According to this present study, zinc plays an essential role in erythroid development, especially in the biosynthesis of heme.

A low hemoglobin level or red blood cell count is defined by the World Health Organization (WHO) as anemia. This can be caused by nutritional deficiencies in iron, folate, or vitamin B12, as well as infection and chronic inflammation.

Even though nutrition-based strategies effectively prevent nutritional anemia, anemia remains prevalent worldwide, affecting approximately 23% of the population. Furthermore, poor nutrition is the leading cause of anemia worldwide, particularly among women of reproductive age and young children.

In humans, erythrocytes in circulation are constantly turned over, with an approximate lifespan of 120 days. Erythrocyte homeostasis of the body is maintained by the supply of new red blood cells, mainly from steady-state erythropoiesis in the bone marrow.

The spleen and liver can become erythropoietic sites for extramedullary erythropoiesis under certain pathological conditions requiring a rapid expansion in red cell production, such as acute hemolytic anemia.

The molecule zinc plays an imperative role in several biological processes in the body, including red blood cell development. However, it is unclear how zinc availability regulates red blood cell development.

There are also epidemiological associations between serum zinc concentrations and anemia risk in humans, and clinical outcomes of poor zinc nutrition cases include symptoms of anemia.

Although zinc status has been recognized as a potential factor in anemia risk, further mechanistic research is needed on the nutritional implications of zinc status on red cell metabolism.

Methodology and Results

It has been demonstrated that G1E-ER4 mouse cells, which have elevated zinc content by development, were used for the in vitro study of terminal erythroid differentiation. When zinc import was restricted, hemoglobin production and hemoglobinization of erythroid progenitors were compromised.

The incorporation of iron synthesizes heme into protoporphyrin. Under zinc restriction, heme production is reduced not because of reduced iron but due to reduced porphyrin synthesis. A second erythropoietic cell model, MEL-DS19, confirmed the importance of zinc for erythroid heme metabolism.

According to the report’s findings, a conventional indicator of iron deficiency anemia, the ZnPPto-heme ratio, also responded differently to zinc restriction than iron deficiency. The results of this study indicate that zinc is a crucial nutrient that contributes to the biosynthesis of erythroid heme and is, therefore, an effective therapeutic target for the treatment of anemia.

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