PCE
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Collated from PsychonautWiki, TripSit, Pharmacology. Where sources differ (e.g. dosing), Compare shows them side by side.
Also known as PCE, EticyclidinePW
PCE may cause psychosis and mania at a significantly higher rate than other dissociatives.[1][2] It is strongly discouraged to use this substance in high doses or multiple days in a row. Please see this section for more details.PW
Insufflated
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 1 mg | 2–4 mg | 4–8 mg | 8–15 mg | —+ |
| Onset | 3–30 minutes |
|---|---|
| Come-up | 30–90 minutes |
| Peak | 2–3 hours |
| Offset | 1–2 hours |
| Total | 4–6 hours |
| After-effects | 4–48 hours |
Oral
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 1 mg | 3–5 mg | 5–10 mg | 10–15 mg | —+ |
| Onset | 30–90 minutes |
|---|---|
| Come-up | 40–120 minutes |
| Peak | 2–3 hours |
| Offset | 1–2 hours |
| Total | 4–8 hours |
| After-effects | 4–48 hours |
Smoked
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 1 mg | 2–4 mg | 4–8 mg | 8–12 mg | —+ |
| Onset | 2–20 minutes |
|---|---|
| Come-up | 20–40 minutes |
| Peak | 2–3 hours |
| Offset | 1–2 hours |
| Total | 4–6 hours |
| After-effects | 4–48 hours |
Dangerous interactionsPW
🧬 Receptor activityPH
Pharmacokinetics
Half-lifePH
Blood: 96 hours; trichloroacetic acid in urine: 80 hours (may be longer depending upon fat deposition); [TDR, p. 1010]
After ingestion of 12-16 g tetrachloroethylene, a 6 year old boy was admitted to the clinic in coma. ... The tetrachloroethylene blood level profile which was determined under hyperventilation therapy could be computer fitted to a two compartment model. Elimination of tetrachloroethylene from the blood compartment occurred via a rapid and a slow process with half-lives of 30 min and 35 hours, respectively. These values compared favorably with the half-lives of 160 min and 33 hours under normal respiratory conditions. ...
The elimination of tetrachloroethylene in expired air ranged from 50 to 150 ppm (339 to 1,017 mg/cu m) for up to 8 hr. Biological half-life for fat stores was 71.5 hr.
The biological half-life of tetrachloroethylene metabolites (as measured as total trichloro-compounds) is 144 hours.
The excretion via blood and lungs occurred at 3 different rate constants with half-lives of 12-16 hr, 30-40 hr, and about 55 hr, respectively, 20, 50, and 100 hr after exposure. Trichloroacetic acid was excreted from blood with a half-life of 75-80 hr ... The half-life of this metabolite in urine /is/ about 6 days.
Half-lives for respiratory elimination range from 1 to 72 hr.
AbsorptionPH
The mutagenicity of tetrachloroethene (tetra) and its S conjugate, S-(1,2,2-trichlorovinyl)glutathione (TCVG) was investigated using a modified Ames preincubation assay. TCVG was a potent mutagen in presence of rat kidney particulate fractions containing high concentrations of gamma-glutamyl transpeptidase (GGT) and dipeptidases. Purified tetra was not mutagenic without exogenous metabolic activation or under conditions favoring oxidative metabolism. Preincubation of tetra with purified rat liver glutathione (GSH) S-transferases in presence of GSH and rat kidney fractions resulted in a time-dependent formation of TCVG as determined by (HPLC) analysis and in an unequivocal mutagenic response in the Ames test. Experiments with tetra in the isolated perfused rat liver demonstrated TCVG formation and its excretion with the bile; bile collected after the addition of tetra to the isolated perfused liver was unequivocally mutagenic in bacteria in the presence of kidney particulate fractions. The mutagenicity was reduced in all cases by the GGT inhibitor serine borate or the beta-lyase inhibitor aminooxyacetic acid. These results support the suggestion that cleavage of the GSH S conjugate formed from tetra by the enzymes of the mercapturic acid pathway and by beta-lyase may be involved in the nephrocarcinogenic effects of this haloalkene in rats.
This article reports on the development of a "harmonized" PBPK model for the toxicokinetics of perchloroethylene (tetrachloroethylene or perc) in mice, rats, and humans that includes both oxidation and glutathione (GSH) conjugation of perc, the internal kinetics of the oxidative metabolite trichloroacetic acid (TCA), and the urinary excretion kinetics of the GSH conjugation metabolites N-Acetylated trichlorovinyl cysteine and dichloroacetic acid. The model utilizes a wider range of in vitro and in vivo data than any previous analysis alone, with in vitro data used for initial, or "baseline," parameter estimates, and in vivo datasets separated into those used for "calibration" and those used for "evaluation." Parameter calibration utilizes a limited Bayesian analysis involving flat priors and making inferences only using posterior modes obtained via Markov chain Monte Carlo (MCMC). As expected, the major route of elimination of absorbed perc is predicted to be exhalation as parent compound, with metabolism accounting for less than 20% of intake except in the case of mice exposed orally, in which metabolism is predicted to be slightly over 50% at lower exposures. In all three species, the concentration of perc in blood, the extent of perc oxidation, and the amount of TCA production is well-estimated, with residual uncertainties of approximately 2-fold. However, the resulting range of estimates for the amount of GSH conjugation is quite wide in humans (approximately 3000-fold) and mice (approximately 60-fold). While even high-end estimates of GSH conjugation in mice are lower than estimates of oxidation, in humans the estimated rates range from much lower to much higher than rates for perc oxidation. It is unclear to what extent this range reflects uncertainty, variability, or a combination. Importantly, by separating total perc metabolism into separate oxidative and conjugative pathways, an approach also recommended in a recent National Research Council review, this analysis reconciles the disparity between those previously published PBPK models that concluded low perc metabolism in humans and those that predicted high perc metabolism in humans. In essence, both conclusions are consistent with the data if augmented with some additional qualifications: in humans, oxidative metabolism is low, while GSH conjugation metabolism may be high or low, with uncertainty and/or interindividual variability spanning three orders of magnitude. More direct data on the internal kinetics of perc GSH conjugation, such as trichlorovinyl glutathione or tricholorvinyl cysteine in blood and/or tissues, would be needed to better characterize the uncertainty and variability in GSH conjugation in humans.
Tetrachloroethylene is a volatile, lipophilic small molecule that is rapidly and extensively absorbed after inhalation and oral exposure. It can also be rapidly absorbed through the skin, but dermal absorption appears to be a less important route of exposure. In humans, inhalation exposure to tetrachloroethylene typically results, within a few hours of exposure, in a pseudoequilibrium between inspired air and blood although there can be substantial interindividual differences in absorption behavior. After oral dosing in animals, peak blood tetrachloroethylene concentrations are typically reached within 15-30 min, and systemic bioavailability is typically greater than 80%; once absorbed, tetrachloroethylene is rapidly distributed throughout the body, and well-perfused tissues reach a pseudoequilibrium with blood within a few minutes.
Because of its lipophilicity, the highest concentrations of tetrachloroethylene are found in adipose tissue. In humans, the fat-to-blood concentration ratio has been estimated to be as high as 90:1. Relatively high concentrations are also observed in the liver and brain. On the basis of animal studies and sparse human data, the brain concentration of tetrachloroethylene is 4-8 times the blood concentration.
For more Absorption, Distribution and Excretion (Complete) data for Tetrachloroethylene (32 total), please visit the HSDB record page.
MetabolismPH
Despite the low overall metabolism of tetrachloroethylene compared with other chlorinated solvents, its metabolism has been studied extensively in both human volunteers and laboratory animals, using both in vivo and in vitro techniques. The studies showed that many metabolites are produced, including some known to be cytotoxic, mutagenic or both. Tetrachloroethylene metabolism can be viewed as having three pathways. The first is cytochrome P-450-mediated (CYP-mediated) oxidation. The second and third share a starting point: direct conjugation with glutathione to S-(1,2,2-trichlorovinyl)glutathione (TCVG) and then further processing to S-(1,2,2-trichlorovinyl)-L-cysteine (TCVC). For the second pathway, beta-lyase catalyzes the formation of reactive products from TCVC. The third pathway is independent of beta-lyase: TCVC is processed further by acetylation and sulfoxidation reactions. Genotoxic and cytotoxic metabolites are formed by each of these pathways. The predominant metabolic pathway is the CYP path, followed by the beta-lyase pathway and then the beta-lyase independent pathway. The TCVC derivatives are toxicologically important but quantitatively minor metabolites.
Trichloroethylene (TRI) and tetrachloroethylene (TETRA) are solvents that have been widely used in a variety of industries, and both are widespread environmental contaminants. ... Seven human volunteers were exposed by inhalation to 1 ppm of TRI or TETRA for 6 hr, with biological samples collected for analysis during exposure and up to 6 days postexposure. Concentrations of TRI, TETRA, free trichloroethanol (TCOH), total TCOH (free TCOH plus glucuronidated TCOH), and trichloroacetic acid (TCA) were determined in blood and urine; TRI and TETRA concentrations were measured in alveolar breath. Toxicokinetic time courses and empirical analyses of classical toxicokinetic parameters were compared with those reported in previous human volunteer studies, most of which involved exposures that were at least 10 fold higher. Qualitatively, TRI and TETRA toxicokinetics were consistent with previous human studies. Quantitatively, alveolar retention and clearance by exhalation were similar to those found previously but blood and urine data suggest a number of possible toxicokinetic differences. For TRI, data from the current study support lower apparent blood-air partition coefficients, greater apparent metabolic clearance, less TCA production, and greater glucuronidation of TCOH as compared to previous studies. For TETRA, the current data suggest TCA formation that is similar or slightly lower than that of previous studies. Variability and uncertainty in empirical estimates of total TETRA metabolism are substantial, with confidence intervals among different studies substantially overlapping. ...
The two major products of tetrachloroethylene metabolism by the CYP pathway are trichloroacetyl chloride and oxalyl chloride.
The beta-lyase pathway: Tetrachloroethylene is conjugated with glutathione to S-(1,2,2-trichlorovinyl) glutathione and is later processed by gamma-glutamyl transpeptidase and aminopeptidase to S-(1,2,2-trichlorovinyl)-L-cysteine (TCVC).
For more Metabolism/Metabolites (Complete) data for Tetrachloroethylene (19 total), please visit the HSDB record page.
Tetrachloroethylene is readily absorbed following inhalation, oral, and dermal exposure. Once tetrachloroethylene is absorbed, its relatively high lipophilicity results in distribution to
fatty tissue. Some tetrachloroethylene is metabolized to trichloroacetic acid (TCA) by cytochrome P-450 enzymes and the glutathione-conjugation pathway, then excreted in the urine. The remaining unmetabolized tetrachloroethylene is exhaled. (L116)
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Fact-sheets from PsychonautWiki. Harm-reduction reference only — not medical advice.