Cell/cellular toxicity

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. 

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. 

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

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. 

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. 

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)... 

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-... 

Miret, S., De Groene, E.M. and Klaffke, W. (2007) Comparison of in vitro assays of cellular toxicity in the human hepatic cell line HepG2. Journal of Biomolecular Screening, 11, 184-193. 

While there seems to be little in common between intractable epilepsy and cancer, researchers in each field have focused on a common mechanism underlying multidrug resistance a cellular pump called P-glycoprotein (Pgp). Pgp protects cells from toxic substances by actively excreting the toxic agent. The pumps reside in tissues that are extensively exposed to toxic material liver, lungs, kidney, intestine, placenta, and blood-brain barrier. How-... 

The effect of echinacea on the immune system is controversial. In vivo human studies using commercially marketed formulations of E purpurea have shown increased phagocytosis, total circulating white blood cells, monocytes, neutrophils, and natural killer cells but not immunostimulation. In vitro, Epurpurea juice increased production of interleukins-1, -6, and -10, and tumor necrosis factor- by human macrophages. Enhanced natural killer cell activity and antibody-dependent cellular toxicity was also observed with E purpurea extract in cell lines from both healthy and immunocompromised patients. Studies using the isolated purified polysaccharides from Epurpurea have also shown cytokine activation. Polysaccharides by themselves, however, are unlikely to accurately reproduce the activity of the entire extract. 

Method Size of DNA Target Cells Transfection Efficiency Transfection Cellular Toxicity Gene Expression Preparation Application... 

This could cause dangerous opening of the calcium channel, because if too much calcium enters the cell through open channels, it would poison the cell by activating intracellular enzymes (Fig. 10—28) that form potentially dangerous free radicals (Fig. 10—29). Too many free radicals would eventually overwhelm the cell with toxic actions on cellular membranes and organelles (Fig. 10-30), ultimately killing the cell (Fig. 10-31). 

G-CSF activates neutrophils, transforming them into cells capable of respiratory burst and release of secretory granules. It also modulates the expression of adhesion molecules on neutrophils as well as CD1 lb/CD18 and plasma elastase antigen levels. G-CSF induces proliferation of endothelial cells, phagocytic activity of neutrophils, reactive oxygen intermediate production by neutrophils and antibody-dependent cellular toxicity by neutrophils. 

Cell injury can be initiated by a number of mechanisms, such as inhibition of enzymes, depletion of cofactors or metabolites, depletion of energy (ATP) stores, interaction with receptors, and alteration of cell membranes. In recent years attention has focused on the role of biotransformation of chemicals to highly reactive metabolites that initiate cellular toxicity. Many compounds, including clinically useful drugs, can cause cellular damage through metabolic activation of the chemical to highly reactive compounds, such as free radicals, carbenes, and nitrenes (Chapters 7 and 8). 

Mechanisms such as conjugation of the reactive chemical with glutathione are protective mechanisms that exist within the cell for the rapid removal and inactivation of many potentially toxic compounds. Because of these interactions, cellular toxicity is a function of the balance between the rate of formation of reactive metabolites and the rate of their removal. Examples of these interactions are presented in the following discussions of specific hepatotoxicants. 

Evaluate the function of human and macaque granulosa, trophoblast and endometrial cells, and macaque embryos in response to 2,3,7,8-TCDD while being cultured in vitro, and the cellular mechanisms by which primate reproductive cells sustain toxic damage... 

The interaction between DNA and carbon nanotubes is stable enough to allow separation of the dispersed nanotubes into well-defined subpopulations.46 55-57 Recently, ssDNA-wrapped SWNTs were separated into multiple fractions with different length distributions, and each fraction was examined for cellular toxicity to various cell lines.55 As demonstrated experimentally, while the longer SWNTs (>200nm) were excluded by cells, the shorter ones were found to internalize into the cytoplasm,... 

Although the use of simple test systems to predict genetic effects in whole mammals is desirable, comparison of dosages in submammalian systems with human exposure is extremely complex. The nature of the exposure, cellular toxicity, and units of measurement differ markedly from one type of organism to another. Molecular dosimetry that measures adducts in DNA is promising,1-3 237-239 jjUt the ability to relate exposures in short-term test systems, including mammalian cell cultures, to human risks is primitive. There are much better grounds for qualitative than for quantitative extrapolation. 

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