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Allelic association study between phospholipase A2 genes and bipolar affective disorder
Author(s) -
MeiraLima Ivanor,
Jardim Daniela,
Junqueira Ricardo,
Ikenaga Elisa,
Vallada Homero
Publication year - 2003
Publication title -
bipolar disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.285
H-Index - 129
eISSN - 1399-5618
pISSN - 1398-5647
DOI - 10.1034/j.1399-5618.2003.00025.x
Subject(s) - allele , genotype , phospholipase a2 , phospholipase , phospholipase a , biology , allele frequency , genetics , gene , microbiology and biotechnology , medicine , biochemistry , enzyme
Objectives: 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. Methods: 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 Ban I cPLA2 and Avr II iPLA2 polymorphisms was performed, and an ATT repeat in sPLA2 was assessed using a semiautomated genetic analyzer (ALFexpress). Results: There was no significant difference observed in the allelic and genotypic distribution between the BPAD and control groups for cPLA2 (genotype: χ 2 = 0.8, 2df, p = 0.6; allele χ 2 = 0, 1df, p = 0.9), iPLA2 (genotype: χ 2 = 1.7, 2df, p = 0.4; allele: χ 2 = 0.3, 1df, p = 0.6), and sPLA2 (allele: χ 2 = 3.6, 6df, p = 0.8). Conclusion: Our results failed to demonstrate that the studied PLA2 polymorphisms were associated with an increased risk for BPAD in our sample.