Background: Cellular metabolism is most invariant process, occurring in all living organisms, which involves mitochondrial proteins from both nuclear and mitochondrial genomes. The mitochondrial DNA (mtDNA) copy number, protein-coding genes (mtPCGs) expression, and activity vary between various tissues to fulfill specific energy demands across the tissues.
Methods And Results: In present study, we investigated the OXPHOS complexes and citrate synthase activity in isolated mitochondria from various tissues of freshly slaughtered buffaloes (n = 3). Further, the evaluation of tissue-specific diversity based on the quantification of mtDNA copy numbers was performed and also comprised an expression study of 13 mtPCGs. We found that the functional activity of individual OXPHOS complex I was significantly higher in the liver compared to muscle and brain. Additionally, OXPHOS complex III and V activities was observed significantly higher levels in liver compared to heart, ovary, and brain. Similarly, CS-specific activity differs between tissues, with the ovary, kidney, and liver having significantly greater. Furthermore, we revealed the mtDNA copy number was strictly tissue-specific, with muscle and brain tissues exhibiting the highest levels. Among 13 PCGs expression analyses, mRNA abundances in all genes were differentially expressed among the different tissue.
Conclusions: Overall, our results indicate the existence of a tissue-specific variation in mitochondrial activity, bioenergetics, and mtPCGs expression among various types of buffalo tissues. This study serves as a critical first stage in gathering vital comparable data about the physiological function of mitochondria in energy metabolism in distinct tissues, laying the groundwork for future mitochondrial based diagnosis and research.
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http://dx.doi.org/10.1007/s11033-023-08416-2 | DOI Listing |
Alzheimers Dement
December 2024
University of Kansas Medical Center, Kansas City, KS, USA.
Background: Mitochondrial dysfunction is an early and prominent feature of Alzheimer's disease (AD). We have recently published that lower brain mitochondrial DNA copy number (mtDNAcn) is associated with increased risk of AD neuropathological change and reduced cognitive performance. Here, we addressed how mtDNAcn affects cell-type specific phenotypes.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
King's College London, London, London, United Kingdom.
Background: Diabetes increases the risk of Alzheimer's disease (AD), and mitochondrial dysfunction is implicated in both diseases. We previously detected mitochondrial DNA copy number (MtDNA-CN) changes in human parietal cortex that differed between diabetic AD and non-diabetic AD. We hypothesize that MtDNA-CN changes may be indicative of different underlying mechanisms.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Esophageal cancer is a highly aggressive disease, and acquired resistance to chemotherapy remains a significant hurdle in its treatment. mtDNA, crucial for cellular energy production, is prone to mutations at a higher rate than nuclear DNA. These mutations can accumulate and disrupt cellular function; however, mtDNA mutations induced by chemotherapy in esophageal cancer remain unexplored.
View Article and Find Full Text PDFFront Cell Dev Biol
December 2024
A. N. Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia.
Mitochondria are semi-autonomous organelles containing their own DNA (mtDNA), which is replicated independently of nuclear DNA (nDNA). While cell cycle arrest halts nDNA replication, mtDNA replication continues. In , flow cytometry enables semi-quantitative estimation of mtDNA levels by measuring the difference in signals between cells lacking mtDNA and those containing mtDNA.
View Article and Find Full Text PDFNat Sci Sleep
December 2024
Department of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, People's Republic of China.
Purpose: Sleep apnea (SA), associated with absent neural output, is characterised by recurrent episodes of hypoxemia and repeated arousals during sleep, resulting in decreased sleep quality and various health complications. Mitochondrial DNA copy number (mtDNA-CN), an easily accessible biomarker in blood, reflects mitochondrial function. However, the causal relationship between mtDNA-CN and SA remains unclear.
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