Classes of Toxicants

Considerable interest has developed concerning the nature of the mixed function oxidase system in fish and the role that this system may play in the development of toxic responses in these animals. Studies have shown that components of the mixed function oxidase system are present in relatively high concentrations in fish liver (4, 5, 6) and that the enzyme systems in this organ are capable of many of the biotransformation reactions already described for the mammalian liver (7, 8, 9). The presence of this complement of enzymes in the livers of many fishes suggests that this organ too may be particularly sensitive to insult from sub lethal concentrations of many waterborne toxicants. For this reason, methods to evaluate liver function in fish may be particularly useful in identifying the sublethal effects of certain classes of toxicants. 

Such essential limitations may markedly decrease the reliability and predictive capacity of quantitative structure-toxicity relationships (STRs) in haloalkenes and all other classes of toxic xenobiotics, but recognition of limitations does not suppress the need for predictive tools. In fact, any approach, empirical or mechanistic, that is able to uncover qualitative STR trends and to assign a priori labels of potential toxicity is certainly welcome. 

SPMD sample extracts, e.g., certain organochlorine pesticides (OCPs), are known to inhibit cholinesterase activity. Therefore, these results were not unexpected. However, it was surprising that a similar response was not observed with brain cholinesterase activity. It is possible that brain cells can more readily metabolize the chemicals, that the chemicals did not pass the brain blood barrier or that the effects occurred earlier in the exposure period, effectively allowing the activity to recover. Considering the numerous neurotoxic chemicals potentially entering aquatic ecosystems or present as airborne vapor phase chemicals, the neurotoxic mode of action related to exposure to contaminants is of increasing interest. Evidence presented in this work demonstrate that SPMDs concentrate members of this class of toxicants. 

Epidemiology studies are, of course, useful only after human exposure has occurred. For certain classes of toxic agents, carcinogens being the most notable, exposure may have to take place for several decades before the effect, if it exists, is observable - some adverse effects, such as cancers, require many years to develop. The obvious point is that epidemiology studies cannot be used to identify toxic properties prior to the introduction of a chemical into commerce. This is one reason toxicologists were invented ... 

Table 1 lists some allelopathlc plants of interest to foresters, together with the classes of toxic compounds produced and examples of species they are reported to suppress. The list is not exhaustive many species that may be allelopathlc have not been studied in depth. One easily observed effect—though sometimes difficult to distinguish from effects of competition—is the exclusion of shrubs, herbs, and other trees from beneath the crowns of particular tree species. 

Attempts to define the scope of toxicology, including that which follows, must take into account that the various subdisciplines are not mutually exclusive and are frequently interdependent. Due to overlapping of mechanisms as well as use and chemical classes of toxicants, clear division into subjects of equal extent or importance is not possible. 

Combustion products are not properly a use class but are a large and important class of toxicants, generated primarily from fuels and other industrial chemicals. 

The two classes of toxicant-protein interactions encountered may be defined as (1) specific, high affinity, low capacity, and (2) nonspecific, low affinity, high capacity. The term high affinity implies an affinity constant (/(binding) of the order of 108 M-1, whereas low affinity implies concentrations of 104 M-1. Nonspecific, low-affinity binding is probably most characteristic of nonpolar compounds, although most cases are not as extreme as that shown in Figure 6.10. 

An exhaustive review of the mechanisms by which chemicals cause acute toxicity is beyond the scope of this chapter. However, certain mechanisms of toxicity are relevant since they are common to many important classes of toxicants. Some of these mechanisms of acute toxicity are discussed. 

As previously described for the male reproductive toxicity, the class of toxicants affecting germ cells can alter the structure of genetic material (chromosomal aberrations, alterations in meiosis, DNA synthesis, and replication). Mature oocytes have a DNA repair capacity different from that of mature sperm, but this capacity decreases at the period of meiotic maturation. 

In cases where the toxicant has not been conclusively identified in the final effluent, the TTE approach must be used cautiously. Streams selected for TTE should be based on some knowledge of the type of process stream, effect of the effluent treatment plant on source stream toxicity, or Phase I TIE results. For example, a Phase I TIE conducted on the suspect source stream(s) could be used to ensure that it contains the sample class of toxicant(s) as the final effluent. The Phase I TIE may also suggest a possible treatment option for the TTE (z. e., addition of EDTA Novak et al., 2002). 

Toxicants can affect any type of tissue in any organ. Different classes of toxicants affect various tissues to varying degrees and in a variety of ways, depending on the nature of the toxicant, the kind of receptor that it attacks, the nature of the binding of the toxicant to the receptor, and the routes, transport, and metabolism of the toxicant in the organism. 

The neuronopathic symptoms described above are caused by substances that attack and destroy the cell bodies of neurons. Another class of toxic effects occurs as the result of deterioration of nerve axons and its surrounding myelin. Symptoms resulting from this effect are called axonopa-thies. A classic toxicant cause of axonopathies is that of y-diketones, most commonly 2,5-hex-anedione ... 

Explain what is shown by the following general reaction in terms of the metabolism of an important class of toxic compounds ... 

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