The fate of 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) following oral administration to man

Gehring, P.J.; Kramer, C. G.; Schwetz, Bernard A.; Rose, James Q.; Rowe, V. K.

doi:10.1016/0041-008x(73)90271-8

Cited by 56 publications

(18 citation statements)

References 4 publications

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“…This should be checked, although present lack of understanding of the role of this enzyme system makes toxicological assessment impossible. Along these lines, it has been shown that these chlorophenoxy acids do not accumulate in human tissue after single dose ingestion, although short term plasma levels in human subjects of over 0.1 mm have been reported (2,4 …”

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confidence: 99%

2,4-Dichlorophenoxyacetic Acid Inhibits the Outer Membrane NADH Dehydrogenase of Plant Mitochondria

Mannella¹,

Bonner²

1978

Plant Physiol.

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The NADH dehydrogenase of potato (Solanum tuberosum) and mung bean (Phaseolus aureus) outer mitochondrial membranes is specifically inhibited by both 2,4-dchlorophenoxyacetic and 2,4,5-trichlorophenoxyacetic acids but not by the natural auxin indole-3-acetic acid.The chemical agent 2,4-D is widely used as a selective herbicide although its biochemical mode of action is not fully understood. We have found that 2,4-D inhibits the NADH dehydrogenase system associated with the outer membranes of potato (Solanum tuberosum) and mung bean (Phaseolus aureus) mitochondria. [ Inhibition by 2,4-D is detectable only at initial NADH levels below this value (Fig. 2), indicating that 2,4-D acts at the dehydrogenase. The mode of inhibition of the NADH dehydrogenase by 2,4-D is complex, appearing competitive with NADH at concentrations of this substrate just below 0.2 mm and uncompetitive at very low NADH concentrations (Fig. 2 and ref. 3). At an initial NADH level of 0.1 mm, concentrations of 2,4-D approaching its water solubility limit (about 2 mM) produce essentially complete inhibition of this outer mitochondrial membrane activity, while inhibiting the microsomal NADH-Cyt c oxidoreductase to a far lesser extent (Fig. 1). It was found that the related compound 2,4,5-trichlorophenoxyacetic acid is also a specific inhibitor of the outer mitochondrial membrane NADH dehydrogenase while IAA, the natural auxin whose hormonal action appears to be mimicked by these chlorophenoxy acids, is not.Since the function of the NADH dehydrogenase-Cyt bs,% system of the outer mitochondrial membrane is not known, the physiological relevance of its inhibition by these compounds is unclear. A possibility suggested by these results is that this electron transfer system is involved, in plants, in

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confidence: 99%

2,4-Dichlorophenoxyacetic Acid Inhibits the Outer Membrane NADH Dehydrogenase of Plant Mitochondria

Mannella¹,

Bonner²

1978

Plant Physiol.

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“…Now 2,3,7,8-tetrachlorodibenzo-p-dioxin has a high toxicity in adult animals (Schwetz et al, 1973) and induces severe lesions in the liver, thymus and other organs in the rat, mouse and guinea-pig and also causes anomalies in mouse foetuses (Moore et al, 1973). This fact suggested that the carcinogenic agent in 2,4,5-T could be the contaminating dioxins (Ton That Tung, 1973).…”

Section: Discussionmentioning

confidence: 99%

“…Considering that the 2,4,5-T preparation we used contained 0 05 ppm dioxins, the dioxin dose was thus less than 1 ng/kg body weight, i.e. 5 x 104 times lower than the LD50 for mice (50 ,tg) administered in a single dose (Schwetz et al, 1973).…”

Section: Discussionmentioning

confidence: 99%

“…The work by Gehring et al (1973) on 2,4,5-T showed that the kinetics of excretion of 2,4,5-T was extremely variable from one species to another. The half-life of 2,4,5-T in the plasma after a dose of 5 mg/kg was found to be 4-7 h in the rat, 77 h in the dog and 23 h in man.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies on its toxicity (Grigsby and Farwell, 1950;Drill and Hiratzka, 1953;Rowe and Hymas, 1954) and metabolism (Piper et al, 1973;Gehring et al, 1973) have been performed. Courtney et al (1970) showed that it was teratogenic for mice, but such an action was not confirmed in rats and rabbits (Emerson et al, 1971;Sparschu et al, 1971).…”

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confidence: 99%

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Bioassay of 2, 4, 5-trichlorophenoxyacetic acid for carcinogenicity in mice

Muranyi-Kovacs¹,

Rudali²,

Imbert³

1976

Br J Cancer

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Summary.-Adult mice of strains C3Hf and XVII/G received 2,4,5-T by continuous oral administration (80 ppm in the diet). The 2,4,5-T preparation contained less than 005 ppm of dioxins. In 2,4,5-T-treated C3Hf mice a significant increase in the incidence of neoplastic lesions was found. No significant difference was found in the XVII/G strain between the treated and control mice. Rare forms of tumours, which were not observed in the controls, were present in the 2,4,5-T-treated C3Hf mice.

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2,4,5‐Trichlorphenoxyessigsäure (2,4,5‐T) einschl. Salze und Ester [MAK Value Documentation in German language, 1995]

2012

The MAK‐Collection for Occupational Health and Safety

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Veröffentlicht in der Reihe Gesundheitsschädliche Arbeitsstoffe , 21. Lieferung, Ausgabe 1995 Der Artikel enthält folgende Kapitel: Allgemeiner Wirkungscharakter Wirkungsmechanismus Toxikokinetik Erfahrungen beim Menschen Tierexperimentelle Befunde und in‐vitro‐Untersuchungen Akute Toxizität Subakute, subchronische und chronische Toxizität Wirkung auf Haut und Schleimhäute Allergene Wirkung Reproduktionstoxizität Genotoxlzität Kanzerogenität Bewertung

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The fate of 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) following oral administration to man

Cited by 56 publications

References 4 publications

2,4-Dichlorophenoxyacetic Acid Inhibits the Outer Membrane NADH Dehydrogenase of Plant Mitochondria

2,4-Dichlorophenoxyacetic Acid Inhibits the Outer Membrane NADH Dehydrogenase of Plant Mitochondria

Bioassay of 2, 4, 5-trichlorophenoxyacetic acid for carcinogenicity in mice

2,4,5‐Trichlorphenoxyessigsäure (2,4,5‐T) einschl. Salze und Ester [MAK Value Documentation in German language, 1995]

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