Xenobiotic chemicals

Lewis DL, Hodson RE, Freeman LF III. 1984. Effects of microbial community interactions on transformation rates of xenobiotic chemicals. Appl Environ Microbiol 48 561-565. 

Guengerich P (1990) Enzymatic oxidation of xenobiotic chemicals. CritRev Biochem Mol Biol 25 97-153. 

Sabljic A (1989) Quantitative modeling of soil sorption for xenobiotic chemicals. Environ Health Persp 83 179-190... 

Rollins-Smith, L.A., Hopkins, B.D., and Reinert, L.K. An amphibian model to test the effects of xenobiotic chemicals on development of the hematopoietic system, Environ. Toxicol. Chem., 23, 2863, 2004. 

Sherratt TN, Roberts G, Williams P et al (1999) A life-history approach to predicting the recovery of aquatic invertebrate populations after exposure to xenobiotic chemicals. Environ Toxicol Chem 18 2512-2518... 

Nonpolar compounds, including the majority of xenobiotic chemicals and some metal complexes [249-252], generally diffuse passively through the lipid portions of the membrane by simple diffusion [21,246,253,254]. In this case, internalisation rates are reflected by compound permeability in the bilipid membrane [254,255] and can be predicted by Fick s law [254,256] ... 

Okey, A.B., Franc, M.A., Moffat, I.D., Tijet, N., Boutros, P.C., Korkalainen, M., Tuomisto, J. and Pohjanvirta, R. (2005) Toxicological implications of polymorphisms in receptors for xenobiotic chemicals the case of the aryl hydrocarbon receptor. Toxicology and Applied Pharmacology, 207, S43-S51. 

Schwitzguebel, J.-P., and Vanek, T., 2003, Some fundamental advances for xenobiotic chemicals, in Phytoremediation Transformation and control of contaminants, S. C. McCutcheon, J. L. Schnoor, eds., John Wiley Sons, Inc., Hoboken, pp. 123-157. 

There are many factors, both chemical and biological, which affect the disposition of xenobiotics. Chemical factors include size and structure, pKa, chirality, and lipophilicity. Biological factors include species, sex and strain, genetic factors, hormonal influences, disease and pathological conditions, age, stress, diet, dose, enzyme induction and inhibition, and tissue and organ specificity. All of these factors can affect the toxicity of a chemical by changing its disposition, especially its metabolism. 

Chemical injury may occur when a living cell comes into contact with a chemical foreign to its system. Chemicals which enter the living organism which are foreign to the system are known as xenobiotics. Chemical injury may be external as a relatively non-selective process wherein an overall disruption takes plase. An example of this would be an acid burn on the surface of the skin, wherein a general protein coagulation takes place with tissue and cellular disruption. The process of absorption is not specifically involved in this type of chemical injury. 

Agents that selectively induce or inhibit the xenobiotic metabolizing enzymes may alter the toxicity of xenobiotic chemicals. 

Carbonyl reduction is a metabolic pathway widely distributed in nature. Many endogenous substances, such as prostaglandins, biogenic amines, and steroids, together with xenobiotic chemicals of several varieties, are transformed to the corresponding alcohols before further metabolism and elimination. Carbonyl reduction in several continuous cell lines was investigated using metyrapone as a substrate ketone. Quercitrin was reported to inhibit carbonyl reductase. 

The purpose of the gastrointestinal tract is to digest and absorb food. As a result, it is a major site for absorption of xenobiotic chemical substances. Many environmental toxicants enter the food chain and are absorbed together with food. In occupational settings, airborne toxic substances enter the mouth from breathing and, if not inhaled, can be swallowed and absorbed from the gastrointestinal tract. 

Boethling, R.S. 1993. Biodegradation of xenobiotic chemicals. In Handbook of Hazardous Materials. M. Corn, ed., pp 55-67. Academic Press, New York. 

Xenobiotics Chemicals that have no relevant function for maintenance and... 

Clearly, in some cases, cancer is the result of the action of synthetic and naturally occurring chemicals. The role of xenobiotic chemicals in causing cancer is called chemical carcinogenesis.10 It is often regarded as the single most important facet of toxicology and clearly the one that receives the most publicity. 

Insofar as toxicological chemistry is concerned, the major function of the liver is to metabolize xenobiotic substances through phase I and phase II reactions. Because of this function, the liver is a crucial organ in the study of toxicological chemistry. Since it processes xenobiotic chemicals,... 

Other than ethanol, the xenobiotic chemical best known to cause steatosis is carbon tetrachloride, CC14. This compound was once widely used in industry as a solvent, and even in consumer items as a stain remover. As discussed in some detail in Chapter 16, it is converted by enzymatic action in the liver to C13C- radical, then by reaction with 02 to Cl3COO- radical, which reacts with unsaturated lipids in the liver to cause fatty liver. 

LB Willett Ohio State University, Wooster, OH Cattle methods to detect and monitor occurrence of potentially hazardous xenobiotics in their environment methods to reduce or eliminate exposure determine mechanisms by which xenobiotics are transported, bound, and mobilized study target organ modification caused by xenobiotic chemicals U. S. Department of Agriculture Cooperative State Research Service... 

The expression level of DMEs is not a fixed immutable property of the individual. Many DMEs are highly responsive to environmental influences—for example, to modulation by endogenous regulatory signals or to induction by xenobiotic chemicals. The five P450 enzymes that typically are most abundant in human liver (CYPs 3A4, 2C9, 1A2, 2E1, and 2C19) (6,7) all are subject, to various degrees, to induction by xenobiotic chemicals as are important Phase II enzymes in the GST or UGT families. 

Although this chapter emphasizes up-regulation (induction) of DMEs by xenobiotic chemicals there are abundant examples of down-regulation (suppression) of DME levels by xenobiotic chemicals, perhaps even involving some of the same regulatory pathways responsible for induction (reviewed in Refs. 20 and 21). 

---