Two-wavelength excitation spectroscopy for non-invasive detection of the iron deficiency indicator zinc protoporphyrin IX

2021 ◽  
Author(s):  
Herbert Stepp ◽  
Christian Homann ◽  
Georg Hennig ◽  
Michael Vogeser
Keyword(s):  
Iron Deficiency ◽  
Protoporphyrin Ix ◽  
Zinc Protoporphyrin ◽  
Non Invasive

The Ratio of Erythrocyte Zinc-Protoporphyrin to Protoporphyrin IX in Disease and its Significance in the Mechanism of Lead Toxicity on Haem Synthesis

1998 ◽  
Vol 35 (3) ◽  
pp. 422-426 ◽  
Author(s):  
Joanna C Nelson ◽  
Marie Westwood ◽  
K R Allen ◽  
K E Newton ◽  
J H Barth
Keyword(s):  
Iron Deficiency ◽  
Protoporphyrin Ix ◽  
Lead Toxicity ◽  
Normal Subjects ◽  
Zinc Protoporphyrin ◽  
Mechanism Of Formation ◽  
Erythropoietic Protoporphyria ◽  
Iron Deficient ◽  
Significant Difference ◽  
Exposed Workers

Protoporphyrin and zinc-protoporphyrin were measured in the erythrocytes of normal subjects, workers exposed to lead and patients with iron deficiency and erythropoietic protoporphyria (EPP). Results showed significantly higher levels of zinc-protoporphyrin in the lead-exposed workers ( P < 0·0001), patients with iron deficiency ( P < 0·0001) and EPP patients ( P < 0·001) compared with normal subjects. The lead-exposed workers showed the highest levels of zinc-protoporphyrin, which were significantly greater than both the iron-deficient and EPP patients ( P < 0·0001). They also showed a higher ratio of zinc-protoporphyrin to free protoporphyrin compared with normal subjects ( P < 0·0001) but no significant difference in this ratio was found when compared with iron-deficient patients ( P = 0·1). These results are discussed in light of the controversy concerning the mechanism of formation of zinc-protoporphyrin in lead exposure.

scholarly journals Non-invasive detection of iron deficiency by fluorescence measurement of erythrocyte zinc protoporphyrin in the lip

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Georg Hennig ◽  
Christian Homann ◽  
Ilknur Teksan ◽  
Uwe Hasbargen ◽  
Stephan Hasmüller ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Zinc Protoporphyrin ◽  
Fluorescence Measurement ◽  
Non Invasive

scholarly journals Prenatal Iron Deficiency and Replete Iron Status Are Associated with Adverse Birth Outcomes, but Associations Differ in Ghana and Malawi

2019 ◽  
Vol 149 (3) ◽  
pp. 513-521 ◽  
Author(s):  
Brietta M Oaks ◽  
Josh M Jorgensen ◽  
Lacey M Baldiviez ◽  
Seth Adu-Afarwuah ◽  
Ken Maleta ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Birth Outcomes ◽  
Regression Models ◽  
Iron Status ◽  
Secondary Data ◽  
Hemoglobin Concentration ◽  
Late Pregnancy ◽  
Zinc Protoporphyrin ◽  
Adverse Birth Outcomes ◽  
Soluble Transferrin Receptor

ABSTRACTBackgroundPrevious literature suggests a U-shaped relation between hemoglobin concentration and adverse birth outcomes. There is less evidence on associations between iron status and birth outcomes.ObjectiveOur objective was to determine the associations of maternal hemoglobin concentration and iron status with birth outcomes.MethodsWe conducted a secondary data analysis of data from 2 cohorts of pregnant women receiving iron-containing nutritional supplements (20–60 mg ferrous sulfate) in Ghana (n = 1137) and Malawi (n = 1243). Hemoglobin concentration and 2 markers of iron status [zinc protoporphyrin and soluble transferrin receptor (sTfR)] were measured at ≤20 weeks and 36 weeks of gestation. We used linear and Poisson regression models and birth outcomes included preterm birth (PTB), newborn stunting, low birth weight (LBW), and small-for-gestational-age.ResultsPrevalence of iron deficiency (sTfR >6.0 mg/L) at enrollment was 9% in Ghana and 20% in Malawi. In early pregnancy, iron deficiency was associated with PTB (9% compared with 17%, adjusted RR: 1.63; 95% CI: 1.14, 2.33) and stunting (15% compared with 23%, adjusted RR: 1.44; 95% CI: 1.09, 1.94) in Malawi but not Ghana, and was not associated with LBW in either country; replete iron status (sTfR <10th percentile) was associated with stunting (9% compared with 15%, adjusted RR: 1.71; 95% CI: 1.06, 2.77) in Ghana, but not PTB or LBW, and was not associated with any birth outcomes in Malawi. In late pregnancy, iron deficiency was not related to birth outcomes in either country and iron-replete status was associated with higher risk of LBW (8% compared with 16%, adjusted RR: 1.90; 95% CI: 1.17, 3.09) and stunting (6% compared with 13%, adjusted RR: 2.14; 95% CI: 1.21, 3.77) in Ghana, but was not associated with birth outcomes in Malawi.ConclusionsThe associations of low or replete iron status with birth outcomes are population specific. Research to replicate and extend these findings would be beneficial. These trials were registered at clinicaltrials.gov as NCT00970866 (Ghana) and NCT01239693 (Malawi).

Detection of iron-deficiency anemia in hospitalized patients by zinc protoporphyrin

1996 ◽  
Vol 244 (1) ◽  
pp. 91-101 ◽  
Author(s):  
Shan S. WongA ◽  
Ala S. Qutishat ◽  
Jason Lange ◽  
Terrie G. Gornet ◽  
L. Maximilian Buja
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Hospitalized Patients ◽  
Deficiency Anemia ◽  
Zinc Protoporphyrin

scholarly journals Influence of meat source, pH and production time on zinc protoporphyrin IX formation as natural colouring agent in nitrite-free dry fermented sausages

Meat Science ◽  
2018 ◽  
Vol 135 ◽  
pp. 46-53 ◽  
Author(s):  
Hannelore De Maere ◽  
Sylvie Chollet ◽  
Jos De Brabanter ◽  
Chris Michiels ◽  
Hubert Paelinck ◽  
...  
Keyword(s):  
Protoporphyrin Ix ◽  
Zinc Protoporphyrin ◽  
Production Time ◽  
Fermented Sausages ◽  
Dry Fermented Sausages

scholarly journals Zinc Protoporphyrin/Heme Ratios (ZnPP/H) as a Potential Newborn Screen for Iron Deficiency.

2010 ◽  
Vol 83 (Suppl_1) ◽  
pp. 585-585
Author(s):  
Steven Marmer ◽  
Melinda Chen ◽  
Beth Fischer ◽  
Vidya Sridhar ◽  
Sharon Blohowiak ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Zinc Protoporphyrin ◽  
Newborn Screen

scholarly journals Recognized and Emerging Features of Erythropoietic and X-Linked Protoporphyria

Diagnostics ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 151
Author(s):  
Elena Di Pierro ◽  
Francesca Granata ◽  
Michele De Canio ◽  
Mariateresa Rossi ◽  
Andrea Ricci ◽  
...  
Keyword(s):  
Biosynthetic Pathway ◽  
Aminolevulinic Acid ◽  
Protoporphyrin Ix ◽  
Limiting Factor ◽  
Zinc Protoporphyrin ◽  
Complete Understanding ◽  
Inherited Disorders ◽  
Rate Limiting ◽  
Systemic Accumulation ◽  
Made In

Erythropoietic protoporphyria (EPP) and X-linked protoporphyria (XLP) are inherited disorders resulting from defects in two different enzymes of the heme biosynthetic pathway, i.e., ferrochelatase (FECH) and delta-aminolevulinic acid synthase-2 (ALAS2), respectively. The ubiquitous FECH catalyzes the insertion of iron into the protoporphyrin ring to generate the final product, heme. After hemoglobinization, FECH can utilize other metals like zinc to bind the remainder of the protoporphyrin molecules, leading to the formation of zinc protoporphyrin. Therefore, FECH deficiency in EPP limits the formation of both heme and zinc protoporphyrin molecules. The erythroid-specific ALAS2 catalyses the synthesis of delta-aminolevulinic acid (ALA), from the union of glycine and succinyl-coenzyme A, in the first step of the pathway in the erythron. In XLP, ALAS2 activity increases, resulting in the amplified formation of ALA, and iron becomes the rate-limiting factor for heme synthesis in the erythroid tissue. Both EPP and XLP lead to the systemic accumulation of protoporphyrin IX (PPIX) in blood, erythrocytes, and tissues causing the major symptom of cutaneous photosensitivity and several other less recognized signs that need to be considered. Although significant advances have been made in our understanding of EPP and XLP in recent years, a complete understanding of the factors governing the variability in clinical expression and the severity (progression) of the disease remains elusive. The present review provides an overview of both well-established facts and the latest findings regarding these rare diseases.

scholarly journals Inhaled carbon monoxide does not cause pulmonary vasodilation in the late-gestation fetal lamb

2000 ◽  
Vol 278 (4) ◽  
pp. L779-L784 ◽  
Author(s):  
Theresa R. Grover ◽  
Robyn L. Rairigh ◽  
Jeanne P. Zenge ◽  
Steven H. Abman ◽  
John P. Kinsella
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
Vascular Tone ◽  
Ductus Arteriosus ◽  
Protoporphyrin Ix ◽  
Left Lung ◽  
Late Gestation ◽  
Zinc Protoporphyrin ◽  
Pulmonary Vasodilation

As observed with nitric oxide (NO), carbon monoxide (CO) binds and may activate soluble guanylate cyclase and increase cGMP levels in smooth muscle cells in vitro. Because inhaled NO (INO) causes potent and sustained pulmonary vasodilation, we hypothesized that inhaled CO (ICO) may have similar effects on the perinatal lung. To determine whether ICOcan lower pulmonary vascular resistance (PVR) during the perinatal period, we studied the effects of ICOon late-gestation fetal lambs. Catheters were placed in the main pulmonary artery, left pulmonary artery (LPA), aorta, and left atrium to measure pressure. An ultrasonic flow transducer was placed on the LPA to measure blood flow to the left lung. After baseline measurements, fetal lambs were mechanically ventilated with a hypoxic gas mixture (inspired O2fraction < 0.10) to maintain a constant fetal arterial [Formula: see text]. After 60 min (baseline), the lambs were treated with ICO[5–2,500 parts/million (ppm)]. Comparisons were made with INO(5 and 20 ppm) and combined INO(5 ppm) and ICO(100 and 2,500 ppm). We found that ICOdid not alter left lung blood flow or PVR at any of the study doses. In contrast, low-dose INOdecreased PVR by 47% ( P < 0.005). The combination of INOand ICOdid not enhance the vasodilator response to INO. To determine whether endogenous CO contributes to vascular tone in the fetal lung, zinc protoporphyrin IX, an inhibitor of heme oxygenase, was infused into the LPA in three lambs. Zinc protoporphyrin IX had no effect on baseline PVR, aortic pressure, or the pressure gradient across the ductus arteriosus. We conclude that ICOdoes not cause vasodilation in the near-term ovine transitional circulation, and endogenous CO does not contribute significantly to baseline pulmonary vascular tone or ductus arteriosus tone in the late-gestation ovine fetus.

NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

2004 ◽  
Vol 286 (1) ◽  
pp. R94-R100 ◽  
Author(s):  
Zonghai Ruan ◽  
Toshishige Shibamoto ◽  
Tomohiro Shimo ◽  
Hideaki Tsuchida ◽  
Tomonobu Koizumi ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Protoporphyrin Ix ◽  
Fold Increase ◽  
Liver Weight ◽  
Zinc Protoporphyrin ◽  
Hepatic Congestion ◽  
Occlusion Technique ◽  
Venous Resistance ◽  
Synthase Inhibitor ◽  
Guinea Pig Liver

The pathophysiology of the hepatic vascular response to anaphylaxis in guinea pig is not known. We studied effects of anaphylaxis on hepatic vascular resistances and liver weight in isolated perfused livers derived from guinea pigs sensitized with ovalbumin. We also determined whether nitric oxide (NO) or carbon monoxide (CO) modulates the hepatic anaphylaxis. The livers were perfused portally and recirculatingly at constant flow with diluted blood. With the use of the double-occlusion technique to estimate the hepatic sinusoidal pressure (Pdo), portal venous resistance (Rpv) and hepatic venous resistance (Rhv) were calculated. An antigen injection caused venoconstriction characterized by an increase in Rpv greater than Rhv and was accompanied by a large liver weight gain. Pretreatment with the NO synthase inhibitor NG-nitro-l-arginine methyl ester, but not the heme oxygenase inhibitor zinc protoporphyrin IX, potentiated the antigen-induced venoconstriction by increasing both Rpv and Rhv (2.2- and 1.2-fold increase, respectively). In conclusion, anaphylaxis causes both pre- and postsinusoidal constriction in isolated guinea pig livers. However, the increases in postsinusoidal resistance and Pdo cause hepatic congestion. Endogenously produced NO, but not CO, modulates these responses.

scholarly journals A Novel Mechanism for NF-κB-activation via IκB-aggregation: Implications for Hepatic Mallory-Denk-Body Induced Inflammation

2020 ◽  
Vol 19 (12) ◽  
pp. 1968-1985
Author(s):  
Yi Liu ◽  
Michael J. Trnka ◽  
Shenheng Guan ◽  
Doyoung Kwon ◽  
Do-Hyung Kim ◽  
...  
Keyword(s):  
Protein Aggregation ◽  
Nuclear Import ◽  
Cell Model ◽  
Protoporphyrin Ix ◽  
Zinc Protoporphyrin ◽  
Primary Hepatocytes ◽  
Protein Aggregate ◽  
Nuclear Entry ◽  
Antibody Recognition ◽  
Bona Fide

Mallory-Denk-bodies (MDBs) are hepatic protein aggregates associated with inflammation both clinically and in MDB-inducing models. Similar protein aggregation in neurodegenerative diseases also triggers inflammation and NF-κB activation. However, the precise mechanism that links protein aggregation to NF-κB-activation and inflammatory response remains unclear. Herein we find that treating primary hepatocytes with MDB-inducing agents (N-methylprotoporphyrin (NMPP), protoporphyrin IX (PPIX), or Zinc-protoporphyrin IX (ZnPP)) elicited an IκBα-loss with consequent NF-κB activation. Four known mechanisms of IκBα-loss i.e. the canonical ubiquitin-dependent proteasomal degradation (UPD), autophagic-lysosomal degradation, calpain degradation and translational inhibition, were all probed and excluded. Immunofluorescence analyses of ZnPP-treated cells coupled with 8 M urea/CHAPS-extraction revealed that this IκBα-loss was due to its sequestration along with IκBβ into insoluble aggregates, thereby releasing NF-κB. Through affinity pulldown, proximity biotinylation by antibody recognition, and other proteomic analyses, we verified that NF-κB subunit p65, which stably interacts with IκBα under normal conditions, no longer binds to it upon ZnPP-treatment. Additionally, we identified 10 proteins that interact with IκBα under baseline conditions, aggregate upon ZnPP-treatment, and maintain the interaction with IκBα after ZnPP-treatment, either by cosequestering into insoluble aggregates or through a different mechanism. Of these 10 proteins, the nucleoporins Nup153 and Nup358/RanBP2 were identified through RNA-interference, as mediators of IκBα-nuclear import. The concurrent aggregation of IκBα, NUP153, and RanBP2 upon ZnPP-treatment, synergistically precluded the nuclear entry of IκBα and its consequent binding and termination of NF-κB activation. This novel mechanism may account for the protein aggregate-induced inflammation observed in liver diseases, thus identifying novel targets for therapeutic intervention. Because of inherent commonalities this MDB cell model is a bona fide protoporphyric model, making these findings equally relevant to the liver inflammation associated with clinical protoporphyria.

Sign in / Sign up

Export Citation Format

Share Document