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Cells death

Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh NC 27695 [Pg.287]

National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 [Pg.287]

Molecular and Biochemical Toxicology, Fourth Edition, edited by Robert C. Smart and Ernest Hodgson Copyright 2008 John Wiley Sons, Inc. [Pg.287]


Methods to Detect and Quantitate Viral Agents in Fluids. In order to assess the effectiveness of membrane filtration the abihty to quantitate the amount of vims present pre- and post-filtration is critical. There are a number of techniques used. The method of choice for filter challenge studies is the plaque assay which utilizes the formation of plaques, localized areas in the cell monolayer where cell death caused by viral infection in the cell has occurred on the cell monolayer. Each plaque represents the presence of a single infectious vims. Vims quantity in a sample can be determined by serial dilution until the number of plaques can be accurately counted. The effectiveness of viral removal may be determined, as in the case of bacterial removal, by comparing the vims concentration in the input suspension to the concentration of vims in the effluent. [Pg.143]

Therapeutic opportunities for NO synthons include angina, for which nitroglycerin is effectively used, as well as penile erectile dysfunction. NOS inhibitors have demonstrated some protection in cerebral ischemia models and may be potentially beneficial in alleviating cell death associated with cerebral ischemia. l-NMA is under clinical study for treatment of sepsis. [Pg.565]

Polyethers. Antibiotics within this family contain a number of cycHc ether and ketal units and have a carboxyHc acid group. They form complexes with mono- and divalent cations that ate soluble ia aoapolar organic solvents. They iateract with bacterial cell membranes and allow cations to pass through the membranes causiag cell death. Because of this property they have been classified as ionophores. Monensia, lasalocid, and maduramicia are examples of polyethers that are used commercially as anticoccidial agents ia poultry and as growth promotants ia mmiaants. [Pg.474]

The main types of cellular injury induced by chemical compounds are necrotic and apoptotic (programmed) cell death. Necrosis implies chaotic ending... [Pg.284]

In apoptotic cell death, several factors such as growth factors, NO, the tumor suppressor gene p53, and the protein encoded by this gene contribute to the process that leads to cell death. One of the functions of p53 protein is the activation of apoptosis if a cell is transformed to a malignant cell. Apoptosis typically leads to the formation of smaller membrane-encapsulated particles within the cell. Apoptotic cell death begins in the nucleus and proceeds to other parts of the cell. The death process may be quite advanced before it can... [Pg.285]

Nucleic acids in the DNA contain a high number of nucleophilic sites that can be attacked by electrophilic intermediates (metabolites) of chemical compounds. DNA adducts formed may cause alterations in the expression of a critical gene in the cell and thus lead to cell death. For example, modification of p53 tumor suppressor gene may inactivate the functions of the p53 protein and render cells sensitive to malignant transformation. Also, formation of RNA adducts may inhibit key cellular events because RNA is essential for protein synthesis. [Pg.288]

Orrenius, S., McCabe, M. J., and Nicotera, P. (1992). Ca- -dependenr mechanisms of cytotoxicity and programmed cell death. Toxicol. Lett. 64/64, 357-364. [Pg.340]

Bursch, W. Oberhammer, F., and Schulte-Herrnann, R. (1992). Cell death by apoptosis and its protective role against di.sease. Trends Pharmacol. Set. 1.3(6), 245-251. [Pg.341]

Fiirvonen M.-R., Nevalainen, A., N, Monkkonen, J., and Savolainen, K. (1997). Streptomyces spores trom mouldy houses induce nitric acid, TTNFa and 11,-6 secretion from R.AW264.7 macrophage cell line without causing subsequent cell death. Environ. Toxicol. Pharmacol. 4, 57-63. [Pg.344]

FIGURE 1.25 The virus life cycle. Viruses are mobile bits of genetic iuformatiou encapsulated in a protein coat. The genetic material can be either DNA or RNA. Once this genetic material gains entry to its host cell, it takes over the host machinery for macromolecular synthesis and subverts it to the synthesis of viral-specific nucleic acids and proteins. These virus components are then assembled into mature virus particles that are released from the cell. Often, this parasitic cycle of virus infection leads to cell death and disease. [Pg.31]

ITowever, most normal somatic cells lack telomerase. Consequently, upon every cycle of cell division when the cell replicates its DNA, about 50-nucleotide portions are lost from the end of each telomere. Thus, over time, the telomeres of somatic cells in animals become shorter and shorter, eventually leading to chromosome instability and cell death. This phenomenon has led some scientists to espouse a telomere theory of aging that implicates telomere shortening as the principal factor in cell, tissue, and even organism aging. Interestingly, cancer cells appear immortal because they continue to reproduce indefinitely. A survey of 20 different tumor types by Geron Corporation of Menlo Park, California, revealed that all contained telomerase activity. [Pg.382]

If the cells are in the exponential growth period and there is no cell death rate, a 0. The net cell concentration is ... [Pg.90]


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