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Systemic toxicology
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
W.M. Haschek, N.H. Stacey, C. Winder
Haematotoxicity can be targeted to cells of the bone marrow or those in the circulation (Irons 1985). Injury to the pluripotent stem cells or their microenvironment can result in underproduction of all cell types. Once differentiation begins, individual cell types can be affected, either in the bone marrow or in the blood, leading to a decrease in cell numbers of a particular cell type or abnormal function of that cell type. Direct toxicity to circulating cells results in an increased demand on the bone marrow resulting in increased cell proliferation (hyperplasia) and decreased differentiation time. Abnormal cell function will not be discussed in detail, since the target organs lie outside the haematopoietic system (see Bloom and Brandt (2002) for an in-depth discussion). A decrease in erythrocyte numbers, mean corpuscular volume (MCV), mean corpuscular haemoglobin content (MCH) or any combination thereof, is termed anaemia. A decrease in white blood cells is termed cytopenia (granulocytopenia, lymphocytopenia or thrombocytopenia depending on the cell type affected) or pancytopenia if all white cells are affected. Effects will vary in severity and reversibility, depending on the chemical and exposure conditions. Possible outcomes are recovery following cessation of exposure, persistence of changes, or progression to aplastic anaemia, myelodysplastic syndrome, or leukaemia (Rosner and Grunwald 1990).
Petroleum Hydrocarbons
Published in G. Mattney Cole, Assessment and Remediation of Petroleum Contaminated Sites, 2018
The most important chronic effect of benzene exposure is destruction of bone marrow cells. With continued exposure there is severe bone marrow damage which results in pancytopenia, a deficiency of all elements of the blood and results in increased susceptibility to infection and hemorrhagic conditions. Eventually, continued exposure leads to the development of a distinctive type of leukemia called acute myelogenous leukemia.
Trichoderma after crossing kingdoms: infections in human populations
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Uener Ribeiro dos Santos, Jane Lima dos Santos
T. longibrachiatum was reported in oncology patients with hematological cancer that displayed anemia, leukopenia, decreased platelet count, pancytopenia, and/or decreased count in neutrophils (Alanio et al. 2008; Chretien et al. 2016; Lagrange-Xélota et al. 2008; Myoken et al. 2002; Richter et al. 1999; Sautour et al. 2018; Seguin et al. 1995), which are frequent driving factors for other fungal infections, as noted in iatrogenic immunosuppression following steroid therapy or even other immunosuppressive treatment. IgG and IgE serum levels were decreased in some of these infections (Santillan Salas et al. 2011; Tang et al. 2003). Skin infection in a hematological pediatric patient also presented lung colonization and, similar to other immunocompromised patients, exhibited multiple complications over several months (Román-Soto, Álvarez-Rojas, and García-Rodríguez 2019). Patients with pulmonary infections frequently presented with fever, dyspnea, cough, and also demonstrated shortness of breath (Georgakopoulou et al. 2021; Lagrange-Xélota et al. 2008; Rodríguez Peralta et al. 2013; Sautour et al. 2018; Yu et al. 2021; Zhou et al. 2020).
The potential interaction of environmental pollutants and circadian rhythm regulations that may cause leukemia
Published in Critical Reviews in Environmental Science and Technology, 2022
Francisco Alejandro Lagunas-Rangel, Błażej Kudłak, Wen Liu, Michael J. Williams, Helgi B. Schiöth
Exposure to benzene has toxic effects on the blood and bone marrow cells leading to leukopenia, pancytopenia, aplastic anemia, and leukemia (Snyder & Hedli, 1996). The hematotoxic effects of benzene and its metabolites, such as phenol, catechol, hydroquinone, 1,2,4-benzenetriol, transtrans-muconic acid and L-phenylmercapturic acid, are due to the fact that these can covalently bind to DNA and other macromolecules and induce damage, cause the overproduction of reactive oxygen species (ROS), as well as other mechanisms that are not yet fully understood (Park et al., 2008; Snyder & Hedli, 1996). Notably, among the genes most affected by exposure to benzene are those of the circadian rhythms, possibly due to the activation of the aryl hydrocarbon receptor (AhR) that has direct effects on the HSPCs (Figure 3) (Gasiewicz, Singh, & Casado et al., 2010; Park et al., 2008). AhR is expressed in hematopoietic stem cells (HSCs), in which it is a crucial mediator for their growth and differentiation by regulating c-MYC, OCT4, HIF-1α, NOTCH, and HES-1 signaling. AhR expression leads mainly to the myeloid line, being particularly important in the generation of erythrocytes and monocytes, although it is also important for the differentiation of naïve lymphocytes (Angelos & Kaufman, 2018; Casado et al., 2010; Lindsey & Papoutsakis, 2012). AhR forms a heterodimer with BMAL1 and, in turn, prevents its heterodimerization with CLOCK, thus acting as a transcriptional repressor for CCGs. Difficulty expressing PER1 reduces the robustness of the rhythm and slows down the clock progression (Tischkau, 2011; Xu et al., 2010).
Urinary concentrations of amphenicol antibiotics in relation to biomarkers of oxidative DNA and RNA damage in school children
Published in Journal of Environmental Science and Health, Part A, 2022
Yang Geng, Man Hu, Yuan Yao, Ming Zhan, Ying Zhou
The Pearson correlation analysis and repeated measurements analysis did not find that urinary levels of FF in school children were potentially correlated to 8-OHdG and 8-OHG. One of possible explanations might be that children were exposed to FF at much lower levels of 0.05 μg/L (median) in this study than dose used in pervious in vivo studies.[9–11,37–40] For example, Ren et al.[52] studied the toxic and side effects of FF in swimming crabs, and found that high doses (40 and 80 mg/kg) of FF caused oxidative damage to biomolecules. Recently Han et al.[24] reported that high doses (greater than 0.60 g/L) rather than low doses (0.15 g/L) of FF had effect on oxidative stress damage to hepatocyte in broiler. These animal studies demonstrated that high doses of FF would cause oxidative stress damage. Furthermore, as the analogue of CAP and TAP, FF manifests lower toxicity (e.g., reversible bone marrow depression, aplastic anemia with pancytopenia) compared with CAP and TAP. It suggests that FF would contribute less oxidative damage to cells and tissue compared with CAP and TAP at the same exposure levels. In fact, the exposure levels of FF in children was lowest in comparison to those of CAP (median, 1.44 μg/L) and TAP (median, 0.32 μg/L) in this study. In addition, we did not determine the urinary amounts of florfenicol amine (FFA), a major metabolite of FF which was excreted in urine along with FF[53] and had longer elimination half-time compared with FF,[54–56] and so possibly underestimate FF exposure in this study. It’s worthy of further investigation of the relationship between the total internal exposure levels of FF and FFA and oxidative damage in the future study.