Toxicity detoxification

Primary degradation produces organic derivatives of a contaminant. The resulting one or more products exhibit their own properties, reactivities, fates, and effects. The metabolites may be either less toxic (detoxification) or even more hazardous than the parent compound (toxification). 

Trivalent arsenic is less abundant in nature, but considerably more toxic. Detoxification of arsenite results in the same methylated species as those arising from arsenate. However, because trivalent arsenic binds tightly to thiol-containing molecules in tissues, it is much less easily detoxified and excreted. 

Many poisons are dealt with by the liver which attempts to render the poison less toxic (detoxification) before it is excreted. Sometimes the poison damages or destroys liver cells but fortunately the liver has such a large reserve of cells that a great deal of damage is necessary to affect its function adversely. Liver damage may result from certain types of industrial poisons as well as from excessive consumption of alcohol. 

Detoxifica.tlon. Detoxification systems in the human body often involve reactions that utilize sulfur-containing compounds. For example, reactions in which sulfate esters of potentially toxic compounds are formed, rendering these less toxic or nontoxic, are common as are acetylation reactions involving acetyl—SCoA (45). Another important compound is. Vadenosylmethionine [29908-03-0] (SAM), the active form of methionine. SAM acts as a methylating agent, eg, in detoxification reactions such as the methylation of pyridine derivatives, and in the formation of choline (qv), creatine [60-27-5] carnitine [461-06-3] and epinephrine [329-65-7] (50). 

The metaboHsm of a material may result in the formation of a transformation product of lower intrinsic toxicity than the parent molecule ie, a process of detoxification has occurred. In other cases, the end result is a metaboHte, or metaboHtes, of intrinsically greater toxicity than the parent molecule, ie, metaboHc activation has occurred. Some examples of detoxification and metaboHc-activation processes are given in Table 2. 

The kidney is an important organ for the excretion of toxic materials and their metaboHtes, and measurement of these substances in urine may provide a convenient basis for monitoring the exposure of an individual to the parent compound in his or her immediate environment. The Hver has as one of its functions the metaboHsm of foreign compounds some pathways result in detoxification and others in metaboHc activation. Also, the Hver may serve as a route of elimination of toxic materials by excretion in bile. In addition to the Hver (bile) and kidney (urine) as routes of excretion, the lung may act as a route of elimination for volatile compounds. The excretion of materials in sweat, hair, and nails is usually insignificant. 

Fig. 3. Schematic representation showing the anatomical basis for differences in the quantitative supply of absorbed material to the Hver. By swallowing (oral route), the main fraction of the absorbed dose is transported direcdy to the Hver. FoUowing inhalation or dermal exposure, the material passes to the pulmonary circulation and thence to the systemic circulation, from which only a portion passes to the Hver. This discrepancy in the amount of absorbed material passing to the Hver may account for differences in toxicity of a material by inhalation and skin contact, compared with its toxicity by swallowing, if metaboHsm of the material in the Hver is significant in its detoxification or metaboHc activation.

Exposure studies have been made using mice and rats (257). These experiments have demonstrated species differences in butadiene toxicity and carcinogenicity. Butadiene was found to be a potent carcinogen in the mouse, but only a weak carcinogen in the rat. The interpretations have focused on differences in toxification rates and detoxification metaboHsms as causative factors (257). The metaboHsm is beHeved to proceed through intermediates involving butadiene monoepoxide and butadiene diepoxide (257). A similar mechanism has been proposed for its biodegradation pathway (258). 

Also, wet air oxidation offers an alternative to conventional incineration for the destmction and detoxification of dilute ha2ardous and toxic waste waters. A 98% removal efficiency of dyehouse effluent has been claimed by wet air oxidation (203). 

Drugs and other chemicals such as food additives or insecticides foreign to the body undergo enzymatic transformations that result in loss of pharmacological activity detoxification), or lead to the formation of metabolites with therapeutic or toxic effects bioactivation). 

Chemical treatment is a class of processes in which specific chemicals are added to wastes or to contaminated media in order to achieve detoxification. Depending on the nature of the contaminants, the chemical processes required will include pH adjustment, lysis, oxidation, reduction or a combination of these. Thus, chemical treatment is used to effect a chemical transformation of the waste to an innocuous or less toxic form. In addition, chemical treatment is often used to prepare for or facilitate the treatment of wastes by other technologies. Figure 12 identifies specific treatment processes which perform these functions. 

Solidification/Stabilization technologies are techniques designed to be used as final waste treatment. A major role of these processes is posttreatment of residuals produced by other processes such as incineration or chemical treatment. In some cases, solidification/ stabilization processes can serve as the principal treatment of hazardous wastes for which other detoxification techniques are not appropriate. High volume, low toxicity wastes (such as contaminated soils) are an example of this application. 

Detoxification. Destroys or reduces toxics that may otherwise create adverse environmental impacts. 

Detoxification The process of decomposition of toxic substances in the body to produce harmless substances, which are duty eliminated from the body. 

MDR-ABC Transporters. Figure 3 Detoxification cellular mechanisms. X, toxic compound X-OH, oxidized toxic compound GS-X, conjugated toxic compound OATP, organic anion transporting proteins CYPs, cytochromes GSH, glutathion UDPGIcUA, Uridine 5-diphosphoglucuronic acid PAPs, 3-phosphoadenylylsulfate. 

Rate of detoxification. Quite rapid, incapacitating dosages lose their effects in 5 to 10 minutes Skin and eye toxicity. Highly irritating but not toxic... 

A susceptible population will exhibit a different or enhanced response to methyl parathion than will most persons exposed to the same level of methyl parathion in the environment. Reasons may include genetic makeup, age, health and nutritional status, and exposure to other toxic substances (e g., cigarette smoke). These parameters result in reduced detoxification or excretion of methyl parathion, or compromised fimction of organs affected by methyl parathion. Populations who are at greater risk due to their imusually high exposure to methyl parathion are discussed in Section 6.7 Populations With Potentially High Exposures. 

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