Meira-Lima Ivanor, Jardim Daniela, Junqueira Ricardo, Ikenaga Elisa, Vallada Homero
Laboratory of Neuroscience, Institute of Psychiatry, University of Sao Paulo Medical School, Sao Paulo, SP, Brazil.
Bipolar Disord. 2003 Aug;5(4):295-9. doi: 10.1034/j.1399-5618.2003.00025.x.
In vivo studies demonstrating that lithium is a powerful phospholipase A2 (PLA2) inhibitor suggest that PLA2 activation, and subsequent cell signaling overactivation by increased fatty acid release may be the primary abnormality in bipolar affective disorder (BPAD), thus making PLA2 genes attractive candidates for the susceptibility to BPAD. The present study investigates polymorphisms in cytosolic phospholipase A2 (cPLA2), calcium-independent phospholipase A2 (iPLA2), and secretory phospholipase (sPLA2) genes in a Brazilian sample.
A cross-sectional study was performed with 181 unrelated DSM-IIIR BPAD subjects and 312 controls. A polymerase chain reaction-restriction fragment length polymorphism assay for BanI cPLA2 and AvrII iPLA2 polymorphisms was performed, and an ATT repeat in sPLA2 was assessed using a semiautomated genetic analyzer (ALFexpress).
There was no significant difference observed in the allelic and genotypic distribution between the BPAD and control groups for cPLA2 (genotype: chi2 = 0.8, 2df, p = 0.6; allele chi2 = 0, 1df, p = 0.9), iPLA2 (genotype: chi2 = 1.7, 2df, p = 0.4; allele: chi2 = 0.3, 1df, p = 0.6), and sPLA2 (allele: chi2 = 3.6, 6df, p = 0.8).
Our results failed to demonstrate that the studied PLA2 polymorphisms were associated with an increased risk for BPAD in our sample.
体内研究表明锂是一种强大的磷脂酶A2(PLA2)抑制剂,这表明PLA2激活以及随后因脂肪酸释放增加导致的细胞信号过度激活可能是双相情感障碍(BPAD)的主要异常情况,因此使PLA2基因成为BPAD易感性的有吸引力的候选基因。本研究调查了巴西样本中胞质磷脂酶A2(cPLA2)、钙非依赖性磷脂酶A2(iPLA2)和分泌性磷脂酶(sPLA2)基因的多态性。
对181名无亲属关系的DSM-IIIR BPAD受试者和312名对照进行了横断面研究。进行了针对BanI cPLA2和AvrII iPLA2多态性的聚合酶链反应-限制性片段长度多态性分析,并使用半自动遗传分析仪(ALFexpress)评估了sPLA2中的ATT重复序列。
在BPAD组和对照组之间,cPLA2(基因型:χ2 = 0.8,2自由度,p = 0.6;等位基因χ2 = 0,1自由度,p = 0.9)、iPLA2(基因型:χ2 = 1.7,2自由度,p = 0.4;等位基因:χ2 = 0.3,1自由度,p = 0.6)和sPLA2(等位基因:χ2 = 3.6,6自由度,p = 0.8)的等位基因和基因型分布没有显著差异。
我们的结果未能证明所研究的PLA2多态性与我们样本中BPAD风险增加有关。