Mitochondrial:nuclear DNA (mtDNA:nDNA) ratios in blood cells were investigated in relation to selected human immunodeficiency virus antiretroviral drug regimens. Patients (n = 214) continually received a regimen consisting of either (1) saquinavir (SAQ) + ritonavir (RTV) + either nevirapine (NVP) or lamivudine (3TC) (n=32) or (2) SAQ+RTV (+/- either NVP or 3TC) + either stavudine (d4T) (n=127), didanosine (ddI) (n=19), d4T+ddI (n=21), or zidovudine (ZDV) (n=15), for >/=4 months. NVP- or 3TC-only regimens were associated with median mtDNA:nDNA ratios that were significantly higher than those for ddI- and d4T+ddI-containing regimens (P<.01) but that were not significantly higher than those for d4T- or ZDV-containing regimens. Patients received thymidine analogue- and/or ddI-containing regimens for a shorter time (median, 14 vs. 24 months; P<.01). Because of survivor-bias effect, these results may represent a conservative estimate of these nucleosides' effect on mtDNA.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1086/375353 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Mitochondrial diseases, caused by mutations in either nuclear or mitochondrial DNA (mtDNA), currently have limited treatment options. For mtDNA mutations, reducing mutant-to-wild-type mtDNA ratio (heteroplasmy shift) is a promising therapeutic option, though current approaches face significant challenges. Previous research has shown that severe mitochondrial dysfunction triggers an adaptive nuclear epigenetic response, characterized by changes in DNA methylation, which does not occur or is less important when mitochondrial impairment is subtle.
View Article and Find Full Text PDFPhylogenetic analysis of the complete mitochondrial genome of the orange-winged sulphur butterfly Mell 1913 (Insecta: Lepidoptera: Pieridae: Coliadinae).
Mitochondrial DNA B Resour
November 2024
Department of Biological Sciences, University of Manitoba, Winnipeg, Canada.
Article Synopsis
- Mell 1913 is a butterfly species unique to China, primarily found in forest canopies, and its mitochondrial genome has been sequenced, revealing a typical butterfly gene arrangement.
- The mitochondrial genome comprises 13 protein-coding genes, 22 tRNAs, and 2 rRNAs, with notable aspects such as atypical start codons and completing stop codons inferred from the mRNA.
- Phylogenetic analysis indicates that Mell 1913's mitogenome is closely related to other butterflies in the Coliadinae subfamily, supporting some previous molecular studies while challenging a morphology-based hypothesis on its relationships.
Transfer of mitochondrial DNA into the nuclear genome during induced DNA breaks.
Nat Commun
November 2024
State Key Laboratory of Protein and Plant Gene Research, Genome Editing Research Center, School of Life Sciences, PKU-THU Center for Life Sciences, Peking University, Beijing, China.
Mitochondria serve as the cellular powerhouse, and their distinct DNA makes them a prospective target for gene editing to treat genetic disorders. However, the impact of genome editing on mitochondrial DNA (mtDNA) stability remains a mystery. Our study reveals previously unknown risks of genome editing that both nuclear and mitochondrial editing cause discernible transfer of mitochondrial DNA segments into the nuclear genome in various cell types including human cell lines, primary T cells, and mouse embryos.
View Article and Find Full Text PDFMicrocystin-LR in drinking water: An emerging role of mitochondrial-induced epigenetic modifications and possible mitigation strategies.
Toxicol Rep
December 2024
Division of Environmental Biotechnology, Genetics & Molecular Biology (EBGMB), ICMR-National Institute for Research in Environmental Health (NIREH), Bhopal, India.
Algal blooms are a serious menace to freshwater bodies all over the world. These blooms typically comprise cyanobacterial outgrowths that produce a heptapeptide toxin, Microcystin-LR (MC-LR). Chronic MC-LR exposure impairs mitochondrial-nuclear crosstalk, ROS generation, activation of DNA damage repair pathways, apoptosis, and calcium homeostasis by interfering with PC/MAPK/RTK/PI3K signaling.
View Article and Find Full Text PDFMitochondrial-Derived Peptide MOTS-c Suppresses Ovarian Cancer Progression by Attenuating USP7-Mediated LARS1 Deubiquitination.
Adv Sci (Weinh)
November 2024
State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and Department of Physiology and Pathophysiology, Air Force Medical University, Xi'an, 710032, China.
Mitochondrial-nuclear communication plays a vital role in maintaining cellular homeostasis. MOTS-c, a short peptide derived from the 12S rRNA of mitochondrial DNA, has been suggested as a retrograde mitochondrial signal. Although recent clinical studies have suggested a possible link between MOTS-c and human cancer, the role of MOTS-c in tumorigenesis has yet to be investigated.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!