Principles of Ecotoxicology
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Environmental pollution is caused by a wide range of chemicals released as a consequence of human activities. This book aims to identify major classes of pollutants and their environmental fate, before going on to consider the effects that they might have on individual organisms and ecosystems. The book progresses from the molecular basis of pollutant toxicity to consequent effects at higher levels of organization - cellular, whole organism, population, community and ecosystem.; The book defines ecotoxicology as the study of the harmful effects of chemicals upon ecosystems. It is an interdisciplinary subject which represents a synthesis of elements from the disciplines of chemistry, biochemistry, toxicology, physiology, population ecology and population genetics. In contrast to "classical" toxicology, the ultimate concern is for the effects at the level of populations and consequent effects at the level of populations.
Today, a large number of organophosphorous compounds are marketed as insecticides, and most follow the basic formula shown in Figure 1.5. Most organophosphorous insecticides (OPs) are liquids of lipophilic character and some volatility; a few are solids. They are generally less stable than organochlorine insecticides and more readily broken down by chemical or biochemical agents (Eto, 1974; Fest and Schmidt, 1982). Thus they tend to be relatively short-lived when free in the environment and the
phases, equilibrium is reached when the chemical has the same fugacity in all phases. In any one phase: f= C Z where C is the concentration of a chemical in the phase, Z is the fugacity capacity constant, and f is the fugacity. Consider now a two-phase system in equilibrium, f1 = f2 where f1 and f2 are fugacities in phase 1 and phase 2, respectively. Thus: 46 Principles of Ecotoxicology, Fourth Edition C1 C2 = Z1 Z2 or C1 C2 = = K12 Z1 Z2 where K12 is the partition
cofactors (Figure 5.4). Epoxide hydrolases of the endoplasmic reticulum hydrate epoxides generated by microsomal monooxygenases. In some cases, this represents a protective function, because the epoxides are strong electrophiles that can form adducts with cellular macromolecules (see Chapter 7). Epoxide hydrolases can metabolize endogenous and xenobiotic substrates. Epoxides of steroids and of insect juvenile hormone are examples of endogenous substrates. As with monooxygenases and esterases,
mixtures; the toxicity of a mixture can greatly exceed the total toxicities of its component chemicals (Chapter 9). Tests of environmental samples such as water, sediment, soil, and air can measure the toxicity of mixtures. If these tests are accompanied by chemical analyses, the measured toxicity may be compared with toxicity predicted from the detected residues of chemicals (toxicities of individual chemicals determined by analysis are calculated and are then combined to yield predicted
estrogenic or androgenic receptors; in other words, they may act as antiestrogens or antiandrogens. In this case, the normal action of the hormone is inhibited because binding to the receptor is retarded. The antiandrogenic action of p,p´-DDE in rats has been attributed to this mechanism (Kelce et al., 1995). 7.4.8 Reactions with Protein Sulfhydryl (SH) Groups The Hg2+ and Cd2+ ions are toxic to many animals. The main reason appears to be their ability to combine with sulfhydryl (thiol) groups,