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[A preliminary study on the mechanism of neurotoxicity of MDMA--oxidative stress harm].

Abstract

OBJECTIVE

Establishing a long-term neurotoxic model to explore the mechanism of neurotoxicity of 3,4-methylenedioxymethamphetamine (MDMA) and the putative protection conferred by Vit C against oxidative stress harm.

METHODS

Male Wistar rats were randomly assigned to control group (A) and MDMA treatment groups(B, C, D, E). Rats of group B were given MDMA 20 mg/kg; groups C, D, E were given Vit C 250 mg/kg 30 min before administration of MDMA (Vit C 30 min group) and 3 h (Vit C 3 h group) and 5 h (VitC 5 h group) after administration of MDMA, respectively. Rats of control group were treated with the same volume of saline. Concentrations of ATP and ADP in brain cortex and 5-HT in hippocampus and occipital cortex were measured by high perfor-mance liquid chromatography; the expression of SERT mRNA was detected by in situ hybridization; and the expression of protein GFAP was detected by immunohisto-chemistry.

RESULTS

hours after MDMA treatment, the concentration of ATP in brain cortex was lessened, compared with control (P <0.05). On the 7th day after MDMA treatment, the concentration of 5-HT in rat hippocampus and occipital cortex was decreased, compared with control (P<0.05). The expression of SERT mRNA in hippocampus was decreased, whereas the expression of GFAP in brain tissue was increased (P<0.05). The adminstration of Vit C 30 min before MDMA treatment and 3 h after MDMA treatment did not curb the decrease of ATP, 5-HT and the expression of SERT mRNA, but Vit C administrated 5 h after MDMA treatment could curb the decrease of ATP and the functional markers of 5-HT. And Vit C given at three time points did downregulate the GFAP expression.

CONCLUSION

MDMA could deplete the direct energetic substance ATP. MDMA could exert neurotoxic effect on 5-HT system. Vit C given 5 h after MDMA administration could provide neuroprotection for ATP and 5-HT system.

Authors+Show Affiliations

Center of Psychology Health, West China Hospital, Sichuan University, Chengdu 610041, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

chi

PubMed ID

16608072

Citation

Li, Su-Xia, et al. "[A Preliminary Study On the Mechanism of Neurotoxicity of MDMA--oxidative Stress Harm]." Sichuan Da Xue Xue Bao. Yi Xue Ban = Journal of Sichuan University. Medical Science Edition, vol. 37, no. 2, 2006, pp. 191-5.
Li SX, Sun AM, Wang X, et al. [A preliminary study on the mechanism of neurotoxicity of MDMA--oxidative stress harm]. Sichuan Da Xue Xue Bao Yi Xue Ban. 2006;37(2):191-5.
Li, S. X., Sun, A. M., Wang, X., Li, J., Peng, Z. G., Kuang, W. H., & Huang, M. S. (2006). [A preliminary study on the mechanism of neurotoxicity of MDMA--oxidative stress harm]. Sichuan Da Xue Xue Bao. Yi Xue Ban = Journal of Sichuan University. Medical Science Edition, 37(2), pp. 191-5.
Li SX, et al. [A Preliminary Study On the Mechanism of Neurotoxicity of MDMA--oxidative Stress Harm]. Sichuan Da Xue Xue Bao Yi Xue Ban. 2006;37(2):191-5. PubMed PMID: 16608072.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [A preliminary study on the mechanism of neurotoxicity of MDMA--oxidative stress harm]. AU - Li,Su-Xia, AU - Sun,Ai-Min, AU - Wang,Xue, AU - Li,Jing, AU - Peng,Zu-Gui, AU - Kuang,Wei-Hong, AU - Huang,Ming-Sheng, PY - 2006/4/13/pubmed PY - 2007/3/28/medline PY - 2006/4/13/entrez SP - 191 EP - 5 JF - Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition JO - Sichuan Da Xue Xue Bao Yi Xue Ban VL - 37 IS - 2 N2 - OBJECTIVE: Establishing a long-term neurotoxic model to explore the mechanism of neurotoxicity of 3,4-methylenedioxymethamphetamine (MDMA) and the putative protection conferred by Vit C against oxidative stress harm. METHODS: Male Wistar rats were randomly assigned to control group (A) and MDMA treatment groups(B, C, D, E). Rats of group B were given MDMA 20 mg/kg; groups C, D, E were given Vit C 250 mg/kg 30 min before administration of MDMA (Vit C 30 min group) and 3 h (Vit C 3 h group) and 5 h (VitC 5 h group) after administration of MDMA, respectively. Rats of control group were treated with the same volume of saline. Concentrations of ATP and ADP in brain cortex and 5-HT in hippocampus and occipital cortex were measured by high perfor-mance liquid chromatography; the expression of SERT mRNA was detected by in situ hybridization; and the expression of protein GFAP was detected by immunohisto-chemistry. RESULTS: hours after MDMA treatment, the concentration of ATP in brain cortex was lessened, compared with control (P <0.05). On the 7th day after MDMA treatment, the concentration of 5-HT in rat hippocampus and occipital cortex was decreased, compared with control (P<0.05). The expression of SERT mRNA in hippocampus was decreased, whereas the expression of GFAP in brain tissue was increased (P<0.05). The adminstration of Vit C 30 min before MDMA treatment and 3 h after MDMA treatment did not curb the decrease of ATP, 5-HT and the expression of SERT mRNA, but Vit C administrated 5 h after MDMA treatment could curb the decrease of ATP and the functional markers of 5-HT. And Vit C given at three time points did downregulate the GFAP expression. CONCLUSION: MDMA could deplete the direct energetic substance ATP. MDMA could exert neurotoxic effect on 5-HT system. Vit C given 5 h after MDMA administration could provide neuroprotection for ATP and 5-HT system. SN - 1672-173X UR - https://www.unboundmedicine.com/medline/citation/16608072/[A_preliminary_study_on_the_mechanism_of_neurotoxicity_of_MDMA__oxidative_stress_harm]_ L2 - https://medlineplus.gov/clubdrugs.html DB - PRIME DP - Unbound Medicine ER -