scholarly journals The elevation of blood levels of zinc protoporphyrin in mice following whole body irradiation

Blood ◽  
1984 ◽  
Vol 63 (5) ◽  
pp. 1159-1167
Author(s):  
TL Walden ◽  
PS Draganac ◽  
WR Farkas

Elevation of zinc protoporphyrin (ZPP) levels in the blood has served as an indicator of lead poisoning and iron deficiency anemia for many years. We have discovered that sublethal doses of whole body irradiation with x-rays also elevates ZPP 2–3-fold over normal levels. The ZPP level does not begin to increase until days 12–14 postirradiation and peaks between days 18 and 20 before returning to normal levels between days 28 and 35. Increasing the radiation dose delays the onset of the rise in ZPP, but does not affect the magnitude of the elevation. At lethal doses, ZPP elevation is not observed. Neither of the two previously described mechanisms that cause elevations of ZPP, namely iron deficiency and inhibition of ferrochelatase, are responsible for the radiation-induced elevation of ZPP. The elevation of ZPP appears to be correlated with the recovery of the hematopoietic system from radiation injury.

Blood ◽  
1984 ◽  
Vol 63 (5) ◽  
pp. 1159-1167 ◽  
Author(s):  
TL Walden ◽  
PS Draganac ◽  
WR Farkas

Abstract Elevation of zinc protoporphyrin (ZPP) levels in the blood has served as an indicator of lead poisoning and iron deficiency anemia for many years. We have discovered that sublethal doses of whole body irradiation with x-rays also elevates ZPP 2–3-fold over normal levels. The ZPP level does not begin to increase until days 12–14 postirradiation and peaks between days 18 and 20 before returning to normal levels between days 28 and 35. Increasing the radiation dose delays the onset of the rise in ZPP, but does not affect the magnitude of the elevation. At lethal doses, ZPP elevation is not observed. Neither of the two previously described mechanisms that cause elevations of ZPP, namely iron deficiency and inhibition of ferrochelatase, are responsible for the radiation-induced elevation of ZPP. The elevation of ZPP appears to be correlated with the recovery of the hematopoietic system from radiation injury.


2008 ◽  
pp. 753-760
Author(s):  
D Driák ◽  
J Österreicher ◽  
Z Řeháková ◽  
Z Vilasová ◽  
J Vávrová

Gastrointestinal form is the second stage of acute radiation syndrome (ARS) with a threshold dose of 8 Gy in man. It represents an absolutely lethal clinical-pathological unit, necrohemorrhagic enteritis and proctocolitis, with unknown causal therapy. Elk-1 is a protein acting as a transcription factor activating specified genes. The purpose of our study was to examine the expression of phospho-Elk-1 in irradiated jejunum and transversal colon of rats with radiation-induced enterocolitis and to assess the importance of this transcriptional factor as a biodosimetric marker of radiation-induced enteropathy. The laboratory rats were randomly divided into 21 groups, 10 animals per group, and irradiated with whole body γ-irradiation of 1, 5, 10, 15, and 20 Gy. Samples of jejunum and transversal colon were taken 24, 48, 72, and 96 hours later, immunohistochemically stained, and the phospho-Elk-1 expression was examined using computer image analysis. A group of 10 shamirradiated animals was used as control. Significantly increased expression of phospho-Elk-1 in rat jejunum has been found in all time intervals after irradiation by sublethal doses of 1 and 5 Gy, whereas after the irradiation by lethal doses, the expression of phospho-Elk-1 in rat jejunum varied considerably. Significantly increased expression of phospho-Elk-1 in transversal colon has also been found in the first days after irradiation by sublethal doses of 1 and 5 Gy. After irradiation by lethal doses, tere was no uniform pattern of the changes in the expression of phospho-Elk1 in rat transversal colon. The detection of phospho-Elk-1 might be considered as a suitable and very sensitive biodosimetric marker of radiation-induced injury of small and large intestine. According to our knowledge, this is the first study on the phospho-Elk-1 expression in irradiated jejunum and transversal colon in the rat.


1996 ◽  
Vol 244 (1) ◽  
pp. 91-101 ◽  
Author(s):  
Shan S. WongA ◽  
Ala S. Qutishat ◽  
Jason Lange ◽  
Terrie G. Gornet ◽  
L. Maximilian Buja

PEDIATRICS ◽  
1957 ◽  
Vol 20 (5) ◽  
pp. 921-940
Author(s):  
Meinhard Robinow ◽  
Frederic N. Silverman

The different types of injury from external sources of ionizing radiation are briefly described and the manifestations of radiation injury in the fetus, the infant and the child are reviewed. If radiation therapy for malignant disease is excluded from consideration, it is found that x-ray damage to skin, other tissue destruction, and growth impairment are relatively minor radiation hazards compared to the dangers of leukemia and other malignancy and of radiation-induced genetic damage. Consideration is given to somatic radiation injury as largely an individual problem and genetic injury as a population problem. This point of view is reflected in the differing recommendations concerning "permissible doses" for individuals and for populations. Medical radiation represents a major and presumably growing source of exposure to individuals and to the population in the United States. Various ways are shown in which excessive diagnostic exposure to x-rays, especially in children, can be reduced without interference with requirements of diagnosis. Control of avoidable radiation can be accomplished by combined attack from different fronts. The more important approaches to radiation safety are discussed. They include attention to technical detail, personnel monitoring, maintenance of radiation records, radiation safety through legislative control and public education. The responsibility of the physician in promoting public understanding of radiation hazards is emphasized.


2021 ◽  
Vol 8 ◽  
Author(s):  
Shinsuke Nirengi ◽  
Hirokazu Taniguchi ◽  
Aya Ishibashi ◽  
Mami Fujibayashi ◽  
Nao Akiyama ◽  
...  

Background: Hepcidin-25 is a 25 amino acid hepatokine and a key regulator of iron metabolism related to iron deficiency anemia. Recent studies have suggested that an elevated hepcidin level is correlated with low energy availability. Leptin is an appetite-suppressing adipokine and has been reported to stimulate hepcidin production in animals and cultured cells. While leptin is modulated by exercise, it is known that endurance runners and sprinters practice different types of exercise. This study investigated and compared the relationships between hepcidin and leptin levels, iron status, and body fat to understand better the risk of iron deficiency anemia in endurance runners and sprinters.Methods: Thirty-six male college track and field athletes (15 endurance runners and 21 sprinters) were recruited for this study. Dietary intake, body composition, and blood levels of ferritin, hepcidin-25, leptin, and adiponectin were measured. Correlations between hepcidin levels and ferritin, body fat, leptin, and adiponectin were evaluated using Pearson's correlation coefficient for each group.Results: The endurance runners had lower hepcidin levels and higher leptin and adiponectin levels compared with sprinters. Ferritin was positively correlated with hepcidin-25 levels in both the endurance and sprinter groups. A positive correlation was observed between hepcidin-25 and body fat or leptin levels only in sprinters.Conclusion: This is the first study investigating the relationship between blood levels of hepcidin and leptin in athletes. The positive correlation between hepcidin-25 and leptin was observed in sprinters but not endurance runners.


1983 ◽  
Vol 42 (1) ◽  
pp. 29-39 ◽  
Author(s):  
J. F. Loutit ◽  
B. M. Cattanach

SUMMARYA new mutant (Wct) has been identified at the W locus of the mouse. The homozygote is poorly viable. Whereas the heterozygote (Wct / +) is only mildly anaemic like Wυ / +, the double heterozygote Wct + / + Ph is considerably more anaemic than Wυ + / + Ph and it and Wsh + / + Ph have significantly raised leucocyte counts. Wct + / + Ph is also unduly radiosensitive to whole body X-irradiation, 50% dying from haematopoietic failure at a dose of 4·59 ± 0·14 Gy, whereas the median for Wct / + was 6·49 ± 0·28 Gy. Serial blood counts of mice after low- or sub-lethal doses of X-rays revealed significantly more profound depression of counts of both red cells and leucocytes in Wct +, and more notably in Wct + / + Ph, than in + / + or Wsh / + (haematologically normal) iso-dosed mice. We conclude that control of haematopoiesis by chromosome 5 is not confined to the W locus but is shared by the linked gene Ph (and perhaps Rw) and that expression of the change is not limited to the erythron but involves the pluripotent haematopoietic stem cell.


1994 ◽  
Vol 3 (6) ◽  
pp. 275-278
Author(s):  
Lubor Malina ◽  
Stanislav Janous˘ek ◽  
Ladislav Rosa ◽  
Rajmund Porkorny ◽  
Ladislav Pelech

2020 ◽  
Vol 14 (1) ◽  
Author(s):  
Ayisha Ayisha ◽  
Sheema Masood Ali

Plummer-Vinson syndrome (PVS), also called "Paterson-Brown-Kelly syndrome“, is a rare medical syndrome generally affecting middle-aged women. Iron deficiency anemia is the prime etiological factor and other probable factors include malnutrition, genetic predisposition, or autoimmune processes characterized by three distinctive features: iron deficiency anemia, dysphagia, and esophageal web. The dysphagia is generally painless and intermittent or progressive over years, restricted to solids, and associated with weight loss. The exact pathogenesis of PVS is still indistinguishable, but it is interconnected with iron deficiency anemia. Plummer-Vinson syndrome, if left untreated, carries an increased risk of developing squamous cell carcinoma of the upper alimentary tract.In this case report, a 40-year-old female patient presented long-standing dysphagia for months, which progressively developed to postcricoid squamous cell carcinoma by the time she approached to medical treatment. Diagnosis was confirmed through laboratory tests, showing iron deficiency anemia and whole-body positron emission tomography-computed tomography (PET-CT) presenting squamous cell carcinoma in postcricoid region (hypopharynx).


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