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Toxic chemicals narcotics

According to McFarland [26], aquatic toxicity can be considered the result of penetration of toxicant into biophases and its interaction with one or more biochemical sites of action. Thus, he and others have postulated that toxicity is a function of the ability of the chemical to enter biophases and its ability to react with cellular compounds. Bioavailability of chemicals in fish has been shown to be related to chemical flux across fish gills [27], an identified exposure pathway. Flux across fish gills is in turn related to the ability of the chemical to partition between organic and aqueous phases, which is usually correlated with the its octanol-water partition coefficient (logPo/w) [28]. It is therefore not surprising that the acute toxicity of narcotic chemicals has been shown to be related to their propensity to accumulate in the membranes, and hence their logPe/w [29]. [Pg.362]

Veith, G.D., Call, D.J. and Brooke, L.T. (1983) Estimating the acute toxicity of narcotic industrial chemicals to fathead minnows, in W.E. Bishop, R.D. Cardwell and B.B. Heidolph (eds.), Aquatic Toxicology and Hazard Assessment Sixth Symposium, ASTM STP 802, American Society for Testing and Materials, Philadelphia, PA, pp. 90-97. [Pg.66]

Mackay D, Puig H, McCarty LS. 1992b. An equation describing the time course and variability in uptake and toxicity of narcotic chemicals to fish. Environ Toxicol Chem 11 941-951. [Pg.251]

Fig. 2. A simplified example of the general relationships between on the one hand the oc-tanol/water partition coefficient (Ko ) and on the other hand internal effect concentrations (body residues), bioconcentration and acute toxicity for narcotic organic chemicals and small freshwater fish [16], reproduced with permission... Fig. 2. A simplified example of the general relationships between on the one hand the oc-tanol/water partition coefficient (Ko ) and on the other hand internal effect concentrations (body residues), bioconcentration and acute toxicity for narcotic organic chemicals and small freshwater fish [16], reproduced with permission...
If biochemical imbalances do in fact occur, there is in turn the problem of first causes what triggered the imbalance in the first place (The same problem, of course, as with the occurrence of cancer.) The catchall term stress, freqnently mentioned, is intertwined with the culture, medicines, allergies, other biochemical abnormalities, the simplicities and complexities of food and drugs, exposure to toxic or even not-so-toxic chemicals, and hereditary factors, that is, the genetic component, etc. As for narcotic drugs, it is being noticed that drugs used for pain control per se may... [Pg.19]

In 1868 two Scottish scientists, Crum Brown and Fraser [4] recognized that a relation exists between the physiological action of a substance and its chemical composition and constitution. That recognition was in effect the birth of the science that has come to be known as quantitative structure-activity relationship (QSAR) studies a QSAR is a mathematical equation that relates a biological or other property to structural and/or physicochemical properties of a series of (usually) related compounds. Shortly afterwards, Richardson [5] showed that the narcotic effect of primary aliphatic alcohols varied with their molecular weight, and in 1893 Richet [6] observed that the toxicities of a variety of simple polar chemicals such as alcohols, ethers, and ketones were inversely correlated with their aqueous solubilities. Probably the best known of the very early work in the field was that of Overton [7] and Meyer [8], who found that the narcotic effect of simple chemicals increased with their oil-water partition coefficient and postulated that this reflected the partitioning of a chemical between the aqueous exobiophase and a lipophilic receptor. This, as it turned out, was most prescient, for about 70% of published QSARs contain a term relating to partition coefficient [9]. [Pg.470]

Possibly relevant to be added to data base in vitro bioassay general toxicity (extract) in vitro bioassay thyroid hormone disruption (extract) (incl. bioactivation) in vitro estrogenicity or androgenicity (extract) Chemicals that only are toxic in high concentration (narcotics, nanoparticles) Chemical analysis of lipophillic POPs in water... [Pg.100]

An alkaloid is a complex organic chemical substance found in plants, which characteristically combines nitrogen with other elements, has a bitter taste, and typically has some toxic, stimulant, analgesic effects. There are many different alkaloids, 30 of which are found in the opium plant. While morphine is the most important alkaloid in opium—for its natural narcotic qualities as well as providing the chemical structure for heroin—another alkaloid, codeine, is also sought after for its medicinal attributes. Other alkaloids include papaverine, narcotine, nicotine, atropine, cocaine, and mescaline. While the concentration of morphine in opium varies depending on where and how the plant is cultivated, it typically ranges from 3 percent to 20 percent. [Pg.17]

Acute toxicity to aquatic species can be rationalized mechanistically by one of two types of interactions nonspecific mechanisms (called narcosis) or specific mechanisms. The latter involves specific interactions, such as covalent electrophilic reactions with biological macromolecules, or specific noncovalent interactions that cause toxicity, such as uncoupling of phosphorylative oxidation, among others. Most chemicals that are toxic to aquatic organisms are narcotic. Some have both narcotic and specific mechanisms. A narcotic chemical enters the cellular membranes of the organism and, by its mere presence, causes perturbations in the membranes to the extent that alterations in the function of the membranes occur, resulting in toxicity. [Pg.362]

Let us now evaluate how we can assess the baseline toxicity of organic chemicals in a quantitative way. We have already mentioned that certain membrane functions may be disrupted if a chemical occupies a certain volume fraction of that membrane. This means that for two compounds of the same size, we would anticipate that when they are present at equal concentrations in the membrane they would exert the same effect. Furthermore, since the majority of chemicals of interest to us do not differ in size by more than a factor of 3 to 4 (compare molar volumes in Chapter 5, e.g., Fig. 5.2), the membrane concentration required for any compound to cause a narcotic effect will be in the same order of magnitude. Therefore, we may expect that the concentration of a compound required in an environmental medium (e.g., water, air) to cause a narcotic effect in an organism should be inversely proportional to the tendency of the compound to accumulate from that medium into biological membranes. [Pg.375]

You are interested in the well-being of Ampelisca abdita, living in a harbor whose sediments are contaminated with 4-nonylphenol. You remember that the lethal volume fraction of narcotic chemicals in membranes is about 0.01 L compound L I lipid. If the sediment contains 2% organic carbon by weight, and the amphipod is assumed to accumulate body burdens up to equilibrium with the sediments on which it lives, what sediment concentration of 4-nonylphenol should be deemed acceptable with respect to baseline toxicity Assume a log ,lipsw = 5.5 for 4-nonylphenol. Use Eq. 9-26c (alkylated and chlorinated benzenes ) for estimating Kioc. Compare your result with the findings of Fay et al. (2000), who observed a die-off of half the amphipods when they were exposed to about 0.16 g 4-nonylphenol - kg-1 sediment. [Pg.386]

Acetylene (Figure 13.1) is widely used as a chemical raw material and fuel for oxyacetylene torches. It was once the principal raw material for the manufacture of vinyl chloride (see reaction 13.2.4), but other synthetic routes are now used. Acetylene is a colorless gas with an odor resembling garlic. Though not notably toxic, it acts as an asphyxiant and narcotic and has been used for anesthesia. Exposure can cause headache, dizziness, and gastric disturbances. Some adverse effects from exposure to acetylene may be due to the presence of impurities in the commercial product. [Pg.298]

The TU approach, combined with equilibrium partitioning (EqP) and (Q)SAR modeling, was also used by Swartz and DiToro (1997) to develop the XPAII model to predict the toxicity of sediment-associated PAH compounds. A (Q)SAR and EqP method is also presented by Swartz and DiToro (1997) for modeling narcotic chemicals in sediments. In this approach, the sediment quality guideline for a mixture of narcotic chemicals that exhibit additive toxicity could be expressed as the sum of the fraction of the OC-normalized sediment concentrations divided by the SQG for each... [Pg.169]


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