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FISIOLOGIA DEL ERITROCITO

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Ann Hematol 100, 2425–2433 (2021).

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Membrana del eritrocito

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Handbook of Materials Modeling, 2020

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La miosina II participa en el mantenimiento de la forma biconcava y deformabilidad de los hematies.

10.1073/pnas.1718285115

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Metabolismo del

eritrocito

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Metabolismo del

eritrocito

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DISTRIBUCIÓN DEL HIERRO

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Metabolismo del Hierro y Eritropoyesis

Regulación de la Hepcidina

Niveles de hierro
Eritropoyesis
Inflamación

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Sistema de regulación IRP/IRE

Cell. 2004;117(3):285-97.

and HIF2α

and DMT1

Proteins involved in iron storage, erythroid heme synthesis, the TCA cycle, iron export,

and iron uptake are coordinately regulated bythe interaction of the iron regulatory proteins

(IRPs) with conserved RNA secondary structures, the iron-responsive elements (IREs).

The binding of IRPs to single IREs in the 5-untranslated regions (UTRs) of mRNAs

blocks their translation, while IRP binding tomultiple IREs in the 3 UTR stabilizes the

TfR-1 mRNA. IRPs exist in two isoforms, IRP1and IRP2. Increased iron levels favor the

conversion of IRP1 from its active RNA binding form into an Fe-S cluster containing cytoplasmic

aconitase that lacks IRE binding activity as well as the proteasomal degradation

of IRP2. Low iron levels or the action of NO promote accumulation of the active apoprotein form of

IRP1 and stabilize IRP2. In contrast, H2O2 only activates IRP1, while hypoxia

interferes with IRP2 degradation.

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N Engl J Med 2017;377:862-72

Pb

Ojo: Pb, Hexachlorobenzeno, diazinona, dioxina, y arsenico

Metabolismo del Grupo hemo

Siglo XII a XV

1897

The porphyrias are disorders of heme synthesis, which has eight steps (Fig. 1).

Each type of porphyria involves a defect, either inherited or acquired, in a pathway

enzyme. When the defect is physiologically significant, it results in overproduction

of pathway precursors preceding the defective step which enter the circulation and

are excreted into urine or bile. The diseases have been grouped as acute hepatic

porphyrias and photocutaneous porphyrias. The acute porphyrias are due to hepatic

overproduction of the porphyrin precursors, delta aminolevulinic acid and

porphobilinogen, and the symptoms are caused by injury primarily to the nervous

system. Cutaneous porphyria is due to overproduction of photosensitizing porphyrins

by the liver or bone marrow, depending on the type of porphyria.

Acute intermittent porphyria is the acute type most often encountered in clinical

practice.1,2 The most prevalent cutaneous porphyrias are porphyria cutanea tarda

and protoporphyria (Table 1). Hereditary coproporphyria and variegate porphyria

are acute forms in which attacks are much less frequent than in acute intermittent

porphyria, but photocutaneous disease (similar to porphyria cutanea tarda) can

occur. Acute flares are managed as they are in acute intermittent porphyria. Delta

aminolevulinic acid dehydratase deficiency and uroporphyrinogen-III synthase

deficiency (in congenital erythropoietic porphyria)3,4 are very rare and will not be

discussed

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Metabolismo de la Bilirrubina

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Preguntas...