Ferene-S as the chromogen for serum iron determinations

Eskelinen, Sakari; Haikonen, Matti; Räisänen, Simo

doi:10.3109/00365518309168286

Cited by 27 publications

(22 citation statements)

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“…Ferene-S is a chromogenic chelator that has been previously used to measure`loosely' bound and therefore potentially redox-active Fe in biological samples (Artiss et al, 1981;Eskelinen et al, 1983;Qian et al, 1998). We found that on average, homogenized cataractous human lenses contained 2 .…”

Section: Detection Of Lenticular Fe By Ferene-s Chelationmentioning

confidence: 90%

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Distribution of Ferritin and Redox-active Transition Metals in Normal and Cataractous Human Lenses

Garner

Roberg

Qian

et al. 2000

Experimental Eye Research

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Section: Detection Of Lenticular Fe By Ferene-s Chelationmentioning

confidence: 90%

“…Chelatable Fe, which represents a potentially redoxactive pool, was analysed using the chromogenic chelator, Ferene-S (Artiss, Vinogradov and Zak, 1981;Eskelinen, Haikonen and Ra Èisa Ènen, 1983;Qian, Liu and Eaton, 1998). This assay does not detect tightly bound Fe, e.g.…”

Section: Ferene-s Assay For Chelatable Fementioning

confidence: 99%

Distribution of Ferritin and Redox-active Transition Metals in Normal and Cataractous Human Lenses

Garner

Roberg

Qian

et al. 2000

Experimental Eye Research

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“…Following centrifugation, the supernatant was diluted with 5 volumes of water and then analyzed by AAS. To confirm the validity of the TCA method, selected plasma samples were also analyzed for iron using Ferene-S, a spectrophotometric method (Eskelinen et al, 1983).…”

Section: Biochemical Analysesmentioning

confidence: 99%

Copper deficient rats and mice both develop anemia but only rats have lower plasma and brain iron levels

Pyatskowit

Prohaska

2008

Comparative Biochemistry and Physiology Part C: Toxicology &

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Iron homeostasis depends on adequate dietary copper but the mechanisms are unknown. Mice (Mus musculus) and rat (Rattus norvegicus) offspring were compared to determine the effect of dietary copper deficiency (Cu-) on iron status of plasma, liver, brain and intestine. Holtzman rat and Hsd:ICR (CD-1) outbred albino mouse dams were fed a Cu-diet and drank deionized water or Cu supplemented water. Offspring were sampled at time points between postnatal ages 13 and 32. Curat and mouse pups were both anemic, but only rat pups had lower plasma and brain iron levels. Plasma iron was lower throughout the suckling period in Cu-rats but not Cu-mice. Cu-mice derived from dams restricted of Cu only during lactation were also severely anemic without hypoferremia. Intestinal metal analysis confirmed that Cu-pups had major reductions in intestinal concentration of Cu, increased Fe, and normal Zn. However, whole mouse (less the intestine) analysis demonstrated normal content of Fe indicating that the limitation in iron transport by intestinal hephaestin had no consequence to total iron reserves of the mouse. Further research will be needed to determine the reason Cu-mice were anemic since the "ferroxidase" hypothesis does not explain this phenotype.

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“…Following centrifugation, the supernatant was diluted with five volumes of water and then analyzed by AAS. To confirm the validity of the TCA method, selected plasma samples were also analyzed for iron using Ferene-S, a colorimetric method (Eskelinen et al 1983). …”

Section: Biochemical Analysesmentioning

confidence: 99%

Multiple mechanisms account for lower plasma iron in young copper deficient rats

Pyatskowit

Prohaska

2007

Biometals

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Copper deficiency lowers brain copper and iron during development. The reduced iron content could be due to hypoferremia. Experiments were conducted to evaluate plasma iron and "ferroxidase" hypotheses by determining copper and iron status of Holtzman albino rats following gestational/ lactational copper deficiency. Copper deficient (Cu−) dams on treatment for 5 weeks, two of gestation and three of lactation, had markedly lower copper content of milk and mammary tissue, and lower milk iron. Newborn pups from Cu− dams had lower copper and iron concentrations. Compared to Cu+ pups, Cu− pups, analyzed between postnatal age (P) 0 and P26, were smaller, anemic, had lower plasma iron, cardiac hypertrophy, and near zero ceruloplasmin activity. Liver copper in Cu+ pups increased then decreased during development and major reductions were evident in Cu− pups. Liver iron in Cu+ pups decreased with age while nursing but increased after eating solid food. Liver iron was lower in Cu− pups at P0 and P13 and normal at P20 and P26. Small intestinal copper decreased with age in Cu+ pups and was lower in Cu− pups. Intestinal iron levels in Cu-pups were higher than Cu+ pups postweaning in some experiments. Reduction in plasma iron in Cu− pups is likely due to a decreased "ferroxidase" function leading to lower placental iron transport, a lower milk iron diet, and partial block in iron uptake from intestine but is not due to failure to mobilize hepatic iron, in contrast to older rats eating diet with adequate iron.

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Ferene-S as the chromogen for serum iron determinations

Cited by 27 publications

References 0 publications

Distribution of Ferritin and Redox-active Transition Metals in Normal and Cataractous Human Lenses

Distribution of Ferritin and Redox-active Transition Metals in Normal and Cataractous Human Lenses

Copper deficient rats and mice both develop anemia but only rats have lower plasma and brain iron levels

Multiple mechanisms account for lower plasma iron in young copper deficient rats

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