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Toxicants interactions measuring toxicity

McClellan K, Altenburger R, Schmltt-Jansen M (2008) Pollution-induced community tolerance as a measure of species interaction in toxicity assessment. J Appl Ecol 45 1514... [Pg.53]

Some biomarker responses provide evidence only of exposure and do not give any reliable measure of toxic effect. Other biomarkers, however, provide a measure of toxic effects, and these will be referred to as mechanistic biomarkers. Ideally, biomarker assays of this latter type monitor the primary interaction between a chemical and its site of action. However, other biomarkers operating down stream from the original toxic lesion also provide a measure of toxic action (see Figure 14.3 in Chapter 14), as, for instance, in the case of changes in the transmission of action potential... [Pg.84]

The problem of potentiation was discussed earlier (Chapter 2, Section 2.5). Potentiation is often the consequence of interactions at the toxicokinetic level, especially inhibition of detoxication or increased activation. The consequences of such potentiation may be evident not only at the whole animal level but also in enhanced responses of biomarker assays that measure toxicity (Figure 13.3). By contrast, biomarkers of exposure alone are unlikely to give any indication of potentiation at the toxicokinetic level. [Pg.253]

Particular attention is given to the development of new mechanistic biomarker assays and bioassays that can be used as indices of the toxicity of mixtures. These biomarker assays are typically based on toxic mechanisms such as brain acetylcholinesterase inhibition, vitamin K antagonism, thyroxin antagonism, Ah-receptor-mediated toxicity, and interaction with the estrogenic receptor. They can give integrative measures of the toxicity of mixtures of compounds where the components of the mixture share the same mode of action. They can also give evidence of potentiation as well as additive toxicity. [Pg.254]

Measurement of biological interaction effects of organotins with other toxic chemicals under stressful environmental conditions of temperature, oxygen, and other variables (Thompson et al. 1985). [Pg.625]

In aquatic environments, Spear (1981) spotlights three research needs (1) development of analytical procedures for measurement of individual dissolved zinc species, notably the aquo ion and zinc chloride, and for nondissolved species that occur in natural waters (2) separation of natural from anthropogenic influences of sediment-water interactions on flux rates, with emphasis on anoxic conditions, the role of microorganisms, and the stability of organozinc complexes and (3) establishment of toxicity thresholds for aquatic organisms based on bioaccumulation and survival to determine the critical dose and the critical dose rate, with emphasis on aquatic communities inhabiting locales where zinc is deposited in sediments. These research needs are still valid. [Pg.716]

Current research needs include the development of protocols to (1) separate, quantitate, and verify the different chemical species of zinc (2) identify natural from anthropogenic sources of zinc (3) establish toxicity thresholds based on accumulation (4) evaluate the significance of tissue concentrations in target organs as indicators of zinc stress and (5) measure the long term consequences of zinc interactions with other nutrients using animals of various age and nutrient status. [Pg.726]

Commercial PCB mixtures frequently contain impurities that may contribute to the 2,3,7,8-TCDD toxic equivalency factor. These impurities may include other PCBs, dioxins, dibenzofurans, naphthalenes, diphenyl ethers and toluenes, phenoxy and biphenyl anisoles, xanthenes, xanthones, anthracenes, and fluorenes (Jones etal. 1993). PCB concentrations in avian tissues sometimes correlate positively with DDE concentrations (Mora et al. 1993). Eggs of peregrine falcons (Falco peregrinus) from California, for example, contained measurable quantities of various organochlorine compounds, including dioxins, dibenzofurans, mirex, hexachlorobenzene, and / ,//-DDE at 7.1 to 26.0 mg/kg FW PCB 126 accounted for 83% of the 2,3,7,8-TCDD equivalents, but its interaction with other detectable organochlorine compounds is largely unknown (Jarman et al. 1993). [Pg.1286]

Drug Levels in Plasma. Drug levels may also be measured in a clinical trial. Such levels are usually part of a pharmacokinetic analysis but also provide important safety data. This information would be particularly relevant in cases of suspected or actual drug overdosage, drug interactions, to correlate medicine levels with toxic events, or in other situations. It must be clarified whether free levels of the drug and/or the protein bound will be measured by the laboratory. [Pg.806]

Szlinder-Richert J, Cybulska B, Grzybowska J, Bolard J, Borowski E (2004) Interaction of amphotericin B and its low toxic derivative, N-methyl-N-D-fructosyl amphotericin B methyl ester, with fungal, mammalian and bacterial cells measured by the energy transfer method. II Farmaco 59 289-296. [Pg.49]

Without appropriate cleanup measures, BTEX often persist in subsurface environments, endangering groundwater resources and public health. Bioremediation, in conjunction with free product recovery, is one of the most cost-effective approaches to clean up BTEX-contaminated sites [326]. However, while all BTEX compounds are biodegradable, there are several factors that can limit the success of BTEX bioremediation, such as pollutant concentration, active biomass concentration, temperature, pH, presence of other substrates or toxicants, availability of nutrients and electron acceptors, mass transfer limitations, and microbial adaptation. These factors have been recognized in various attempts to optimize clean-up operations. Yet, limited attention has been given to the exploitation of favorable substrate interactions to enhance in situ BTEX biodegradation. [Pg.376]


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