The Metabolic Fate of Endrin in the Rabbit

Bedford, Colin T.; Harrod, R. K.; Hoadley, Elizabeth C.; Hutson, D. H.

doi:10.3109/00498257509056119

Cited by 23 publications

(3 citation statements)

References 12 publications

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“…9-KEN is some fivefold more toxic than endrin to rats and appears to be the ultimate toxic metabolite of endrin (Bedford et al, 1975a;Hutson et al, 1975). Species differences are evident, since Kadous and Matsumura (1982) reported the order of endrin metabolite toxicity to male German cockroaches as 5-OH anti-9-OH 9-keto-, whereas the order on topical application was 9-keto  syn-9-OH  endrin » anti-9-OH to houseflies and 9-syn-OH  9-keto- endrin » anti-9-OH to blowflies (Brooks and Mace, 1987).…”

Section: Inhibitorsmentioning

confidence: 98%

Interactions with the Gamma-Aminobutyric Acid A-Receptor

Brooks¹

2010

Hayes' Handbook of Pesticide Toxicology

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Section: Inhibitorsmentioning

confidence: 98%

Interactions with the Gamma-Aminobutyric Acid A-Receptor

Brooks¹

2010

Hayes' Handbook of Pesticide Toxicology

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“…Figure 4 illustrates the formation of the glucuronide of anti-12-hydroxy-[l^Clendrin under the following conditions: volume, 5 ml; hydroxyendrin, 0.004 mM; UDPGA, 0.75 mM; washed rabbit liver microsomes (4.2 mg/ml) in 0.1 M TRIS-HC1 buffer (pH 7.4 at 37°C); incubation temperature, 37°C. Portions (1 ml) were withdrawn at intervals and partitioned between benzene and water which were then radioassayed to afford the proportions of unchanged substrate and conjugate respectively (22). Triton X-100 had no effect on this reaction, possibly because the very lipophilic anti-12- …”

Section: Type II Metabolismmentioning

confidence: 99%

The Use of Animal Subcellular Fractions to Study Type II Metabolism of Xenobiotics

Crawford

Hutson

1979

Xenobiotic Metabolism: In Vitro Methods

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Type II biotransformations or conjugation reactions are enzyme -catalysed energy-requiring biosyntheses. The ultimate reaction requires a high-energy donor substrate, an acceptor substrate and an appropriate transferase. The high-energy substrate may contain the endogenous conjugating agent (conjugand) (e.g. glucuronic acid, as in UDPGA) or it may contain the xenobiotic (e.g. 4-chlorobenzoic acid, as in 4-chlorobenzoyl-CoA). If the xenobiotic is to be activated to become a donor substrate, other enzymes and high energy substrates (e.g. ATP) are called into action. If we assume for the moment that the low molecular weight substrates for these reactions have equal access to every component in the cell, then the subcellular location of the transferring enzyme will be the controlling factor in the subcellular distribution of the conjugation reaction. History of the TechniqueThe metabolism of foreign compounds has been studied in various subcellular fractions from about 1950. Brodie and coworkers (1) presented the first overview of the enzyme -catalysed metabolism of these compounds in 1958. In the intervening years, the properties of microsomes and other subcellular fractions in relation to the metabolism and toxicity of drugs, pesticides and, more recently, 'environmental' chemicals have received an enormous amount of study. However, it is interesting to note that the best of the earlier reviews of the enzymology of foreign compound metabolism by J. R. Gillette in 1963 (2) contains the essential details of each of the conjugation reactions referred to below. Progress has not been even: it has proved difficult to keep our treatment of glucuronyltransferase within reasonable limits, yet amino acid conjugation, despite some very interesting species differences, has received very little attention at the enzyme level.For our practical purposes, the animal cell can be regarded as composed of nucleus, endoplasmic reticulum, mitochondria 0-8412-0486-l/79/47-097-181$12.25/0

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“…In mice little ketoendrin is formed and in birds none (Stickel et al, 1979;Mount & Oehme, 1981). Endrin and its metabolites are excreted mainly in the bile (Cole et al, 1968), but in rats 50% is excreted in urine (Bedford et al, 1975b).…”

mentioning

confidence: 99%

A Case of Fatal Endrin Poisoning

Runhaar¹,

Sangster²,

Greve

et al. 1985

Human Toxicology

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1 Ingestion of 12 g of endrin by a 49-year-old man caused convulsions persisting for 4 days, hypersalivation, hyperthermia, renal insufficiency, thrombocytopenia and recurrent hypotension. Death followed after 11 days, due to pulmonary complications (infection and haemorrhage) and hypoxaemia causing bradycardia and cardiac arrest. 2 Endrin and dieldrin concentrations in blood 4 hours, 6 and 11 days after ingestion were respectively 450, 86 and 71 μg/l for endrin and 60, 19 and 19 μg/l for dieldrin. Dieldrin was also present, possibly because the endrin preparation contained traces of dieldrin. 3 Endrin concentrations 11 days after ingestion were 0.071 mg/l in blood, in adipose tissue 89.5 mg/kg, in the heart 0.87 mg/kg, in the brain 0.89 mg/kg, in the kidneys 0.55 mg/kg and in the liver 1.32 mg/kg.

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The Metabolic Fate of Endrin in the Rabbit

Cited by 23 publications

References 12 publications

Interactions with the Gamma-Aminobutyric Acid A-Receptor

Interactions with the Gamma-Aminobutyric Acid A-Receptor

The Use of Animal Subcellular Fractions to Study Type II Metabolism of Xenobiotics

A Case of Fatal Endrin Poisoning

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