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Toxicity cellular

Atrophy is the cellular response of size reduction. This response lessens the cell s oxygen, organelle (specialized subunit within a cell with a specific function), and nutrient needs. This may be an effective reaction to diminished resources. Hypertrophy is an increase in cell size. This can be beneficial when increased capacity is demanded of a cell that does not normally divide, such as cardiac or skeletal muscle cells. Hyperplasia refers to an increase in cellular number by division. This is only possible in cells capable of mitosis. During metaplasia one mature ceU type transforms to another mature cell type. This process is used when scar tissue, for example, replaces normal functioning tissue in response to chronic irritation or inflammation. [Pg.334]

Cancer is a specialized response pathway that is a health concern of high importance to toxicologists. In cancer, a cell frequently experiences a mutation that confers unregulated growth. In a promotion event, the cell proliferates and forms a mass, or [Pg.334]


It is likely that ara-HxMP similarly exerts its antiviral activity in the form of the triphosphate, ara-HxTP, since ara-HxTP inhibits HSV-1 DNA polymerase (49). Another possible explanation of the antiviral activity of ara-HxTP is that it is metaboHcaHy converted to ara-AMP. In fact, it has been shown at Wellcome Research Laboratories that ara-HxMP is a substrate for adenylosuccinate synthetase, and that the resulting arabinofuranosyladenylosuccinate is cleaved to ara-AMP by adenylosuccinate lyase (1). The selective action of ara-A against HSV appears to be a consequence of the preferential inhibition of ara-ATP against HSV-1 and HSV-2 polymerases. Ara-ATP also inhibits normal cellular DNA polymerases, which may be the reason for its cellular toxicity. Also, it has been observed that ara-A is incorporated uniformly throughout the HSV-1 genome, which may result in defective viral DNA (50). [Pg.307]

Lash LH, Xu Y, Elfarra AA, et al. 1995. Glutathione-dependent metabolism of trichloroethylene in isolated liver and kidney cells of rats and its role in mitochondrial and cellular toxicity. Drug Metabolism and Disposition 23 846-853. [Pg.276]

The cell surface contains antigens, which are referred to as CD, which stands for cluster of differentiation. The antibodies are produced against a specific antigen. When administered, usually by an intravenous injection, the antibody binds to the antigen, which may trigger the immune system to result in cell death through complement-mediated cellular toxicity, or the antigen-antibody cell complex may be internalized to the cancer cell, which results in cell death. Monoclonal antibodies also may carry radioactivity, sometimes referred to as hot antibodies, and may be referred to as radioimmunotherapy, so the radioactivity is delivered to the cancer cell. Antibodies that contain no radioactivity are referred to as cold antibodies. [Pg.1294]

In the last 30 years, the use of in vitro tools for toxicological studies and evaluation has become relevant and the number of scientific works and techniques has increased day by day. One of the most important advantages of in vitro systems is their ability to serve as model for the central events in the in vivo toxicological process, and a depth evaluation of the intrinsic cellular toxicity can provide useful information for toxicological safety evaluation. [Pg.76]

Frazier JM (1990) Multiple endpoint measurements to evaluate the intrinsic cellular toxicity of chemicals. J Mol Cell Toxicol 3 349-357... [Pg.88]

Basak, S. C., Balasubramanian, K., Gute, B. D., Mills, D., Gorczynska, A., Roszak, S. Prediction of cellular toxicity of halocarbons from computed chemodescriptors A hierarchical QSAR approach. J. Chem. Inf. Comput. Sci. 2003, 43, 1103-1109. [Pg.498]

Schnellman, R.G. and Mandel, L.J. (1986). Cellular toxicity of bromobenzene and bromo-benzene metabolites to rabbit proximal tubules The role and mechanism of 2-bromohy-droquinone. J. Pharmacol. Exp. Then 237 456 161. [Pg.686]

In the E-Screen bioassay, LAS was not effective in promoting cell proliferation (Table 7.3.3). This compound was tested at concentrations of up to 100 pM with no evidence of cellular toxicity. The antiestrogenic effect of this compound was also measured but all samples tested were negative. Because it has been suggested that surfactants of the alkylbenzene sulfonate type are readily degradable and transformed into sulfophenyl carboxylates or SPCs, an important number of SPCs were assayed in the E-Screen test. These SPCs did not induce cell proliferation of MCF7 cells. [Pg.930]

Dillingham EO, Autian J. 1973. Teratogenicity, mutagenicity, and cellular toxicity of phthalate esters. Environ Health Perspect 81-89. [Pg.117]

Garrett NE, Lewtas J. 1983. Cellular toxicity in Chinese hamster ovary cell cultures I. Analysis of cytotoxicity endpoints for twenty-nine priority pollutants. Environ Res 32 455-465. [Pg.121]

Ciranni et al. (1988) found no evidence of fetal cellular toxicity, as measured by a reduction in the polychromatic erythrocyte/normochromatic erythrocyte... [Pg.78]

A large number of studies have investigated the metabolism of benzene per se or in relation to toxification and, particularly, myelotoxicity. Most evidence shows that benzene oxide (10.1, Fig. 10.8) is not the ultimate toxic species, as was initially believed. Indeed, phenol and quinone metabolites of benzene are more active in forming adducts with macromolecular nucleophiles and eliciting cellular toxicity. For example, the efficacy of benzene metabolites (see Fig. 10.8) to inhibit DNA synthesis in a mouse lymphoma cell line decreased in the order benzoquinone (10.17) > hydroquinone (10.16)... [Pg.619]

Evidence of a role of lipid peroxidation in the cellular toxicity of ozone has been obtained in in vitro studies in which human red cells were exposed to this oxidant gas. The possibility that lipid peroxidation is responsible for altered permeability of bacterial cell walls after ozone exposure was proposed by Scott and Lesher and has since been con-... [Pg.347]

Sheeja K, Kuttan G. (2007) Modulation of natural killer activity, antibody dependent cellular toxicity, and antibody dependent complement mediated cytotoxicity by andrographolide in normal and Ehrlich ascites carcinoma bearing mice. Integr Cancer Ther 6 66-73. [Pg.366]


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See also in sourсe #XX -- [ Pg.177 ]

See also in sourсe #XX -- [ Pg.47 ]




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Antibody-dependent cellular toxicity

Cell culture cellular toxicity

Cell/cellular toxicity

Cellular and Molecular Mechanisms of Toxicity

Cellular responses, to toxic compounds

Chemical toxicants, cellular response

Covalent binding cellular toxicity mechanism

Enzyme reactions cellular toxicity, mechanisms

Functional Polymers Cellular Toxicity

Halocarbons, cellular toxicity

Mechanism and Response in Cellular Toxicity

Protective mechanisms against cellular toxicity

Tissue slices, cellular toxicity

Toxicity cellular assays

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