Detoxification product from

Table 16.1 Median lethal doses (at 48 h) of components of Prorhinotermes simplex and Schedorhinotermes lamanianus defensive secretions, and their detoxification products. (From Spanton and Prestwich, 1981)...

STAACK R, KINGSTON s, WALLiG M A and JEFFERY E H (1998) A Comparison of the individual and collective effects of four glucosinolate breakdown products from Brussels sprouts on induction of detoxification enzymes , Toxicol Appl Pharmacol, 149 17-23. 

An a priori classification of these various reactions as either toxification or detoxification is simply impossible, since each product from these various pathways may be toxic or not depending on its chemical properties and own products. Furthermore, the biological context plays a critical role [154], yet this role, best viewed as the influence of biological factors on the relative importance of competitive routes of metabolism, is often underplayed by those who venture to make predictions of metabolic outcome. Indeed, in the cascade of intertwined metabolic routes exemplified by haloalkenes, a small difference in pathway selectivity at an early metabolic crossroad may be amplified downstream, giving rise to major differences in relative levels of metabolites and overall toxicity. 

Uric acid is the end product of the purine metabolism. When uric acid excretion via the kidneys is disturbed, gout can develop (see p. 190). Creatinine is derived from the muscle metabolism, where it arises spontaneously and irreversibly by cyclization of creatine and creatine phosphate (see p. 336). Since the amount of creatinine an individual excretes per day is constant (it is directly proportional to muscle mass), creatinine as an endogenous substance can be used to measure the glomerular filtration rate. The amount of amino acids excreted in free form is strongly dependent on the diet and on the ef ciency of liver function. Amino acid derivatives are also found in the urine (e.g., hippu-rate, a detoxification product of benzoic acid). 

Cyclohexylundecanoic acid has been isolated from bovine milk and characterized (Schogt and Haverkamp Begemann 1965). Brewington et al. (1974) found glucuronides of 17 milk fatty acids in bovine milk. These were presumably detoxification products formed in the liver and, interestingly, included the odd-chain acids, 9 0-17 0. 

The true detoxification products as a rule appear in the urine, while the reactive intermediate toxic products remain in the body, tightly bound to tissue components, and thus chemically sequestered in the tissues. From the toxicological point of view therefore, it is not the percentage of the pharmacon and its metabolites recovered from urine, feces, and from the carcass by extraction that is most important in balance studies it is in fact the fraction of the... 

It would be particularly useful with a feed consisting of products from a previous detoxification step the detoxified material would be in dilute aqueous solution, the form required for supercritical water oxidation. 

The major natural auxin is indole-3-acetic acid (lAA) [42]. A number of related compounds exist in plants, including indolebutyric acid and indoleacetonitrile (Fig. la). These related compounds are active primarily when first converted to lAA [42]. In addition, there are a series of LAA conjugates with sugars and amino acids [43]. Some of these may be detoxification products, but others may be reservoirs of releasable lAA, especially in seeds. Phenylacetic acid (Fig. la) has auxin activity, and exists in sizable amounts in a few plants such as tobacco [42], but it is unclear that this compound actually moves from one part of a plant to another. In addition to the natural auxins, a whole host of synthetic auxins are known. The most widely used are a-naphthaleneacetic acid (NAA) and 2,4-dichlorophenoxyacetic acid (2,4-D) (Fig. la). 

Thiocyanate [SCN ], the anion of thiocyanic acid, is an important waste product from the chemical industry, it is present in various food items, it may be added to dairy milk to promote bacteriostatic processes, and it is synthesixed in the human liver as part of detoxification of cyanide. A special case in medicine has been generation of large amounts of thiocyanate leading to hypothyroidism after sodium nitroprusside infusion for hypertension (Nourok et at, 1964). After oral ingestion thiocyanate is readily absorbed. It is partly bound to albumin in blood, and mainly eliminated by excretion in urine. The half life of thiocyanate in humans is in the order of 1—2 weeks (Scherer, 2006), but varies between individuals. Thiocyanate may have a number of... 

Reactions between the sulfur-containing amino acids cysteine and methionine (Fig. 2.18) and rufhenium(II) arene anticancer complexes are of much interest in view of the strong influence of sulfur amino acids on the intracellular chemistry of platinum drugs, their involvement in detoxification and resistance mechanisms [100]. We found [101] that [(ri -biphenyl)Ru(en)Cl][PF 5] reacts slowly with the thiol amino add L-cysteine in aqueous solution at 310 K, pH 2-5, and only to about 50% completion at a 1 2 mM ratio. Reactions appeared to involve aquation as the first step followed by initial formation of 1 1 adducts via substitution of water by S-bound or O-bound cysteine. Two dinuclear complexes were also detected as products from the reaction. In these reactions half or all of the chelated ethylene-diamine had been displaced and one or two bridging cysteines were present The unusual cluster species (biphenyl) Ru g was also formed espedaUy at higher cysteine concentrations. The reaction was suppressed in 50 mM triethylammo-nium acetate solution at pH > 5 or in 100 mM NaCl suggesting that thiols may not readily inactivate Ru(II)-en arene complexes in blood plasma or in cells. Similarly, reactions with the thioether sulfur of methionine appeared to be relatively weak. Only 27% of [(r -biphenyl)Ru(en)Cl][PF5] reacted with L-methionine (L-MetH) at an initial pH of 5.7 after 48 h at 310 K, and gave rise to only one adduct [(ri -biphenyl) Ru(en) (i-MetH -S)]. ... 

Figure 5.13. Explanation of different toxicity of an alkaloid introduced orally and intravenously. The alkaloid sparteine, when injected, is 20 times as toxic as when given orally. The alkaloid is absorbed slowly from the intestine and is converted in the liver to a detoxification product and then excreted by the kidney, which prevents accumulation in the blood over a dangerous level. When injected the barriers are avoided and the rapid action on the nervous system does not allow the kidney enough time to excrete the compound (Nowacki and Wezyk, 1960). Courtesy of the journal.

---