Zhou Jun-Fu, Zhou Ye-Hua, Zhang Liang, Chen Huai-Hong, Cai Dong
Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Surveillance Station of Drug Abuse, 88 Jiefang Road, Hangzhou 310009, Zhejiang Province, China.
Biomed Environ Sci. 2003 Mar;16(1):53-61.
To investigate whether 3,4-methylenedioxymethamphetamine (MDMA) abuse produces another neurotoxicity which may significantly inhibit the acetylcholinesterase activity and result in severe oxidative damage and liperoxidative damage to MDMA abusers.
120 MDMA abusers (MA) and 120 healthy volunteers (HV) were enrolled in an independent sample control design, in which the levels of lipoperoxide (LPO) in plasma and erythrocytes as well as the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric methods.
Compared with the average values of biochemical parameters in the HV group, those of LPO in plasma and erythrocytes in the MA group were significantly increased (P < 0.0001), while those of SOD, CAT, GPX and AChE in erythrocytes in the MA group were significantly decreased (P < 0.0001). The Pearson product-moment correlation analysis between the values of AChE and biochemical parameters in 120 MDMA abusers showed that significant linear negative correlation was present between the activity of AChE and the levels of LPO in plasma and erythrocytes (P < 0.0005-0.0001), while significant linear positive correlation was observed between the activity of AchE and the activities of SOD, CAT and GPX (P < 0.0001). The reliability analysis for the above biochemical parameters reflecting oxidative and lipoperoxidative damages in MDMA abusers suggested that the reliability coefficient (alpha) was 0.8124, and that the standardized item alpha was 0.9453.
The findings in the present study suggest that MDMA abuse can induce another neurotoxicity that significantly inhibits acetylcholinesterase activity and aggravates a series of free radical chain reactions and oxidative stress in the bodies of MDMA abusers, thereby resulting in severe neural, oxidative and lipoperoxidative damages in MDMA abusers.
研究3,4-亚甲基二氧甲基苯丙胺(摇头丸)滥用是否会产生另一种神经毒性,这种毒性可能会显著抑制乙酰胆碱酯酶活性,并对摇头丸滥用者造成严重的氧化损伤和脂质过氧化损伤。
采用独立样本对照设计,纳入120名摇头丸滥用者(MA)和120名健康志愿者(HV),用分光光度法测定血浆和红细胞中脂质过氧化物(LPO)水平以及红细胞中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPX)和乙酰胆碱酯酶(AChE)的活性。
与HV组生化参数平均值相比,MA组血浆和红细胞中LPO水平显著升高(P < 0.0001),而MA组红细胞中SOD、CAT、GPX和AChE活性显著降低(P < 0.0001)。对120名摇头丸滥用者AChE值与生化参数进行Pearson积差相关分析,结果显示AChE活性与血浆和红细胞中LPO水平呈显著线性负相关(P < 0.0005 - 0.0001),而AChE活性与SOD、CAT和GPX活性呈显著线性正相关(P < 0.0001)。对上述反映摇头丸滥用者氧化和脂质过氧化损伤的生化参数进行可靠性分析,结果显示可靠性系数(α)为0.8124,标准化项目α为0.9453。
本研究结果表明,摇头丸滥用可诱发另一种神经毒性,显著抑制乙酰胆碱酯酶活性,加重摇头丸滥用者体内一系列自由基链式反应和氧化应激,从而导致摇头丸滥用者出现严重的神经、氧化和脂质过氧化损伤。