ABSTRACT
BACKGROUND: The thioredoxin (Trx) system is a reducing complex, consisting of Trx, Trx reductase (TrxR), and NADPH, that scavenges reactive oxygen species. The system is a natural protective mechanism to prevent apoptosis and progression of oxidative stress-related diseases. The present study was conducted to explore possible changes in TrxR activity and gene expression as a response to the oxidative stress during HTLV-1 infection. MATERIALS AND METHODS: Blood samples were collected from 40 HTLV-1-infected patients and 40 age- and sex-matched healthy controls. The patient group consisted of chronic asymptomatic carriers and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM-TSP) patients. A commercial kit was used to measure the TrxR enzyme activity, and real-time polymerase chain reaction was performed to evaluate TrxR gene expression in extracted peripheral blood mononuclear cells (PBMCs). RESULTS: A decreasing pattern of TrxR enzyme activity was observed among control, carrier, and HAM-TSP groups (mean ± SD; controls, 0.1734 ± 0.056; carriers, 0.134 ± 0.065; and HAM-TSP, 0.0928 ± 0.047 µmol/min/mL). Cellular TrxR gene expression showed the same decreasing trend. The fold differences of gene expression in carriers and HAM-TSP groups compared with healthy controls were 0.8 and 0.7 vs 1, respectively. CONCLUSION: We found a reduction in TrxR expression as well as serum enzyme activity in HTLV-1-infected individuals, particularly in HAM-TSP patients. The reduced TrxR activity during HTLV-1 infection may hamper the natural protective mechanisms, thereby contributes to virus-induced complications.
