Biomarkers examples

Different species are used / applicable to different geographic areas. Biomarkers exampled by bacteria (Microtox ) toxicity tests can be conducted in all cases endpoint for this test is enzyme fimction, duration is hours, and amount of sediment required is minimal ( 0.1 L). 

Our new appreciation of the role of inflammation in atherosclerosis shows the way for translation of these novel biological insights to clinical practice, for example by aiding the identification of individuals at risk of adverse cardiovascular events [5]. In this context, inflammatory biomarkers such as CRP merit rigorous consideration for inclusion in risk assessment strategies. In addition, these scientific advances provide a framework... 

The most specific biomarker of exposure to methyl parathion is the presence of the compound in serum or tissue. This is an especially good biomarker for detection shortly after acute exposure. For example, methyl parathion levels were detected in the sera of five men who were exposed for 5 hours in a cotton field 12 hours after it was sprayed with methyl parathion. The route of exposure was dermal, through unprotected hands. Serum levels averaged 156 ppb after 3 hours of the 5-hour exposure, and averaged 101.4 and 2.4 ppb at 7 and 24 hours postexposure, respectively (Ware et al. 1975). 

Some biomarkers only provide a measure of exposure others also provide a measure of toxic effect. Biomarkers of the latter kind are of particular interest and importance and will be referred to as mechanistic biomarkers in the present text. Some mechanistic biomarker assays directly measure effects at the site of action as described in Section 2.4 (see Chapter 4, Table 4.2, for examples). Inhibition of acetylcholinesterase is one example. Others measure secondary effects on the operation of nerves or the endocrine system (examples given in Table 4.2 and Chapters 15 and 16). 

Examples of biomarker assays operating at different levels are given in Table 4.2. The recent development of omics technology should provide strong support to this approach (Box 4.3). Microarray analysis, for instance, can give a time-related sequence of gene responses that relate to the cellular changes of toxicity. 

In predicting the effects of a pollutant on population growth rate, the effects of the chemical on the values of t, I, and n are of central interest. Chemical residue data and biomarker assays that provide measures of toxic effects are relevant here because they can, in concept, be used to relate the effects of a chemical upon the individual organism to a population parameter such as survivorship or fecundity (Figures 4.5 and 4.6). Examples of this are discussed in the second part of the text, including the reduction of survivorship of sparrow hawks caused by dieldrin (Chapter 5), the... 

Another issue is the development and refinement of the testing protocols used in mesocosms. Mesocosms could have a more important role in environmental risk assessment if the data coming from them could be better interpreted. The use of biomarker assays to establish toxic effects and, where necessary, relate them to effects produced by chemicals in the field, might be a way forward. The issues raised in this section will be returned to in Chapter 17, after consideration of the individual examples given in Part 2. 

The toxicology of PCBs is complex and not fully understood. Coplanar PCBs interact with the Ah-receptor, with consequent induction of cytochrome P4501A1/2 and Ah-receptor-mediated toxicity. Induction of P4501A1 provides the basis of valuable biomarker assays, including bioassays such as CALUX. Certain PCBs, for example, 3,3, 4,4 -TCB, are converted to monohydroxymetabolites, which act as thyroxine antagonists. PCBs can also cause immunotoxicity (e.g., in seals). 

This third part of the book will be devoted mainly to the problem of addressing complex pollution problems and how they can be studied employing new biomarker assays that exploit new technologies of biomedical science. Chapter 13 will give a broad overview of this question. The following three chapters, The Ecotoxicological Effects of Herbicides, Endocrine Disrupters, and Neurotoxicity and Behavioral Effects, will all provide examples of the study of complex pollution problems. 

Four examples will now be given of such mechanistic biomarker assays that can give integrative measures of toxic action by pollutants, all of which have been described earlier in the text. Where the members of a group of pollutants share a common mode of action and their effects are additive, TEQs can, in principle, be estimated from their concentrations and then summated to estimate the toxicity of the mixture. In these examples, toxicity is thought to be simply related to the proportion of the total number sites of action occupied by the pollutants and the toxic effect additive where two or more compounds of the same type are attached to the binding site. 

In addition to the foregoing, three further examples in this list (numbers 5-7) deserve consideration. These are (5) interaction of endocrine disrupters with the estrogen receptor, (6) the action of uncouplers of oxidative phosphorylation, and (7) mechanisms of oxidative stress. Until now only the first is well represented by biomarker assays that have been employed in ecotoxicology. 

Recently, there has been a growth of interest in the development of in vitro methods for measuring toxic effects of chemicals on the central nervous system. One approach has been to conduct electrophysiological measurements on slices of the hippocampus and other brain tissues (Noraberg 2004, Kohling et al. 2005). An example of this approach is the extracellular recording of evoked potentials from neocortical slices of rodents and humans (Kohling et al. 2005). This method, which employs a three-dimensional microelectrode array, can demonstrate a loss of evoked potential after treatment of brain tissue with the neurotoxin trimethyltin. Apart from the potential of in vitro methods such as this as biomarkers, there is considerable interest in the use of them as alternative methods in the risk assessment of chemicals, a point that will be returned to in Section 16.8. 

Because of their wide-ranging and holistic character, assays of behavioral effects have been used as screening procedures when testing for neurotoxicity (see, for example, Iversen 1991, Tilson 1993). They can provide sensitive indications of neurotoxic disturbances, which can then be traced back to their ultimate cause by using mechanistic biomarker assays. 

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