Abstract Iron is a limiting nutrient for Symbiodiniaceae (colloquially known as zooxanthellae), with low solubility in seawater. The use of stable, soluble, and chemically defined iron complexes is proposed as a strategy to control the supply of this metal to target organisms. In this work, we investigated the effect of iron(II) and derivatives of iron(III) (desferrioxamine, deferiprone, deferasirox, and HBED) over the growth and metal loading of five Symbiodiniaceae species. Iron supplementation did not affect growth or metal load in species with high iron stocks. In contrast, for species with low iron stocks, hydrophobic Fe(DFX)2 was very efficient in inducing growth and iron loading. Also, the desferrioxamine derivative of iron Fe(DFO) appeared as an interesting, ecologically friendly source of the nutrient. The effect of iron supplementation on the growth of Breviolum minutum submitted to heat shock was also studied. Iron supplementation prior to the heat shock episode increased the heat tolerance of B. minutum. Such findings provide new insights for the strategy of iron supplementation to improve the fitness of Symbiodiniaceae, both in vitro and in the environment.

Objetivo: Avaliar o acúmulo de ferro em diferentes órgãos por meio da ressonância nuclear magnética T2* e correlacionar os resultados aos níveis de ferritina sérica, ferro plasmático lábil e outros órgãos envolvidos. Métodos: Foram avaliados retrospectivamente 115 pacientes talassêmicos (sendo 65 mulheres). A concentração hepática de ferro foi determinada em biópsia de 11 pacientes; os resultados foram comparados com os valores de T2* fígado. Resultados: a ferritina sérica média foi de 2.676,5 +/- 2.051,7 ng/mL. O ferro plasmático lábil foi anormal (> 0,6 Unidades/mL) em 48/83 pacientes (57%). A média dos valores de T2* no fígado foi 3,91 ± 3,95 ms, sugerindo siderose hepática em 92,1% pacientes. A média do T2* cardíaco foi de 24,96 ± 14,17 ms e 36% dos pacientes apresentavam siderose cardíaca (T2* < 20ms), dos quais 19% (22/115) já apresentavam sobrecarga cardíaca grave (T2* < 10 ms). A média de T2* no pâncreas foi de 11,12 ± 11,20 ms, perfazendo um total de 83,5% de pacientes com sobrecarga de ferro pancreático (T2* < 21 ms). Houve correlação significativa, curvilínea e inversa entre T2* fígado e a concentração de ferro hepática (r = −0,878; p <0,001) e correlação moderada entre T2* pâncreas e T2* miocárdio (r = 0,546; p <0,0001). Conclusão: Uma elevada taxa de acometimento hepático, pancreático e cardíaco por sobrecarga férrica foi demonstrada. Os níveis de ferritina não puderam prever sobrecarga de ferro hepático, cardíaco ou pancreáticos medidos por meio da ressonância nuclear magnética T2*. Não houve correlação entre a sobrecarga de ferro no fígado, pâncreas e miocárdio, nem entre a ferritina e os níveis plasmáticos de ferro sérico e os valores de T2* no fígado, coração e pâncreas.

ABSTRACT Objectives: To evaluate the use of magnetic resonance imaging in patients with β-thalassemia and to compare T2* magnetic resonance imaging results with serum ferritin levels and the redox active fraction of labile plasma iron. Methods: We have retrospectively evaluated 115 chronically transfused patients (65 women). We tested serum ferritin with chemiluminescence, fraction of labile plasma iron by cellular fluorescence and used T2* MRI to assess iron content in the heart, liver, and pancreas. Hepatic iron concentration was determined in liver biopsies of 11 patients and the results were compared with liver T2* magnetic resonance imaging. Results: The mean serum ferritin was 2,676.5 +/- 2,051.7 ng/mL. A fraction of labile plasma iron was abnormal (> 0,6 Units/mL) in 48/83 patients (57%). The mean liver T2* value was 3.91 ± 3.95 ms, suggesting liver siderosis in most patients (92.1%). The mean myocardial T2* value was 24.96 ± 14.17 ms and the incidence of cardiac siderosis (T2* < 20 ms) was 36%, of which 19% (22/115) were severe cases (T2* < 10 ms). The mean pancreas T2* value was 11.12 ± 11.20 ms, and 83.5% of patients had pancreatic iron deposition (T2* < 21 ms). There was significant curvilinear and inverse correlation between liver T2* magnetic resonance imaging and hepatic iron concentration (r= −0.878; p < 0.001) and moderate correlation between pancreas and myocardial T2* MRI (r = 0.546; p < 0.0001). Conclusion: A high rate of hepatic, pancreatic and cardiac impairment by iron overload was demonstrated. Ferritin levels could not predict liver, heart or pancreas iron overload as measured by T2* magnetic resonance imaging. There was no correlation between liver, pancreas, liver and myocardial iron overload, neither between ferritin and fraction of labile plasma iron with liver, heart and pancreas T2* values

OBJETIVO: Quantificar a porcentagem de ferro lábil redox ativo em farinhas fortificadas adquiridas no comércio popular. MÉTODOS: Amostras de farinha de trigo, fubá e rosca foram extraídas com tampões miméticos de suco gástrico, saliva e suco intestinal. Os níveis de ferro lábil redox ativo foram determinados por meio da reação de auto-oxidação do ácido ascórbico catalisada pelo ferro, em presença de uma sonda fluorimétrica. RESULTADOS: A fração de ferro lábil redox ativo representa entre 1% e 9% do ferro total nas farinhas estudadas, sendo os menores valores encontrados em condições miméticas do suco gástrico e os maiores nos meios mais alcalinos. Há indícios de que o ferro lábil redox ativo origina-se da decomposição de um complexo entre ferro e ácido fítico. Observa-se uma correlação positiva entre ferro lábil redox ativo e ferro total nas condições de salinidade dos fluidos biomiméticos estudados. CONCLUSÃO: Ferro lábil redox ativo pode ser um fator de risco para pacientes atransferrinêmicos, sistemicamente sobrecarregados com ferro (por exemplo, talassêmicos) ou aqueles com defesas antioxidantes comprometidas por enfermidades. A quantidade de ferro total pode ser preditiva dos níveis de ferro lábil redox ativo absorvidos em cada etapa do trato gastrintestinal após a ingestão de farinhas fortificadas.

OBJECTIVE: To quantify the fraction of redox-active labile iron in iron-fortified flours acquired on the Brazilian market. METHODS: Samples of wheat flour, maize flour and breadcrumbs were extracted with buffers that mimic gastric juice, saliva and intestinal juice. Redox-active labile iron levels were assessed through the reaction of autoxidation of ascorbic acid catalyzed by iron in the presence of a fluorescence probe. RESULTS: Redox-active labile iron represents 1% to 9% of the total iron in the flour and breadcrumb samples, with the lowest values found under gastric juice conditions and the highest in the more alkaline media. Redox-active labile iron possibly arises from the decomposition of an iron-phytic acid complex. A positive correlation between redox-active labile iron and total iron was found in saline biomimetic fluids. CONCLUSION: Redox-active labile iron may be a risk factor for people with impaired antioxidant defenses, such as those who are atransferrinemic or iron overloaded (e.g. thalassemic). Total iron can be used to predict redox-active labile iron absorption at each stage of the gastrointestinal tract after ingestion of iron-fortified flours.