Toxicological profiles - 1,1,2-trichloroethane

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Edwards, S.

1,1,1-Trichloroethane - Wikipedia

Dworatzek, D. Major, and P. EPA R, pp, Ethylene Dibromide. Halogenated alkenes. Halogenated monoaromatics. Polychlorinated biphenyls PCBs. Blood samples were taken at the following intervals during the regimen: 2, 4, 6, 8,10, 12, and 13 weeks and 1 week posttreatment. Five rats at each dosage level were randomly selected to serve as blood donors.

These animals were lightly etherized and 2. Five different rats from each group were utilized for blood sampling at each of the next 2 sampling intervals, so that each animal served once as a blood donor during the first half of the study. On day 51 of the regimen, 1,1-dichloroethylene was mistakenly given in place of TRI to each member of the 2. All of these animals died within 24 h of massive liver damage.

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Fortunately, they were housed in a different isolation module from the 0. The 0. Blood samples were again taken for serum enzyme analysis from alternate animals in these 2 groups every 2 weeks for the reminder of the study. Moribund rats were removed, killed, and examined for gross morphological changes. The terminal sacrifice was performed on day 92, after 13 weeks of the dosing regimen.

Five additional control and five 0. At sacrifice, each rat in the toxicity studies was anesthetized with ether and blood taken by closed-chest cardiac puncture. Serum ornithine carbamoyl-transferase OCT activity was determined by the 14 CO 2 trapping technique of Drotman , as modified by Kyle et al. After taking blood, the abdominal cavity of each animal was opened and the liver excised and weighed. A 1 cm-wide strip of the left median lobe of the liver was removed and placed into buffered formalin. Slides were coded and examined in a single-blind fashion by a veterinary pathologist.

The nonprotein sulfhydryl NPSH content of mg portions of the liver was measured by the technique of Richardson and Murphy A 5-g portion of the central hepatic lobe was removed and microsomes prepared by differential centrifugation. Microsomal protein content was assayed according to Lowry et al. An aliquot of the microsomal suspension was incubated with histidine, EDTA and glucosephosphate. Liberation of inorganic phosphate was the measure of glucosephosphatase GPase activity Reynolds and Yee, GPase activity was monitored as an index of liver microsomal injury.

The liver was perfused in situ with cold normal saline in order to remove as much blood as possible. A 5-g portion of the central lobe of the liver was then taken for preparation of microsomes by differential centrifugation. The total cytochrome P content of hepatic microsomes was determined by the standard spectrophotometric method of Omura and Sato The microsomal protein concentration was measured by the procedure of Lowry et al.

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PROD was assayed by the fluorimetric method of Lubet et al. The fluorimetric technique of Burke and Mayer , as modified by Lubet et al. Rats of — g were given a single oral bolus dose of 5. An additional experiment was conducted to determine whether the time course of CYP2E1 induction varied with dose. Rats were gavaged with 0. Appropriate amounts of TRI were diluted in corn oil, as described for the short-term study protocol. The rats were killed at 24 h post dosing by cervical dislocation, in order to isolate the liver microsomes rapidly and without the use of ether or other anesthetics.

Each microsomal parameter was measured as described above.

Another experiment was carried out to assess the influence of the short-term exposure regimen on hepatic P levels and CYP2E1 activity. Rats were dosed once daily for 5 consecutive days, allowed 2 days of rest, and dosed for 4 additional days.

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Groups of 6 animals per dosage level were sacrificed 1, 5, and 12 days after initiation of the regimen, for analyses of total P levels and CYP2E1 activity. The statistical significance of changes in toxicity and P indices as a function of dose was assessed by one-way analysis of variance. The significance of apparent differences over time between values for adjacent time-points was evaluated by Student-Newman-Keul's test.

The significance of differences between 0-time and late time-points was assesssed by Duncan's multiple range test.

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Data for each index of liver injury in the short-term and subchronic studies were analyzed using a Minitab statistical package Version A response surface model was used to fit each data set Kuehl, Both linear and quadratic equations were derived for the data with respect to effects of TRI dosage and days of dosing.

Regression analysis was utilized to assess the linearity of changes in indices as a function of dose. There was little evidence of toxicity 24 h after a single oral dose of 0, 0. There was no mortality from TRI exposure. Histopathological examination and measurements of liver:body weight, serum enzymes, hepatic NPSH levels, and GPase activity did not reveal hepatocellular damage at any dosage level data not shown. The decision was made to give even higher doses of TRI in the short-term study, in an effort to produce liver injury. The acute oral LD 50 for male rats was reported to be The high, repetitive oral doses of TRI caused multiple fatalities.

This stage was followed by a protracted period of narcosis. Neither CNS effects nor fatalities were observed in the 0. Despite daily gavage dosing with lethal or near-lethal amounts of TRI, there were relatively few manifestations of toxicity in the surviving rats.

Body weight gain was comparable in the 0 and 0. Liver injury was not apparent at any TRI dosage level during the short-term study. No treatment-related lesions were found upon microscopic examination of the liver.