Compensatory cell proliferation

Ledda-Columbano GM, Columbano A, Coni P, et al. 1987a. Liver cell proliferation induced by the mitogen ethylene dibromide, unlike compensatory cell proliferation, does not achieve initiation of rat liver carcinogenesis by diethyinitrosoamine. Cancer Lett 36 247-252. 

The term toxicodynamics means the process of interaction of chemical substances with target sites and the subsequent reactions leading to adverse effects. The toxicodynamic effect is driven by the concentration at the effect site(s) directly or indirectly and may be reversed or modified by several factors such as repair mechanisms for DNA damage and compensatory cell proliferation (EC 2003). 

Hormesis, in which compensatory adaptive changes precede and occur at lower doses than degenerative changes, was detected for half of the toxic drugs for cell proliferation, cell morphology and mitochondria [4, 33]. Hormesis could not be assessed for parameters that normally have low values, such as intracellular calcium measured by fluo4 or membrane permeability measured by toto-3, because assay methods were not sufficiently sensitive. However, for calcium, more sensitive dyes. 

Cell Proliferation as a Compensatory Response to Toxic Tissue Injury... 

Fig. 15.2 Influence of apoptosis on homeostasis of a cell grouping. In a grown organism, the cell number in a tissue is determined by the relation between the rate of cell division and cell death. The rates of both processes are represented in the figure by the size of the arrow. In a normal tissue, the cell number remains constant (homeostasis) since both processes occur at the same rate. Ifthe rate of cell proliferation predominates, diseases occur characterized by increased cell number (e. g., in tumors). In the reverse case, when the rate of cell death predominates, the cell number is reduced in a pathologic fashion. In the absence of compensatory changes in the cell division rate, changes in the extent of apoptosis can lead to either accumulation of cells or loss of cells. According to Thompson, (1995).

A continuation of this line of studies for 6 days to 23 weeks at 300 ppm showed continued decreases in numbers of mature B- and T-lymphocytes produced in the bone marrow, spleen, and thymus (Rozen and Snyder 1985). Abnormalities of humoral and cell-mediated immune responses following benzene exposure are presumably caused by a defect in the lymphoid stem cell precursors of both T- and B-lymphocytes. Bone marrow cellularity increased 3-fold, and the number of thymic T-cells increased 15-fold in benzene-exposed mice between the 6th and the 30th exposure. No corresponding increase in splenic cells was noted. The marked increase in the numbers of cells in bone marrow and thymus was interpreted by the authors to indicate a compensatory proliferation in these cell lines in response to... 

Cardiotoxicity of primary amines (epinephrine, norepinephrine, isoproterenol) was noted earlier, and has been recognized for nearly 100 years. The vascular toxicity of these and related compounds has also recently been recognized. The effects seem to focus on medial cells of the artery wall, rather than on adventitial or endothelial cells. Early changes include loss of medial cells, mineralization, and loss of elastic fibers. Later there is a compensatory proliferation of intimal cells. The vascular toxicity of two related compounds is particularly striking. One of these compounds, allylamine, will be discussed near the end of this chapter. The second is )S-aminoproprionitrile ()S-APN), which is the active agent in the toxic sweet pea, Lathyrus odoratus. Consumption of flour derived from this plant results in lathyrism, a condition often seen in children and young... 

Ma, L., and Weinstein, R. A. (2008). MicroRNAs in malignant progression. Cell Cycle 7(5), 570-572. Maeda, S., Kamata, H., Luo, J. L., Leffert, H., and Karin, M. (2005). IKKbeta couples hepatocyte death to cytokine-driven compensatory proliferation that promotes chemical hepatocarcinogenesis. Cell 121(7), 977-990. 

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