Donating Blood Effects

Ihor

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Anemia, Iron Storage and Ceruloplasmin in Copper Nutrition in the Growing Rat

Abstract

Several studies have shown that copper-deficient animals accumulate iron as anemia persists, indicating the unavailability of absorbed iron for hemoglobin formation. Recently, it was suggested that ceruloplasmin by its ferroxidase activity is the regulating agent that mobilizes the iron from cells to plasma. This experiment was conducted to examine in vivo this suggestion by the periodic monitoring of the levels of liver iron and copper and hemoglobin in relation to ceruloplasmin oxidase activity during a state of copper depletion and subsequent repletion. A total of 230 weanling rats were divided into two groups and fed either a low copper (<1 ppm) or a control diet (35 ppm copper as CuCO3). Both diets contained 135 ppm iron as Fe2O3. After 42 days half the rats on the low copper diet were fed the control diet and continued for another 42 days of repletion. Animals were killed at weekly intervals for 84 days and on days 44 and 47. Hemoglobin, hematocrit, plasma ceruloplasmin oxidase activity, liver iron and liver copper were different (P < 0.05) from the control values starting at day 7 of depletion. Ceruloplasmin activity was reduced to 5% of the control by day 14 of depletion, and an accumulation of iron in the liver amounted to 65% more than the control values by the end of the 42-day depletion period. Hemoglobin and hematocrit values were reduced to 50% of the control values during this period. With copper repletion the marked increase in ceruloplasmin oxidase activity (25-fold in 2 days) corresponded with the rapid removal of iron (30% decrease in 2 days) and the accumulation of copper in the liver. Further increases in the ceruloplasmin activity in the repleted animals were tied with the corresponding removal of iron from the liver during repletion. These changes were followed by a steady increase in hemoglobin and hematocrit values equalling the control values by days 70 and 63 of repletion, respectively. These results are compatible with the suggestion that copper exerts its influence in the metabolism of hemoglobin through ceruloplasmin by mobilizing the absorbed iron, bound to transferrin, from the cells to the plasma.

Anemia, Iron Storage and Ceruloplasmin in Copper Nutrition in the Growing Rat
 

Ihor

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Ceruloplasmin/Transferrin system is related to clinical status in acute stroke.
Abstract

BACKGROUND AND PURPOSE:
In acute stroke, Iron (Fe) may amplify reperfusion injury by catalyzing the conversion of superoxide and hydrogen peroxide into highly reactive radicals. Transferrin (Tf) is the main protein regulating Fe homeostasis, whereas Ceruplasmin (CP) is a circulating ferroxidase enzyme able to oxidize ferrous ions to less toxic ferric forms. This study aims at investigating whether CP, Copper (Cu), Tf, and Fe play a role in the pathophysiology of acute stroke.

METHODS:
We enrolled 35 acute stroke patients and 44 controls. All patients underwent: neurological examination assessed by National Institutes of Health Stroke Scale (NIHSS), ultrasound evaluation of carotid atherosclerosis, brain MRI to quantify ischemic lesion volume and measurement of serum levels of CP, Cu, Tf, Fe, hydro-peroxides, and Total plasmatic antioxidant capacity.

RESULTS:
In patients, NIHSS scores were associated with Tf (r=-0.48, P=0.004), hydro-peroxides (r=0.34, P=0.046), CP (r=0.43, P=0.012), and lesion volume (r=0.50, P=0.004). Lesion volume was inversely associated with Tf (r=-0.44, P=0.012). CP and hydro-peroxides were also largely related (r=0.81, P<0.001). The model multiple R was 0.57, resulting in a 32.5% of explained NIHSS variance with Tf accounting for 23.4% and CP for 9.1%.

CONCLUSIONS:
CP and Tf levels are representative of clinical status in acute stroke patients. Our findings suggest a protective role of Tf in acute stroke and a possible ambivalent role of CP.

Ceruloplasmin/Transferrin system is related to clinical status in acute stroke. - PubMed - NCBI
 

Ihor

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Role of copper in mitochondrial iron metabolism
Heme synthesis by copper-deficient cells was investigated to elucidate the nature of the defect in intracellular iron metabolism. Iron uptake from transferrin by copper-deficient reticulocytes was 52% of normal, and the rate of heme synthesis was 33% of normal. Hepatic mitochondria isolated from copper-deficient animals were deficient in cytochrome oxidase activity and failed to synthesize heme from ferric iron (Fe III) and protoporphyrin at the normal rate. The rate of heme synthesis correlated with the cytochrome oxidase activity. Heme synthesis from Fe(III) and protoporphyrin by normal mitochondria was enhanced by succinate and inhibited by malonate, antimycin A, azide, and cyanide. It is proposed that an intact electron transport system is required for the reduction of Fe(III), thereby providing a pool of ferrous iron (Fe II) for protoheme and heme a synthesis.

Role of copper in mitochondrial iron metabolism | Blood | American Society of Hematology
 

Ihor

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Copper availability contributes to iron perturbations in human nonalcoholic fatty liver disease.
Abstract

BACKGROUND & AIMS:
Iron perturbations are frequently observed in nonalcoholic fatty liver disease (NAFLD). We aimed to investigate a potential association of copper status with disturbances of iron homeostasis in NAFLD.

METHODS:
We retrospectively studied 140 NAFLD patients and 25 control subjects. Biochemical and hepatic iron and copper parameters were analyzed. Hepatic expression of iron regulatory molecules was investigated in liver biopsy specimens by reverse-transcription polymerase chain reaction and Western blot analysis.

RESULTS:
NAFLD patients had lower hepatic copper concentrations than control subjects (21.9 +/- 9.8 vs 29.6 +/- 5.1 microg/g; P = .002). NAFLD patients with low serum and liver copper concentrations presented with higher serum ferritin levels (606.7 +/- 265.8 vs 224.2 +/- 176.0 mg/L; P < .001), increased prevalence of siderosis in liver biopsy specimens (36/46 vs 10/47 patients; P < .001), and with elevated hepatic iron concentrations (1184.4 +/- 842.7 vs 319.9 +/- 451.3 microg/g; P = .020). Lower serum concentrations of the copper-dependent ferroxidase ceruloplasmin (21.7 +/- 4.1 vs 30.4 +/- 6.4 mg/dL; P < .001) and decreased liver ferroportin (FP-1; P = .009) messenger RNA expression were found in these patients compared with NAFLD patients with high liver or serum copper concentrations. Accordingly, in rats, a reduced dietary copper intake was paralleled by a decreased hepatic FP-1 protein expression.

CONCLUSIONS:
A significant proportion of NAFLD patients should be considered copper deficient. Our results indicate that copper status is linked to iron homeostasis in NAFLD, suggesting that low copper bioavailability causes increased hepatic iron stores via decreased FP-1 expression and ceruloplasmin ferroxidase activity thus blocking liver iron export in copper-deficient subjects.

Copper availability contributes to iron perturbations in human nonalcoholic fatty liver disease. - PubMed - NCBI
 

Ihor

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Copper Accumulates in Hemosiderins in Livers of Patients with Iron Overload Syndromes
Abstract

In biology, redox reactions are essential and sometimes harmful, and therefore, iron metabolism is tightly regulated by cuproproteins. Since the state of copper in iron overload syndromes remains unclear, we investigated whether copper metabolism is altered in these syndromes. Eleven patients with iron overload syndromes participated in this study. The clinical diagnoses were aceruloplasminemia (n=2), hemochromatosis (n=5), ferroportin disease (n=2), and receiving excess intravenous iron supplementation (n=2). Liver specimens were analyzed using a light microscope and transmission electron microscope equipped with an X-ray analyzer. In addition to a large amount of iron associated with oxygen and phosphorus, the iron-rich hemosiderins of hepatocytes and Kupffer cells contained small amounts of copper and sulfur, regardless of disease etiology. Two-dimensional imaging clearly showed that cuproproteins were distributed homogenously with iron complexes within hemosiderins. Copper stasis was unlikely in noncirrhotic patients. The enhanced induction of cuproproteins by excess iron may contribute to copper accumulation in hemosiderins. In conclusion, we have demonstrated that copper accumulates in hemosiderins in iron overload conditions, perhaps due to alterations in copper metabolism.

Copper Accumulates in Hemosiderins in Livers of Patients with Iron Overload Syndromes
 

Ihor

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This is a big publication about iron and copper and abstract here doesn't disclose many things as all text. It is advisable to read in full.

Intersection of Iron and Copper Metabolism in the Mammalian Intestine and Liver

Abstract
Iron and copper have similar physiochemical properties; thus, physiologically relevant interactions seem likely. Indeed, points of intersection between these two essential trace minerals have been recognized for many decades, but mechanistic details have been lacking. Investigations in recent years have revealed that copper may positively influence iron homeostasis, and also that iron may antagonize copper metabolism. For example, when body iron stores are low, copper is apparently redistributed to tissues important for regulating iron balance, including enterocytes of upper small bowel, the liver, and blood. Copper in enterocytes may positively influence iron transport, and hepatic copper may enhance biosynthesis of a circulating ferroxidase, ceruloplasmin, which potentiates iron release from stores. Moreover, many intestinal genes related to iron absorption are transactivated by a hypoxia-inducible transcription factor, hypoxia-inducible factor-2α (HlF2α), during iron deficiency. Interestingly, copper influences the DNA-binding activity of the HIF factors, thus further exemplifying how copper may modulate intestinal iron homeostasis. Copper may also alter the activity of the iron-regulatory hormone hepcidin. Furthermore, copper depletion has been noted in iron-loading disorders, such as hereditary hemochromatosis. Copper depletion may also be caused by high-dose iron supplementation, raising concerns particularly in pregnancy when iron supplementation is widely recommended. This review will cover the basic physiology of intestinal iron and copper absorption as well as the metabolism of these minerals in the liver. Also considered in detail will be current experimental work in this field, with a focus on molecular aspects of intestinal and hepatic iron-copper interplay and how this relates to various disease states.

Intersection of Iron and Copper Metabolism in the Mammalian Intestine and Liver
 

tankasnowgod

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@tankasnowgod
Can blood donation also have harmful effects?
My ferritine = 158 ug/l
iron = 23
don't know if it's a good choice for me to give a blood donation, never done that.

Sure, it's possible. Blood donation centers will even tell you straight up there's a possibility of feeling light headed, dizzy, or even fainting. Most of these generally have to do with low blood sugar after the donation. When these do occur, they are usually transient.

The bigger dangers of infection or anemia are largely eliminated due to the screening process, hemoglobin check, and sterilizing the area and instruments.

Overall, it's a pretty safe and straighforward procedure. I think it's wise to do your first donation on a day when you don't have anything else planned, to see how it effects you.
 

Hgreen56

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Sure, it's possible. Blood donation centers will even tell you straight up there's a possibility of feeling light headed, dizzy, or even fainting. Most of these generally have to do with low blood sugar after the donation. When these do occur, they are usually transient.

The bigger dangers of infection or anemia are largely eliminated due to the screening process, hemoglobin check, and sterilizing the area and instruments.

Overall, it's a pretty safe and straighforward procedure. I think it's wise to do your first donation on a day when you don't have anything else planned, to see how it effects you.
thanks.
what is your opinion about my value's ?
is it useful to lowering them by donation or doesn't matter much health wise?
Not sure my value's are low, medium, high.. according to "peat" vision
 
Last edited:

tankasnowgod

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thanks.
what is your opinion about my value's ?
is it useful to lowering them by donation or doesn't matter much health wise?
Not sure my value's are low, medium, high.. according to "peat" vision

I think studies like the Zacharsky studies show long term benefits (like less heart disease) when ferritin is kept under 80. A lot of people aim somewhere in the range of 25-75, which seems to be a pretty good overall range. I personally want to keep ferritin in that range, which is at least half your current test, so blood donation would likely be beneficial.
 

Hgreen56

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Apr 8, 2020
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I think studies like the Zacharsky studies show long term benefits (like less heart disease) when ferritin is kept under 80. A lot of people aim somewhere in the range of 25-75, which seems to be a pretty good overall range. I personally want to keep ferritin in that range, which is at least half your current test, so blood donation would likely be beneficial.
thanks gain.
 

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