Detail of "152-20-5"

Reference

A phosphorothionate isomer protects against the pneumotoxicity caused by O,O,S-trimethyl phosphorothioate

A phosphorothionate isomer protects against the pneumotoxicity caused by O,O,S-trimethyl phosphorothioate. Gandy, Jay; Imamura, Toshiko (Div. Toxicol. Physiol.In this study， 9035-51-2 and 39391-09-8 are also used., Univ. California, Riverside, CA 92521, USA). Toxicol. Appl. Pharmacol., 87(3), 498-508 (English) 1987. CODEN: TXAPA9. ISSN: 0041-008X. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) O,O,S-Tri-Me phosphorothioate (OOS-TMP) [152-20-5], an impurity in many organophosphorus insecticides, causes pneumotoxicity in rats at low doses (20 mg/kg) resulting in increases in bronchopulmonary lavage lactate dehydrogenase (LDH) activity and morphol. alterations of bronchiolar epithelium. Coadministration of the nontoxic isomer, O,O,O-trimethyl phosphorothioate (OOO-TMP) [152-18-1], at 1% of the toxicant dose, protected against the increase in LDH levels and morphol. changes in bronchioles caused by OOS-TMP. Since OOS-TMP appears to require metabolic activation for pneumotoxicity, the effects of OOO-TMP on pulmonary and hepatic cytochrome P 450 [9035-51-2] content and cytochrome P 450-mediated monooxygenases were examd. as possible biochem. mechanism of antagonism. Oral treatment with OOO-TPM (0.5, 0.4, or 4.o mg/kg) decreased pulmonary cytochrome P 450 levels by 23-50% at 2 and 6 h, whereas no changes were detected in hepatic cytochrome P 450 levels. Lung microsomal 7-ethoxycoumarin O-deethylase (7-Ec) [42613-26-3] was inhibited by 71-100%, whereas liver 7-Ec was inhibited by 26-52%. p-Nitroanisole demethylase [9054-86-8] activity was decreased 22-47% following treatment with the 2 highest dose levels of OOO-TMP. Apparently, the lung is a target organ of delayed toxicity produced by OOS-TMP, and the antagonistic effect of OOO-TMP is due to alterations in the metabolic activation processes of OOS-TMP in the lung and(or) liver. .

Selective inhibition of rat pulmonary monooxygenase by O,O,S-trimethyl phosphorothioate treatment

Selective inhibition of rat pulmonary monooxygenase by O,O,S-trimethyl phosphorothioate treatment. Imamura, Toshiko; Gandy, Jay; Fukuto, T. Roy (Dep. Entomol., Univ. Calfornia, Riverside, CA 92521, USA). Biochem. Pharmacol., 32(21), 3191-5 (English) 1983. CODEN: BCPCA6. ISSN: 0006-2952. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) The effects of oral administration of O,O,S-trimethyl phosphorothioate (OOS) [152-20-5] were studied using pulmonary and hepatic microsomal enzymes of rats. The animals were treated with OOS at 10, 20, and 40 mg/kg, and killed on day 3 after treatment. Their relative lung wts. increased markedly at 20 and 40 mg/kg, increasing 94% at the highest dose, whereas the wt. of liver decreased. At 20 mg/kg OOS, the cytochrome P 450 (P 450) [9035-51-2] content of the lung and liver decreased to 83 and 80% of the control levels, resp. Pulmonary microsomal 7-ethoxycoumarin O-deethylase (I) [42613-26-3] decreased in a dose-dependent manner; activities were <10% of control at 40 mg/kg. The activity of pulmonary coumarin hydroxylase [39401-02-0] also decreased following OOS treatment, but the decrease was not dose-dependent since no activity was detectable at >10 mg/kg. In contrast, the effect of OOS treatment on hepatic monooxygenase [9038-14-6] activity was moderate. I activity was not affected by OOS treatment at any dose level, while p-nitroanisole demethylase [79818-30-7] activity was decreased only at 40 mg/kg OOS. Pulmonary malathion carboxylesterase [39391-09-8] activity was not affected by OOS treatment. In contrast, a dose-dependent decrease was obsd. in the liver carboxylesterase [9016-18-6]. Time course effects of OOS treatment on these parameters were examd. by treating rats at 20 mg/kg. The animals were killed 0.5, 1, 3, and 7 days after the treatment. The I activity of pulmonary microsomes was decreased on days 0.5, 1, and 3 after treatment, the max. decrease being obsd. on day 1. Significant decreases were not obsd. in hepatic microsomal activities of I or p-nitroanisole demethylase throughout the exptl. period; rather, these activities were higher on day 7. Hepatic microsomal malathion carboxylesterase was lower on days 0.5, 1, and 3 after OOS treatment.