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Toxic Metal Removal Using Microbial Nanotechnology
Published in Mahendra Rai, Patrycja Golińska, Microbial Nanotechnology, 2020
In spite of Fe being an essential component for hemoglobin, a higher level of Fe poses a toxic threat as excess Fe is deposited in the cells of various organs and tissues, including liver, pancreas, heart, endocrine glands, skin, and joints. This may lead to severe clinical damage such as micronodular cirrhosis of the liver, atrophy of pancreas, hepatocellular liver failure, diabetes mellitus, arthritis, cardiac dysfunction, and even hypogonadism. On the other hand, secondary Fe overload is a result of disorders of erythropoiesis and chronic liver disease where excessive dietary Fe absorption and tissue deposition is observed. Fe-loading associated with refractory anemia with hypercellular bone marrow and ineffective erythropoiesis may also include severe conditions like thalassemia and sideroblastic anemia. Eventually, Fe overload leads to oxidative stress and ROS-mediated damage to lipids, proteins, carbohydrates, and DNA. Further, Fe overload leads to acquired lysosomal storage disease and may lead to damage of hepatic mitochondria, endoplasmic reticulum, and plasma membrane (Britton et al. 2002).
Hypobaric Hypoxia: Adaptation and Acclimatization
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
John H. Coote, James S. Milledge
With acute systemic hypoxia, as occurs on ascent to high altitude, the high gradient of oxygen tension from arteriole and capillary to tissue will inevitably decrease and so oxygen delivery is compromised. There are several changes that attempt to limit the effect on brain function, some of which have been referred to earlier. Acutely, cerebral vessel dilatation increases cerebral blood flow and the carotid chemoreceptor-induced hyperventilation reduces the magnitude of decrease in oxygen tension in the blood supplying the brain. During acclimatization, oxygen delivery is further improved by an increase in the number of red blood cells due to hypoxia-induced release of erythropoietin which stimulates erythropoiesis. Perhaps most importantly, the oxygen environment close to neurons is improved by a lessening of the diffusion distance by angiogenesis leading to an increase in the number of capillaries and small arterioles (Figure 7.9). According to studies on experimental animals exposed to hypobaric hypoxia for three weeks, the number of capillaries in the cortex may double (LaManna et al., 2004; LaManna, 2007). The target genes for erythropoiesis and for angiogenesis are activated by the hypoxia-sensitive transcription factor HIF-1α, as described in a previous section.
Systemic toxicology
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
W.M. Haschek, N.H. Stacey, C. Winder
Haematopoiesis occurs in the bone marrow with differentiated cells entering the circulation to replace senescent cells (Leventhal and Khan 1985; Testa and Gale 1988). Within the bone marrow, haematopoietic cells are located extravascularly and are supported and regulated by stromal cells that produce a variety of growth factors. In addition, erythropoietin, produced by the kidney, is essential for erythropoiesis. The microenvironment of the haematopoietic cells is critical for their proliferation and differentiation. The pluripotent stem cell gives rise to the progenitor cells of all lineages; it has little proliferative capacity in spite of unlimited self-renewal. The progenitor cells have greater proliferative capacity but are committed to a limited number of lineages. The proliferative precursors of each cell lineage give rise to the well-differentiated end-stage cells that enter the circulation. These end-stage cells cannot proliferate, except for monocytes and lymphocytes, and all have a finite lifespan (Young 1988). The two basic cell lineages are the lymphoid (discussed later in the section on the immune system) and haematopoietic, the latter differentiating into the myeloid, erythroid and megakaryocytic series, as shown in Figure 3.1. Differentiated cells released into the circulation consist of granulocytes and monocytes (called macrophages in tissues) from the myeloid lineage, erythrocytes (red blood cells) from the erythroid lineage, and platelets from the megakaryocytic lineage (Irons 1991).
Positive periodic solutions for a delay model of erythropoiesis with iterative terms
Published in Applicable Analysis, 2023
Marwa Khemis, Ahlème Bouakkaz, Rabah Khemis
Almost half a century ago, the Canadian physiologists Leon Glass and Michael Mackey [1] have set down the following first order delay differential equation which is now known as the Mackey–Glass model: This model describes a highly complex process, called erythropoiesis, by which red blood cells (named also erythrocytes, erythroid cells, RBCs) are produced in the marrow of certain bones for releasing them in the bloodstream. Here, (cells/kg) denotes the density of circulating mature human erythroid cells, c (cells/kg-day) is the mortality term, c>0 (days) stands for the death rate of red blood cells, (cells/kg-day) describes the red blood cells reproduction where p>0 (units cells/kg-day) is the maximal erythrocytes production rate, are positive constants and (days) is the time duration of the maturational phase.
Walking exercise and lower-body blood flow restriction: Effects on systemic inflammation, lipid profiles and hematological indices in overweight middle-aged males
Published in Research in Sports Medicine, 2022
Omid Razi, Mohammad Mohammadi, Nastaran Zamani, Anthony C. Hackney, Claire Tourny, Sghaeir Zouita, Ismail Laher, Hassane Zouhal
Training-induced responses of inactive individuals are likely to be increased under hypoxic conditions (Piché et al., 2005). Hypoxia stimulates HIF-2α release and triggers EPO secretion by the kidney and liver. EPO stimulates the bone marrow to release erythrocytes anHGB into the circulation (Koenig & Ernst, 2000), as confirmed by a study reporting that a 4-week exposure to hypoxic conditions increased serum levels of RBC, HCT, and haem (Li et al., 2019). EPO functions as a blood-producing hormone that is released by the kidneys in response to hypoxic conditions and which stimulates RBC production (erythropoiesis) in the bone marrow (Robach et al., 2018). Although this response is influenced by exercise training (Robach et al., 2018), EPO release is also increased under hypoxic conditions too (Choi et al., 1996; Furukawa et al., 2008). HCT percentage is influenced by plasma volume variation, which itself is decreased by exercise training under hypoxic condition (Robach et al., 2018). Our study did not evaluate the role of plasma volume as a contributing factor to changes in HCT which we acknowledge as a limitation of the study. Research on the impact of BFR walk training on cardiovascular risk factors and haematological indices is in its infancy. Additional studies are needed to examine the effects of this training method at higher exercise training intensities and expand on our findings.
Iron balance and iron supplementation for the female athlete: A practical approach
Published in European Journal of Sport Science, 2018
Charles R Pedlar, Carlo Brugnara, Georgie Bruinvels, Richard Burden
The regulation of iron absorption, storage and the regulation of erythropoiesis is under the control of iron protein regulators and hypoxia inducible factors respectively (Kuhn, 2015). Iron absorption is under the control of the peptide hormone hepcidin which was only relatively recently discovered (Nemeth et al., 2004). Briefly, hepcidin is secreted in the liver and increases in response to iron overload (Burden, Morton, Richards, Whyte, & Pedlar, 2015) or inflammation, shutting down iron absorption via ferroportin. Conversely, hepcidin decreases in anaemia, promoting iron absorption. Since exercise results in an inflammatory response, it can transiently increase hepcidin (Burden, Pollock, et al., 2015), potentially reducing the capacity to absorb iron. Therefore, heavy and frequent exercise training bouts may put the athlete at risk of iron deficiency although more studies are needed to understand the longitudinal effects of exercise upon hepcidin. Recent evidence suggests that during recovery from marathon training iron status improves (Pedlar et al., 2017), thus, rest may be an effective means of correcting iron deficiency although more studies are needed.