[No authors listed]
Neurocysticercosis (NCC), caused by cysticerci of Taenia solium is the most common helminthic infection of the central nervous system. Some individuals harboring different stages of cysticerci in the brain remain asymptomatic, while others with similar cysticerci lesions develop symptoms and the reasons remain largely unknown. Inflammatory response to antigens of dying parasite is said to be responsible for symptomatic disease. Reactive oxygen species that are generated in inflammatory conditions can damage cellular macromolecules such as lipids, DNA, and proteins. The glutathione S-transferases (GSTs) are critical for the protection of cells from A total of 250 individuals were included in the study: symptomatic NCCâ=â75, asymptomatic NCCâ=â75, and healthy controlsâ=â100. The individuals carrying the deletions of GSTM1 and GSTT1 were at risk for NCC (ORâ=â2.99, 95Â %CIâ=â1.31-6.82, pâ=â0.0073 and ORâ=â1.94, 95Â %CIâ=â0.98-3.82, pâ=â0.0550 respectively). Further, the individuals with these deletions were more likely to develop symptomatic disease (ORâ=â5.08, 95Â % CIâ=â2.12-12.18, pâ=â0.0001 for GSTM1 and ORâ=â3.25, 95Â %CIâ=â1.55-6.82, pâ=â0.0018 for GSTT1). Genetic variants of GSTM3 and GSTP1 were not associated with NCC. The total GST activity and levels of GSTM1, GSTT1, and GSTM3 were significantly higher in asymptomatic subjects than in symptomatic and healthy controls. Lower GST activity was observed in individuals with GSTM1 and GSTT1 deletions. The present study suggests that the individuals with GSTM1 and GSTT1 deletions are at higher risk to develop symptomatic disease. The higher GST activity and levels of GSTM1, GSTT1, and GSTM3 are likely to play role in maintaining asymptomatic condition.
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