Bioavailability in rats of bound and conjugated plant carbamate insecticide residues

Marshall, T. C.; Dorough, H. W.

doi:10.1021/jf60213a007

Cited by 38 publications

(11 citation statements)

References 10 publications

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“…That the fecal 14C residues indeed were not absorbed from the gut could be confirmed by cannulating the bile duct and radioassaying the bile ...". Published bioavailability studies have indeed examined the bile fluid (Marshall and Dorough, 1977) or have, as an alternative, examined the soluble portion of fecal radio-In the absence of significant radioactivity in the bile fluid, high soluble fecal radioactivity could be formed by the intestinal microflora. In the presence of significant radioactivity in bile fluid, soluble fecal radioactivity could originate from biliary excretion, a process well documented for DDT and related compounds (Hayes, 1975).…”

Section: Introductionmentioning

confidence: 99%

Animal bioavailability of a 3,4-dichloroaniline-lignin metabolite fraction from wheat

Sandermann¹,

Musick²,

Aschbacher³

1992

J. Agric. Food Chem.

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Section: Introductionmentioning

confidence: 99%

Animal bioavailability of a 3,4-dichloroaniline-lignin metabolite fraction from wheat

Sandermann¹,

Musick²,

Aschbacher³

1992

J. Agric. Food Chem.

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“…Many studies have shown that the bioavailability of bound residues is generally low. This has been found to be true for cambendazole (Baer et al 1977), trenbolone acetate (Ross 1980), carbofuran and carbaryl (Marshall and Dorough 1977).…”

Section: Bound Residuesmentioning

confidence: 81%

Toxicological significance of covalently‐bound residues

Rico

Burgat-Sacaze

1984

Food Additives & Contaminants

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Bound residues may be defined in terms of the nonextractable radioactivity which persists in tissues after administration of radiolabelled compounds to an organism. This fraction is found to contain natural endogenous compounds resulting from incorporation of degradation products of the administered substance into intermediary metabolites (amino acids, carbohydrates etc.). However, 'new' compounds are also found which arise from covalent binding of the administered substance or its metabolites to endogenous macromolecules. The former fraction is nontoxic, but in the second case the nature of the covalent binding is important from the toxicological point of view. It is unspecific and irreversible, and often involves the action of short-lived and highly reactive intermediates. The covalent bond is usually thermodynamically irreversible. A good example is provided by bromobenzene, which binds to proteins via the 3,4-epoxide, which is the hepatotoxic agent. From the above considerations it is possible to distinguish two types of metabolites that may be found in foodstuffs prepared from drug-treated animals. The first are represented by the drug itself and its primary metabolites. These compounds are potentially more or less toxic to the consumer. The second type are the covalently bound metabolites. These have lost their reactivity in an irreversible manner and may be considered to have low toxicity to the consumer as well as low bioavailability. Some examples (trenbolone acetate, aflatoxin, carbaryl) are discussed to support this contention.

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“…With increased defecation during exposure, residence time for intestinal contents decreased. Since 3-hydroxycarbofuran undergoes significant enterohepatic circulation, hydrolysis of conjugates in small intestine and subsequent 3-hydroxycarbofuran reabsorption [40,41,Ferguson et al, in review] could also decrease and conjugates could be excreted in feces. Though representing < I % of total "CC/animaI, greater carbofuran (1 1 x ) was measured in feces after 4.1 pm than after 1.5 pm particle inhalation.…”

Section: Discussionmentioning

confidence: 99%

Carbofuran disposition in the rat after aerosol inhalation

Ferguson

Jewell

Krieger

et al. 1982

Enviro Toxic and Chemistry

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-[14C-]Carbonyl carbofuran toxicity, metabolism and pharmacokinetics in male Sprague-Dawley rats were studied after 4.1 pm (50 min, 0.2 and 1.2 pglL) and 1.5 pm (70 min, 0.2 pglL) aerodynamic diameter monodisperse aerosol exposures. Regional carbofuran deposition for each particle size was similar to human and rodent models for insoluble aerosols. Total carbofuran deposition was greater than expected in the rodent model but similar to that in human models.3-Hydroxycarbofuranlcarbofuran ratios in gastrointestinal tract and liver (1.3,3 X greater after 4.1 pm) provided additional deposition indices. Rapid in vitro solubility t,,, (17 min) for 4.1 pm particles and minimal differences in plasma carbamate (% total ''Clanimal) after varied particle size exposure indicated primary clearance by dissolution, irrespective of deposition site. Carbofuran (1.2 pg/L, 4.1pm) inhibited red blood cell acetylcholinesterase (55% at 10 min postexposure with recovery by 2 h). Eight-hour I4C metabolic fate in I4CO, (3 1-38%), urine (9-12%), feces (2-5.5%) and carcass (44-58%) were similar for each particle size. Carbamate pharmacokinetics measured for 2 h postexposure to 4.1 prn particles described monoexponential elimination. Plasma half-lives for carbofuran (36 min) and 3-hydroxycarbofuran (62 min) were similar to those previously determined after oral and i.v. exposures.

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Bioavailability in rats of bound and conjugated plant carbamate insecticide residues

Cited by 38 publications

References 10 publications

Animal bioavailability of a 3,4-dichloroaniline-lignin metabolite fraction from wheat

Animal bioavailability of a 3,4-dichloroaniline-lignin metabolite fraction from wheat

Toxicological significance of covalently‐bound residues

Carbofuran disposition in the rat after aerosol inhalation

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