Mitochondrial defects arise from nucleoside/nucleotide reverse transcriptase inhibitors in neurons: Potential contribution to HIV-associated neurocognitive disorders

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• 作者：Kui-Ming Hung^a ; ^b ; Pei-Chun Chen^b ; Han-Chieh Hsieh^c ; Marcus J Calkins^a ; ^{mjcalkins@mail.ncku.edu.tw}
• 关键词：NRTI ; nucleoside/nucleotide reverse transcriptase inhibitor ; HAND ; HIV-associated neurocognitive disorders ; cART ; combination antiretroviral therapy ; pol γ ; polymerase γ ; mtDNA ; mitochondrial DNA ; ddI ; didanosine ; AZT ; zidovudine ; FTC ; emtricitabine ; TDF ; tenofovir ; ddC ; zalcitabine ; d4T ; stavudine ; 3TC ; lamivudine ; ABC ; abacavir ; PGC-1α ; peroxisome proliferator-activated receptor γ coactivator 1α ; mtUPR ; mitochondrial unfolded protein response ; CO1 ; Cytochrome oxidase I ; ND1 ; NADH Dehydrogenase
• 刊名：Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：1863
• 期：2
• 页码：406-413
• 全文大小：984 K
• 卷排序：1863

文摘

NRTIs can produce mitochondrial toxicity in primary cortical neurons. Sub-chronic treatment with ddI depletes mtDNA in neurons. AZT treatment causes mitochondrial toxicity without mtDNA depletion in neurons. TDF and FTC did not produce observable mitochondrial toxicity in neurons.