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The Kidneys remove toxins from the blood and move waste products into the urine. However, the accumulation of toxins and fluids in the body leads to kidney failure. For example, the overuse of acrylamide and titanium dioxide nanoparticles (TiONPs) in many food and consumer products increases human exposure and risks; however, there are almost no studies available on the effect of TiONPs coadministration with acrylamide on the integrity of genomic and mitochondrial DNA. Accordingly, this study was conducted to estimate the integrity of genomic and mitochondrial DNA in the renal tissue of mice given acrylamide and TiONPs. To achieve this goal, mice were administrated orally TiONPs or/and acrylamide at the exposure dose levels (5 mg/kg b.w) and (3 mg/kg b.w), respectively, five times per week for two consecutive weeks. Concurrent oral administration of TiONPs with acrylamide caused remarkable elevations in the tail length, %DNA in tail and tail moment with higher fragmentation incidence of genomic DNA compared to those detected in the renal tissue of mice given TiONPs alone. Simultaneous coadministration of TiONPs with acrylamide also caused markedly high elevations in the reactive oxygen species (ROS) production and p53 expression level along with a loss of mitochondrial membrane potential and high decreases in the number of mitochondrial DNA copies and expression level of β catenin gene. Therefore, from these findings, we concluded that concurrent coadministration of acrylamide with TiONPs augmented TiONPs induced genomic DNA damage and mitochondrial dysfunction through increasing intracellular ROS generation, decreasing mitochondrial DNA Copy, loss of mitochondrial membrane potential and altered p53 and β catenin genes expression. Therefore, further studies are recommended to understand the biological and toxic effects resulting from TiONPs with acrylamide coadministration.
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http://dx.doi.org/10.1038/s41598-023-40676-7 | DOI Listing |
Mitochondrial DNA A DNA Mapp Seq Anal
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Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou), Guangzhou, China.
Hibernation is an elaborate response strategy employed by numerous mammals to survive in cold conditions that involves active suppression of metabolism. Despite the role of mitochondria as energy metabolism centers during hibernation, the adaptive and evolutionary mechanisms of mitochondrial genes in hibernating animals, like hedgehogs in eulipotyphlan species, are not yet fully understood. In this study, we sequenced and assembled mitochondrial genomes of the hibernating four-toed hedgehog () and the non-hibernating Asian house shrew ().
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September 2025
Department of Obstetrics and Gynecology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu (Z.W.).
Background: Early-onset preeclampsia poses significant risks to maternal and fetal health, necessitating a deeper understanding of its molecular mechanisms and effective therapeutic strategies.
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Nature
September 2025
Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, USA.
Loss-of-function variants in the lipid transporter ABCA7 substantially increase the risk of Alzheimer's disease, yet how they impact cellular states to drive disease remains unclear. Here, using single-nucleus RNA-sequencing analysis of human brain samples, we identified widespread gene expression changes across multiple neural cell types associated with rare ABCA7 loss-of-function variants. Excitatory neurons, which expressed the highest levels of ABCA7, showed disrupted lipid metabolism, mitochondrial function, DNA repair and synaptic signalling pathways.
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Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA; Salk Institute for Biological Studies, La Jolla, CA, 92037, USA; Department of Molecular Biology, University of Utah, Salt Lake City, UT, USA; Department of Biochemistry, University of Utah, Salt Lake Ci
Aging is the greatest risk factor for cardiovascular diseases (CVD) and is characterized by inflammation, oxidative stress, and cellular senescence. Cellular senescence is a state of persistent cell cycle arrest triggered by stressors such as DNA damage and telomere attrition. Senescent endothelial cells (ECs) can impair vascular function and promote inflammation, thereby contributing to CVD progression.
View Article and Find Full Text PDFMech Ageing Dev
September 2025
Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy; Department of Medicine and Surgery, LUM University, Casamassima, Italy.
Age-related skeletal muscle decline is a major contributor to frailty, functional impairment, and loss of independence in advanced age. This process is characterized by selective atrophy of type II fibers, impaired excitation-contraction coupling, and reduced regenerative capacity. Emerging evidence implicates mitochondrial dysfunction as a central mechanism in the disruption of muscle homeostasis with age.
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