PubMed · 2569704
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R Laverty, B J Logan. 1989-08-23. Ecstasy abuse.. https://pubmed.ncbi.nlm.nih.gov/2569704/
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The antiangiogenic effect of Lygodium flexuosum extract was evaluated in Wistar rats intoxicated with N-nitrosodiethylamine (NDEA) in preventive and curative models. In preventive groups, NDEA was administered for 20 weeks. Daily doses of L. flexuosumn-hexane extract (200mg/kg) started 1 week before the onset of NDEA intoxication and continued for 20 weeks. In curative animals, NDEA was administered for 20 weeks followed by treatment with the n-hexane extract of L. flexuosum for 28 days. Rats intoxicated with NDEA had elevated levels of serum gamma-GT, AST, ALT, LDH levels and hepatic MDA and decreased levels of hepatic GSH. When treated with L. flexuosum extract had normal levels of gamma-GT, AST, ALT, LDH levels, hepatic MDA and GSH. NDEA administered rat liver showed an overexpressed levels of angiopoietins 1 (Ang-1) and 2 (Ang-2) and its receptor Tie-2 mRNA. L. flexuosum extract treatment significantly (p<or=0.05) reduced the levels of Ang-1 and Ang-2 and Tie-2 in rat livers evidenced by RT-PCR. Immunohistochemical analysis showed that vascular endothelial growth factor (VEGF) was overexpressed and localized around periportal area of liver sections intoxicated with NDEA and its overexpression was effectively reduced by the treatment with L. flexuosum extract. Histopathological observations also substantiated NDEA-induced hepatotoxicity and the effect was significantly (p<or=0.05) reduced by L. flexuosum extract treatment. Thus, L. flexuosum extract at a dose of 200mg/kg effectively reversed the hepatotoxicity induced by N-nitrosodiethylamine in both experimental models.
Severe and malignant hyperthermia is a frequently reported factor in emergency department (ED) visits and fatalities in which use of amphetamine drugs, such as (+/-)3,4-methylenedioxymethamphetamine (MDMA), (+/-)3,4-methylenedioxyamphetamine (MDA) and (+)methamphetamine (METH), is confirmed. Individuals who use "ecstasy" are also often exposed, intentionally or otherwise, to several of these structurally-related compounds alone or in combination. In animal studies the degree of (subcritical) hyperthermia is often related to the severity of amphetamine-induced neurotoxicity, suggesting health risks to the human user even when emergency medical services are not invoked. A clear distinction of thermoregulatory risks posed by different amphetamines is therefore critical to understand factors that may produce medical emergency related to hyperthermia. The objective of this study was therefore to determine the relative thermoregulatory disruption produced by recreational doses of MDMA, MDA and METH in nonhuman primates. Body temperature and spontaneous home cage activity were monitored continuously in six male rhesus monkeys via radiotelemetric devices. The subjects were challenged intramuscularly with 0.56-2.4 mg/kg MDMA, 0.56-2.4 mg/kg MDA and 0.1-1.0 mg/kg METH. All three amphetamines significantly elevated temperature; however the time course of effects differed. The acute effect of METH lasted hours longer than MDA or MDMA and a disruption of nighttime circadian cooling was observed as long as 18 h after 1.0 mg/kg METH and 1.78-2.4 mg/kg MDA, but not after MDMA. Activity levels were only reliably increased by 0.32 mg/kg METH. It is concluded that while all three substituted amphetamines produce hyperthermia in rhesus monkeys, the effects do not depend on elevated locomotor activity and exhibit differences between compounds. The results highlight physiological risks posed both by recreational use of the amphetamines and by current trials for clinical MDMA use.
BACKGROUND: A sensitive gas chromatography-mass spectrometry method was developed and validated for the simultaneous measurement of MDEA, MDMA, and its metabolites, 3,4-methylenedioxy-N-ethylamphetamine (MDEA), 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy), and its metabolites, 4-hydroxy-3-methoxyamphetamine (HMA), 3,4-methylenedioxyamphetamine (MDA), and 4-hydroxy-3-methoxyamphetamine (HMMA) in human urine. METHODS: We hydrolyzed 1 mL urine, fortified with MDMA-d5, MDA-d5, and MDEA-d6, with 100 microL of concentrated hydrochloric acid at 120 degrees C for 40 min, then added 100 microL 10 N sodium hydroxide and 3 mL phosphate buffer 0.1 N (pH 6.0) were added to hydrolyzed urine specimens before solid-phase extraction. After elution and evaporation, we derivatized extracts with heptafluorobutyric acid anhydride and analyzed with gas chromatography-mass spectrometry operated in EI-selected ion-monitoring mode. RESULTS: Limits of quantification were 25 microg/L for MDEA, MDMA, and its metabolites. Calibration curves were linear to 5000 microg/L for MDEA, MDMA, HMA, MDA, and HMMA, with a minimum r2 > 0.99. At 3 concentrations spanning the linear dynamic range of the assay, mean overall extraction efficiencies from urine were >85.5% for all compounds of interest. Intra- and interassay imprecisions, produced as CV, were <15% for all drugs at 30, 300, and 3000 microg/L. CONCLUSIONS: This gas chromatography-mass spectrometry assay provides adequate sensitivity and performance characteristics for the simultaneous quantification of MDEA, MDMA, and its metabolites HMMA, MDA, and HMA in human urine. The method meets and exceeds the requirements of the proposed Substance Abuse and Mental Health Services Administration's guidelines for federal workplace drug testing of MDEA and MDMA in urine.