or reducing agents were tested to determine their relative efficacy as antagonists in acute intramuscular vanadyl sulphate intoxication in mice. The chelating or reducing agents were administered intraperitoneally to male Swiss mice at doses equal to one-fourth of their respective LD50. Therapeutic effectiveness (TEF) was calculated. In a subsequent experiment, the effect of EDTA, glutathione, DFOA, ascorbic acid, succinic acid, monosodium phosphate, Tiron, DTPA, and 2-mercaptosuccinic acid on the excretion, and distribution of vanadium was determined. Of the compounds examined, Tiron followed by ascorbic acid, and 2-mercaptosuccinic acid were effective in increasing the urinary excretion of vanadium. Tiron, and 2-mercaptosuccinic acid were also effective in reducing the concentration of vanadium found in kidney, the main target organ of vanadium accumulation. Tiron appears to be the most effective agent of those tested in the prevention of acute vanadium (IV) intoxication in mice.

The developmental toxicity of uranium in mice.

To evaluate the developmental toxicity of uranium, 5 groups of 20 pregnant Swiss mice were given by gavage daily doses of 0, 5, 10, 25 and 50 mg/kg of uranyl acetate dihydrate on gestational days 6-15. Cesarean sections were performed on all females on gestation day 18. Fetuses were examined for external, visceral, and skeletal abnormalities. The results indicated that such exposure resulted in maternal toxicity as evidenced by reduced weight gain and food consumption during treatment, and increased relative liver weight. There were no treatment-related effects on the number of implantation sites per dam, or on the incidence of postimplantation loss (resorptions plus dead fetuses). The number of live fetuses per litter and the fetal sex ratio were not affected by the treatment. However, dose-related fetal toxicity, consisting primarily of reduced fetal body weight and body length, and an increased incidence of abnormalities was observed. Malformations (cleft palate, bipartite sternebrae) and developmental variations (reduced ossification and unossified skeletal variations) were noted at the 25 and 50 mg/kg per day test levels. Therefore, administration of uranyl acetate dihydrate during organogenesis in mice produced maternal toxicity at 5, 10, 25 and 50 mg/kg per day. The "no observable effect level" (NOEL) for fetotoxicity including teratogenicity was below 5 mg/kg per day, as some anomalies were observed at this dose. There was no evidence of embryolethality at any dosage level used in this study.

Reproductive toxicity evaluation of vanadium in male mice.

The reproductive toxicity of vanadium was studied in mice. Male Swiss mice were exposed to sodium metavanadate at doses of 0, 20, 40, 60, and 80 mg/kg per day given in the drinking water for 64 days. To evaluate the fertility of the vanadium-treated animals, males were mated with untreated females for 4 days. A significant decrease in the pregnancy rate was observed at 60 and 80 mg/kg per day of sodium. metavanadate. However, metavanadate did not reduce fertility in male mice at 20 and 40 mg/kg per day. Reproductive toxicity was measured by sperm count, sperm motility, organ weights, and histologic evaluation of the testes. Decreased body and epididymis weight was only observed in the 80 mg/kg per day group, while testicular weights were not altered by the treatment with all doses used. Sperm count was significantly decreased at 40, 60, and 80 mg/kg per day, but the sperm motility was unaffected. Histopathological examination revealed that the testes were normal and that the epididymis of treated male mice contained normal appearing sperm. The no observed adverse effect level (NOAEL) was 40 mg/kg per day. Consequently, vanadium would not cause any adverse effect on fertility or testicular function in male mice at the concentrations usually ingested by humans through the diet and drinking water.

Vanadium treatment of diabetic Sprague-Dawley rats results in tissue vanadium accumulation and pro-oxidant effects.

The effect of sodium metavanadate (NaVO3) consumption on trace element metabolism, components of the antioxidant defense system and lipid oxidative damage were studied in control (CON) and streptozotocin-induced diabetic (DIAB) rats. Ten days after injection, CON and DIAB rats received either 0 mM NaVO3/80 mM NaCl (0 group) or 1.2 mM NaVO3/80 mM NaCl (1.2V group) in their drinking water. DIAB groups had higher food and fluid intakes than the CON groups; vanadium (V) groups had lower food and fluid intakes than the saline groups. Vanadium therapy lowered plasma glucose concentrations of DIAB rats. The following parameters were similar among the groups: plasma Zn, Cu and Fe concentrations, plasma ceruloplasmin activity, liver Zn, Cu, Mn and Fe concentrations, kidney Mn and Fe concentrations, liver non-Se-dependent glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Red) and Mn-SOD activities, liver reduced glutathione (GSH) and oxidized glutathione (GSSG) concentrations and kidney non-Se-dependent GSH-Px activity. Kidney Zn and Cu concentrations were higher in DIAB rats than in CON rats. The CON-1.2V and DIAB-1.2V groups had V accumulation in the liver and kidney. Liver CuZn-SOD and Se-dependent GSH-Px and kidney CuZn-SOD and GSH-Red activities were lower in DIAB rats compared to CON rats; kidney Mn-SOD and kidney Se-dependent GSH-Px activities were higher in DIAB rats than CON rats. Vanadium treatment did not cause significant alterations in the antioxidant defense system; however, tissue vanadium concentrations were positively correlated to TBARS production. These results show that diabetes caused significant alterations in the antioxidant defense system and that V therapy was associated with a marked deterioration in health of both control and diabetic rats.

Meso-2,3-dimercaptosuccinic acid (DMSA) affects maternal and fetal copper metabolism in Swiss mice.

Meso-2,3-dimercaptosuccinic acid (DMSA) is a chelating agent used to treat heavy metal intoxication. DMSA has been reported to be teratogenic in the mouse, and it has been suggested that this teratogenicity may be secondary to DMSA-induced alterations in Zn metabolism. In the present study, 0, 400 or 800 mg DMSA/kg body weight were administered on gestation days 6-15 to pregnant Swiss mice by gavage (PO) or subcutaneous injection (SC). Mice were fed a diet containing 14 micrograms Zn, 10 micrograms Cu, 120 micrograms Fe, 1175 micrograms Mg and 6.8 mg Ca/g diet. A sub-group of mice in the 800 mg DMSA/kg SC group was fed a diet containing 250 micrograms Zn/g. DMSA administration did not result in overt maternal toxicity. There was no effect of the drug on fetal or placental weight, or on crown-rump length. However, some fetuses from DMSA-treated dams were characterized by skeletal abnormalities including supernumerary ribs, unossified anterior phalanges and malformed sternebrae. Drug exposure was not associated with consistent changes in tissue Zn, Fe, Ca or Mg levels. Supplemental Zn had no marked effects on the fetus. Fetal liver Cu concentrations exhibited dose-dependent decreases with increasing DMSA dose. This finding suggests that the developmental toxicity of DMSA may be mediated through disturbed maternal/fetal copper metabolism.

The effect of age on aluminum retention in rats.

The present study was designed to assess potential changes in aluminum (Al) retention during advanced age. Young (21 day old), adult (8 months), and old (16 months) rats were exposed to 0, 50, and 100 mg Al/kg/day administered as aluminum nitrate in drinking water for a period of 6.5 months. Urinary Al levels were measured after 3 and 6.5 months of Al exposure. Organ weights and tissue Al concentrations were examined at 6.5 months of Al administration. Differences in the tissue accumulation of Al with age included higher liver, kidneys, spleen, bone and testes levels in old rats than in tissues of both young or adult animals. In contrast, brain concentrations were higher in young rats. Urinary Al levels of young, adult or old Al-exposed rats showed different trends at 6.5 months of Al exposure: compared with young values adult values declined, while those of old rats tended to increase further. The current results show that tissue Al retention patterns may be significantly altered depending on the age at Al exposure. This finding may be of concern for future investigations on the potential role of Al in certain neurological disorders.

Chelation therapy in aluminum-loaded rats: influence of age.

The influence of age at which aluminum (Al) exposure was initiated on the efficacy of chelation therapy in mobilizing Al was investigated in two groups of male rats exposed to this element at two different stages of the life cycle. Young (21 days old) and old (18 months) rats were exposed to 0 and 50 mg Al/kg/day administered as Al nitrate in drinking water for a preliminary period of 14 days followed by a period of 100 days, in which Al-exposed animals received 100 mg Al/kg/day. At the end of the period of exposure, Al-loaded rats in each age group were given one of the following treatments: s.c. deferoxamine (DFO), oral 1,2-dimethyl-3-hydroxypyrid-4-one (L1) and 1-(p-methylbenzyl)-2-ethyl-3-hydroxypyrid-4-one (MeBzEM) at doses of 0.89 mmol/kg/day for 5 consecutive days. Another group of Al-exposed rats received a concurrent administration of s.c. DFO and oral L1 both at 0.45 mmol/kg/day. During chelation therapy urines were collected daily. Control groups included rats exposed and unexposed to Al. Oral administration of L1 was the most effective treatment in enhancing urinary Al excretion in both age groups of Al-loaded rats. This beneficial effect was similar for old and young animals. Concurrent administration of DFO and L1 had no advantages over the use of either single agent, while MeBzEM was not effective in mobilizing Al from Al-exposed rats.

Comparative aluminum mobilizing actions of deferoxamine and four 3-hydroxypyrid-4-ones in aluminum-loaded rats.

The efficacy of the Al chelating drugs deferoxamine (DFO) and the hydoxypyridones (HPs): 1,2-dimethyl-3-hydroxypyrid-4-one (L1), 1-[3-hydroxy-2-methyl-4-oxopyridyl]-2-ethanesulfonic acid (L6), 1-benzyl-(4-carboxylic acid)-3-hydroxy-2-methyl-4-oxopyridine (Bzcal) and 1-(p-methylbenzyl)-2-ethyl-3-hydroxypyrid-4-one (MeBzEM) in increasing Al excretion and reducing tissue Al accumulation has been compared in adult male rats which had previously received Al nitrate nonahydrate i.p. at 0.16 mmol/kg per day for 2 months. At the end of this period, DFO was injected s.c. and the HPs were given by gavage at 0.89 mmol/kg per day for five consecutive days. Total urines were collected 24 h after each chelator administration. Following chelation treatment animals were killed and samples of brain, bone, liver, kidney, and spleen were collected. DFO administration increased to about 4 x the cumulative urinary Al elimination for 5 days, while the excretion of Al into urine caused by Bzcal, L1, and MeBzEM administration was about twice that of the control group. On the other hand, treatment with Bzcal, DFO, and MeBzEM for 5 days significantly reduced the Al levels in bone by 31, 33, and 29%, and the Al concentrations in brain by 46, 69, and 71%, respectively. These results suggest that oral administrations of MeBzEM and Bzcal can be potential alternatives to parenteral administration of DFO in Al removal.