Toxicity of O,O,S-trimethyl and triethyl phosphorothioate to the rat

Nm, Mallipudi; Umetsu, Noriharu; Rf, Toia; Re, Talcott; Tr, Fufuto

doi:10.1021/jf60222a011

Cited by 58 publications

(21 citation statements)

References 9 publications

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“…Previous investigations reported that acute administration of OOS-TMP to rats leads to a delayed toxicity (death occurring 4 to 28 days after treatment). Symptoms of this delayed toxicity include body weight loss, and red staining around the eyes, nose and mouth [25][26][27]. Although the mechanism of this delayed toxicity remains unknown, histopathological and biochemical studies suggest that the lung may be a principle target organ of the delayed toxicity caused by OOS-TMP [28][29][30].…”

Section: Discussionmentioning

confidence: 99%

Effects of acute administration of O,O,S-trimethyl phosphorothioate on the respiratory burst and phagocytic activity of splenic and peritoneal leukocytes

Rodgers

Ellefson

1988

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An impurity in malathion, O,O,S-trimethyl phosphorothioate (OOS-TMP), was previously shown to be immunosuppressive. The immune cell type which induced immune suppression caused by OOS-TMP at 24 hrs after administration was found to be splenic macrophages. Further characterization of macrophages from OOS-TMP treated mice indicated that OOS-TMP led to macrophage differentiation. In this study, these initial studies were continued and extended to examine the effects of OOS-TMP on splenic and peritoneal macrophages at various times following exposure. Administration of OOS-TMP increased the size heterogeneity of cell volume, phagocytic capability and respiratory burst activity of splenic and peritoneal macrophages. However, by day 7 splenic and peritoneal macrophages from treated animals had size frequency histograms, phagocytic capability and respiratory burst activity similar to control. These data would suggest that macrophages not previously exposed to OOS-TMP migrated to the spleen and peritoneum of treated animals. This migration may allow the restoration of the ability of splenocytes from treated animals to generate an immune response. Alternatively, these data may indicate that 7 days following exposure to OOS-TMP, the differentiative state of the splenic and peritoneal macrophages of treated mice had decayed and hence these cells had regained resident characteristics.

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Section: Discussionmentioning

confidence: 99%

Effects of acute administration of O,O,S-trimethyl phosphorothioate on the respiratory burst and phagocytic activity of splenic and peritoneal leukocytes

Rodgers

Ellefson

1988

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“…Therefore, if a byproduct generated from OMT degradation retains the P@O bond, it still has an acute toxicity. For example, the oral LD 50 values in rats are 840 and 15 mg kg À1 for TMP and STMP, respectively (Mallipudi et al, 1979;Meister, 1991). The toxicity of STMP is two times as high as that of OMT (i.e., 30 mg kg À1 ) (NCILB, 1973).…”

Section: Toxicity Change Of Omt Solutionmentioning

confidence: 99%

Kinetics and mechanism for omethoate degradation by catalytic ozonation with Fe(III)-loaded activated carbon in water

2013

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“…The nontoxic ionic metabolites thus produced are readily excreted in the urine (March et al, 1956;Casida et al, 1963;Plapp and Tong, 1966;Talcott et al, 1979aTalcott et al, , 1979bTalcott et al, , 1979c. The recent discovery of the toxicity of some impurities in technical organophosphorus pesticides has led to reevaluation of the safety of several of these compounds (Mallipudi et al, 1979). In contrast to acute intoxication by an anticholinesterase organophosphate insecticide such as parathion, longer holding periods were required to determine LD SO values in rats treated with the impurities 0,0,5-trimethyl phosphorothioate and 0,0,5-triethyl phosphorothioate, particularly at lower doses.…”

Section: Introductionmentioning

confidence: 99%

“…Although the mode of action of these delayed toxic compounds is not known, they were shown to inhibit carboxylesterases and cholinesterases (Mallipudi et al, 1979;Talcott et al, 1979c;Umetsu et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

Delayed toxicity and delayed neurotoxicity of phosphorothioate and phosphonothioate esters

Armstrong

et al. 1981

Journal of Toxicology and Environmental Health

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The delayed neurotoxicity to hens and delayed toxicity to rats of the isomeric trimethyl phosphonothioates, trimethyl phosphate, and a series of the methyl and ethyl esters of methyl-, ethyl-, and phenylphosphonate and phosphonothioates were examined. All the O,O-dialkyl phosphonothioates, phosphorothioates, and their corresponding oxons were relatively nontoxic to rats, with oral LD50 values greater than the 150-450 mg/kg tested. The O,S-dialkyl phosphorothioate esters were highly acutely toxic. The rat acute LD50 values for O,S-dimethyl methylphosphonothioate and O,S-diethyl ethylphosphonothioate were 3 and 8 mg/kg. O,S-Diethyl ethylphosphonothioate and O,O, S-trimethyl phosphorothioate were the only compounds tested that showed delayed toxicity to rats. The delayed LD50 values for these two compounds were 7 and 15-20 mg/kg, respectively, with rats dying 3-22 d after treatment The delayed toxic effects were associated with continual loss of weight, reaching 18-46% at the time of death. Of this series of compounds, only O,O-diethyl phenylphosphonothioate and its oxon showed delayed neurotoxicity to hens 45 d after treatment. The minimum effective dose for these two compounds was 25 mg/kg.d administered ip for 10 d. These findings suggest that delayed neurotoxicity in hens is not due to the same mechanism as delayed toxicity in rats.

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Toxicity of O,O,S-trimethyl and triethyl phosphorothioate to the rat

Cited by 58 publications

References 9 publications

Effects of acute administration of O,O,S-trimethyl phosphorothioate on the respiratory burst and phagocytic activity of splenic and peritoneal leukocytes

Effects of acute administration of O,O,S-trimethyl phosphorothioate on the respiratory burst and phagocytic activity of splenic and peritoneal leukocytes

Kinetics and mechanism for omethoate degradation by catalytic ozonation with Fe(III)-loaded activated carbon in water

Delayed toxicity and delayed neurotoxicity of phosphorothioate and phosphonothioate esters

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