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The acute oral toxicity of parathion in relation to dietary protein

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Summary

The clinicopathological syndrome of acute oral toxicity to parathion (98.5% technical) was determined in male albino rats fed for 28 days from weaning on a diet containing 3.5% protein as casein (group I), normal amounts of protein as casein (26% group II), and normal amounts of mixed natural protein as laboratory chow. The LD50±S.E. was found to be 4.86±0.31 mg/kg in group I, 37.1±4.9 mg /kg in group II and 23.4±5.4 mg/kg in group III. The LD50 in group I was significantly lower than that in group II which, in turn, was significantly higher than that in group III. Most deaths occurred at 10–35 hours in all three groups. The clinical syndrome of intoxication was essentially the same in all three groups and included signs of cholinergic stimulation such as diarrhea, sialarrhea and dacryorrhea, of stimulation of the central nervous system such as piloerection, tremors, and exophthalmos, alternating with signs of depression of the central nervous system such as hyporeflexia, drowsiness, ataxia, prostration and pallor. These signs were accompanied by anorexia, oligodipsia, hypothermia, loss of body weight, oliguria, proteinuria, hematuria and glucosuria. At autopsy there were found a very mild local irritant gastroenteritis, vascular congestion of many organs, a contracted spleen and, when death was delayed, gastric ulcers and degenerative changes in organs such as the liver and kidneys. Most organs were dehydrated and had lost weight. The survivors appeared normal by the 4th day but there was a persistent hematuria, glucosuria and proteinuria. Organ weights and water contents were mostly within normal limits at 2 weeks and 1 month but autopsy at these intervals occasionally disclosed healed or healing abscesses, indicating that resistance to infection had been lowered by parathion, and other residual changes such as a megacolon and hydrated muscle.

Zusammenfassung

Die akute perorale Toxizität von Parathion (98,5% technisch) wurde an jungen, männlichen Albino-Ratten bestimmt. Die Tiere in Gruppe I erhielten eine gereinigte Diät, in der Eiweiß als Casein in sehr geringen Mengen (3,5%) enthalten war, in Gruppe II die gleiche Nahrung wie Gruppe I, jedoch mit Casein in normaler Menge (26%), und in Gruppe III die übliche gepreßte Trockennahrung (Chow). Die LD50±S.F. betrug in Gruppe I 4,86±0,31 mg/kg Körpergewicht, 37,1±4,9 mg/kg in Gruppe II, und 23,4±5,4 mg/kg in Gruppe III. Das klinisch-pathologische Vergiftungssyndrom war im wesentlichen in allen 3 Gruppen gleich. Die klinischen Manifestationen umfaßten: Haaraufrichtung, Diarrhöe, Sialarrhoe, Dakryorrhoe, Hemodakryorrhoe, Nasenbluten, Exophthalmus, Zittern, Hyporeflexie, Lustlosigkeit, Ataxie, Anorexie, Oligodipsie, Körpergewichtsverlust, Oligurie, Albuminurie, Hematurie, und Glykosurie. Die meisten Todesfälle traten nach 10–35 Std ein. Bei der Autopsie fanden sich geringe akute Enteritis, ausgedehnte Erweiterung der venösen Capillaren, degenerative Veränderungen in Leber und Nieren und Wasserverlust und Gewichtsverlust der Körperorgane. Die Überlebenden schienen nach 4 Tagen wieder normal zu sein, die Organgewichte sowie der Wassergehalt lagen nach 2 Wochen und nach 1 Monat in den Normbereichen.

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References

  • Ball, W. L., J. W. Sinclair, M. Crevier, andK. Kay: Modification of parathion's toxicity for rats by pretreatment with, chlorinated hydrocarbon insecticides. Canad. J. Biochem.32, 440–445 (1954).

    Google Scholar 

  • Boyd, E. M.: Food and drug toxicity: a summary of recent studies. J. clin. Pharmac.8, 281–284 (1968a).

    Google Scholar 

  • —: Predictive drug toxicity: assessment of drug safety before human use. Canad. med. Ass. J.98, 278–293 (1968b).

    Google Scholar 

  • - Dietary protein and pesticide toxicity. Bull. Wld Hlth Org., in press (1969).

  • —, andM. A. Boulanger: Insecticide toxicology. Augmented susceptibility to carbaryl toxicity in albino rats fed purified casein diets. J. agr. Food Chem.16, 834–838 (1968).

    Google Scholar 

  • -, and E.Carsky: The acute oral toxicity of the herbicide chlorpropham in albino rats fed diets containing varying amounts of protein. Arch. environm. Hlth, in press (1969a).

  • Boyd, E. M., andE. Carsky: Kwashiorkorigenic diet and diazinon toxicity. Acta Pharmacol. (Kbh.)27, 284–294 (1969b).

    Google Scholar 

  • —, andC. P. Chen: Lindane toxicity and protein-deficient diet. Arch. environm. Hlth17, 156–163 (1968).

    Google Scholar 

  • —, andE. S. De Castro: Protein-deficient diet and DDT toxicity. Bull. Wld Hlth Org.38, 141–150 (1968).

    Google Scholar 

  • —, andI. Dobos: Protein-deficiency and tolerated oral doses of endosulfan. Arch. int. Pharmacodyn.,178, 152–165 (1969a).

    Google Scholar 

  • - -The acute oral toxicity of monuron in albino rats fed from weaning on different diets. J. agr. Food Chem., in press (1969b).

  • —, andL. M. Knight: Postmortem shifts in the weight and water levels of body organs. Toxicol. appl. Pharmacol.5, 119–128 (1963).

    Google Scholar 

  • —, andC. J. Krijnen: Toxicity of captan and protein-deficient diet. J. clin. Pharmacol.8, 225–234 (1968).

    Google Scholar 

  • - - The influence of protein intake on the acute oral toxicity of carbaryl. J. clin. Pharmacol., in press (1969a).

  • - - Dietary protein and DDT toxicity. Bull. environm. Contam. Toxicol., in press (1969b).

  • -, and V.Krupa: The acute oral toxicity of demeton in albino rats fed from weaning on diets of varying protein content. Canad. J. pharmaceut. Sci., in press (1969).

  • -, and J.Stefec: Dietary protein and pesticide toxicity: endrin. Canad. med. Ass. J., in press (1969).

  • —, andT. K. Tanikella: The acute oral toxicity of malathion in relation to dietary protein. Arch. f. Toxikol.24, 292–303 (1969).

    Google Scholar 

  • -, and F. I.Taylor: The acute oral toxicity of chlordane in albino rats fed for 28 days from weaning on a protein-deficient diet. Ind. Med. Surg., in press (1969).

  • Colhoun, E. H.: Physiological events in organophosphorus poisoning. Canad. J. Biochem.37, 1127–1134 (1959).

    Google Scholar 

  • De Castro, E. S., andE. M. Boyd: Organ weights and water content of rats fed protein-deficient diets. Bull. Wld Hlth Org.38, 971–979 (1968).

    Google Scholar 

  • Ecobichon, D. J., andW. Kalow: Action of organophosphorus compounds upon esterases in human liver. Canad. J. Biochem.41, 1537–1546 (1963).

    Google Scholar 

  • Frawley, J. P., E. C. Hagan, andO. G. Fitzhugh: A comparative pharmacological and toxicological study of organic phosphate-anticholinesterase compounds. J. Pharmacol. exp. Ther.105, 156–165 (1952).

    Google Scholar 

  • Gaines, T. B.: The acute toxicity of pesticides to rats. Toxicol. appl. Pharmacol.2, 88–99 (1960).

    Google Scholar 

  • Hegsted, D. M., andY.-O. Chang: Protein utilization in growing rats. I. Relative growth index as a bioassay procedure. J. Nutr.85, 159–168 (1965).

    Google Scholar 

  • Khera, K. S., andD. A. Lyon: Chick and duck embryos in the evalution of pesticide toxicity. Toxicol. appl. Pharmacol.13, 1–15 (1968).

    Google Scholar 

  • Mayer, J., andE. A. Arees: Ventromedial glucoreceptor system. Fed. Proc.27, 1345–1348 (1968).

    Google Scholar 

  • McFarland, L. Z., andP. B. Lacy: Acute anticholinesterase toxicity in ducks and Japanese quail. Toxicol. appl. Pharmacol.12, 105–114 (1968).

    Google Scholar 

  • Meeter, E., andO. L. Wolthuis: The effects of cholinesterase inhibitors on the body temperature of the rat. Europ. J. Pharmac.4, 18–24 (1968).

    Google Scholar 

  • Murphy, S. D., R. R. Lauwerys, andK. L. Cheever: Comparative anticholin-esterase action of organophosphorus insecticides in vertebrates. Toxicol. appl. Pharmacol.12, 22–35 (1968).

    Google Scholar 

  • Nakatsugawa, T., N. M. Tolman, andP. A. Dahm: Degradation and activation of parathion analogs by microsomal enzymes. Biochem. Pharmacol.17, 1517–1528 (1968).

    Google Scholar 

  • O'Brien, R. D.: The effect of SKF 525 A (2-diethylaminoethyl, 2∶2-diphenyl-valerate hydrochloride) on organophosphate metabolism in insects and mammals. Biochem. J.79, 229–235 (1961).

    Google Scholar 

  • —: The role of activating and degrading enzymes in determining species specificity of toxicants. Ann. N.Y. Acad. Sci.123, 156–162 (1965).

    Google Scholar 

  • Seume, F. W., J. E. Casida, andR. D. O'Brien: Effects of parathion and malathion separately and jointly upon rat esterases in vivo. J. agr. Food Chem.8, 43–47 (1960).

    Google Scholar 

  • Taylor, W. J. R., andZ. N. Gaut: Poisoning with the newer organophosphorus insecticides. Int. J. Clin. Pharmac. Ther. Toxicol.3, 175–183 (1968).

    Google Scholar 

  • Vukovitch, R. A., A. J. Triolo, andJ. M. Coon: Protective effect of chlorpromazine on parathion and paraoxon toxicity in mice. Fed. Proc.27, 597 (1968).

    Google Scholar 

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This project was assisted by grants from the World Health Organization and the Medical Research Council of Canada.

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Boyd, E.M., Chen, C.P. & Liu, S.J. The acute oral toxicity of parathion in relation to dietary protein. Arch. Toxikol. 25, 238–253 (1969). https://doi.org/10.1007/BF00577780

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