tailieunhanh - Báo cáo Y học: Azidothymidine causes functional and structural destruction of mitochondria, glutathione deficiency and HIV-1 promoter sensitization

Mitochondrial functional and structural impairment and generation of oxidative stress have been implicated in aging, various diseases and chemotherapies. This study analyzed azidothymidine (AZT)-caused failures in mitochondrial functions, in redox regulation and activation of the HIV-1 gene expression. We monitored intracellular concentrations of ATP and glutathione (GSH) as the indicators of energy production and redox conditions, respectively, during the time-course experiments with U937 and MOLT4 human lymphoid cells in the presence of AZT ( mgÆmL)1) or H2O2 ( mM) for 15–25 days. . | Eur. J. Biochem. 269 2782-2788 2002 FEBS 2002 doi Azidothymidine causes functional and structural destruction of mitochondria glutathione deficiency and HIV-1 promoter sensitization Tokio Yamaguchi 1 lyoko Katoh2 and Shun-ichi Kurata1 1Department of Biochemical Genetics Medical Research Institute Tokyo Medical and Dental University Tokyo Japan 2Ikawa Laboratory RIKEN The Institute of Physical and Chemical Research Wako Saitama Japan Mitochondrial functional and structural impairment and generation of oxidative stress have been implicated in aging various diseases and chemotherapies. This study analyzed azidothymidine AZT -caused failures in mitochondrial functions in redox regulation and activation of the HIV-1 gene expression. We monitored intracellular concentrations of ATP and glutathione GSH as the indicators of energy production and redox conditions respectively during the time-course experiments with U937 and MOLT4 human lymphoid cells in the presence of AZT mg-mL-1 or H2O2 mM for l i -55 days. Moochondrial DA A integrity and NF-KB-driven HIV-1 promoter activity were also assessed. ATP concentration began to decrease within several days after exposure to AZT or H2O2 and the decrease continued to reach 30-40 of the normal level. However decline of GSH was detectable after a retention period for at least 5-6 days and progressed likewise. PCR analyses found that mitochondrial DNA destruction occurred when the ATP and GSH depletion had progressed detecting a difference in the deletion pattern between AZT and H2O2-treated cells. The GSH decrease coincided with HIV-1 promoter sensitization detected by enhanced DNA binding ability of NF-KB and induction of the gene expression upon H2O2-rechallenge. Our results suggest that in the process of AIDS myopathy development AZT or oxidative agents directly impair the energy-producing system of mitochondria causing dysfunction of cellular redox control which eventually leads to loss

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