Objective To explore the role of antioxidant enzymes and free radicals in the pathogensis of schizophrenia and effects of risperidone treatment.Methods Ninety first-episode schizophrenia inpatients according to the Dignostic and Statistical Manual of Mental Disorder Fouth Edition,were treated only with risperidone, observed for 12 weeks, and the clinical effects estimated with the Positive and Negative Syndrome Scale (PANSS).The biological markers including total anti-oxidant activity (TAC), total superoxide dismutase (T-SOD), cupro-zinc superoxide dismutase (Cu-ZnSOD), manganecesuperoxide dismutase (Mn-SOD), malondialdehyde (MDA) and S100B, were measured both in patients and controls (87 subjects).Results Activity of T-SOD and Cu-ZnSOD, S100B were significant increased in patients compare to controls [(732±126)×102U/Lvs.(672±115)×102 U/L;(578±175)×102 U/Lvs.(440±148)×102 U/L;(180±181) ng/Lvs.(101±115)ng/L;t=3.2, 5.6, 2.2;v=169,169, 60; P< 0.05].Mn-SOD activity was marked lower in patients compared to controls [(153±145)×102U/Lvs.(232±161)×102 U/L,t=-3.3,v =169, P<0.05].TAC activity was higher posttreatment compare to baseline [(150 ± 54)×102 U/L vs.( 174 ± 59)×102 U/L; t = - 2.6,v= 66,P<0.05].Mn-SOD activity in pre-treatment set up the regression equation with the improvement of PANSS total score(R =0.62 ,R2 = 0.38, F = 7.89, P = 0.02).TAC activity in pre-treatment set up the regression equation with the improvement of positive symptoms ( R = 0.71, R2 = 0.50,F=12.9,P = 0.00).Mn-SOD activity in pre-treatment and the changes in TAC between post-treatment and pre-treatment set up regression equation with the improvement negative symptoms( R =0.76, R2 = 0.58, F = 8.24, P = 0.00).Conclusion The free radicals and antioxidant enzymes may be involved in the pathology of schizophrenia, and risperidone treatment may improve antioxidant activity of first-episode schizophrenic patients.%目的 探讨自由基、抗氧化酶在精神分裂症病理机制中的作用,并观察利培酮对抗氧化酶、丙二醛的影响.方法 符合美国精神障碍诊断与统计手册第4版诊断标准的精神分裂症首次发病(以下简称首发)住院患者90例(患者组),采用单一利培酮4～6 mg治疗,观察周期为12周,以阳性和阴性症状量表(PANSS)评定精神症状,并检测血清总抗氧化活力(TAC)、总超氧化物歧化酶(T-SOD)活力、铜锌超氧化物歧化酶(Cu-ZnSOD)活力、锰超氧化物歧化酶(Mn-SOD)活力及丙二醛(MDA)和S100B的含量.选择87名正常健康人作为对照(对照组).结果 患者组T-SOD(732±126)×102U/L,Cu-ZnSOD活力(578±175)×102U/L,S100B蛋白含量(180±181)ng/L,均显著高于对照组[(672±115)×102U/L,(440±148)×102U/L,(101±115)ng/L;t=3.2,5.6,2.2;v=169,169,60;P均<0.05].而Mn-SOD活力[(153±145)×102 U/L]显著低于对照组[(232±161)×102 U/L;t=-3.3,v=169,P<0.05].治疗后TAC活力[(150±54)×102 U/L]较治疗前[(174±59)×102U/L]显著提高;t=-2.6,v=66,P<0.05.治疗前Mn-SOD与PANSS总分减分值可建立回归方程(R=0.62,R2=0.38,F=7.89,P=0.02);治疗前TAC与阳性症状减分值可建立回归方程(R=0.71,R2=0.50,F=12.9,P=0.00);治疗前Mn-SOD、治疗前后TAC差值与阴性症状减分值可建立回归方程(R=0.76,R2=0.58,F=8.24,P=0.00).结论 自由基代谢、氧化应激可能参与精神分裂症发病机制;利醅酮提高了首发患者的总抗氧化活力.
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