scholarly journals Reduced metabolic rate and oxygen radicals production in stored insect sperm

2012 ◽  
Vol 279 (1736) ◽  
pp. 2196-2203 ◽  
Author(s):  
Anne-Cécile Ribou ◽  
Klaus Reinhardt
Keyword(s):  
Metabolic Rate ◽  
Cellular Senescence ◽  
Oxygen Radicals ◽  
Ros Production ◽  
Time Resolved ◽  
Sperm Density ◽  
Insect Sperm ◽  
Important Means ◽  
Diploid Cells ◽  
Rank Differences

Females of internally fertilizing species can significantly extend sperm lifespan and functionality during sperm storage. The mechanisms for such delayed cellular senescence remain unknown. Here, we apply current hypotheses of cellular senescence developed for diploid cells to sperm cells, and empirically test opposing predictions on the relationship between sperm metabolic rate and oxygen radical production in an insect model, the cricket Gryllus bimaculatus . Using time-resolved microfluorimetry, we found a negative correlation between metabolic rate (proportion of protein-bound NAD[P]H) and in situ intracellular oxygen radicals production in freshly ejaculated sperm. In contrast, sperm stored by females for periods of 1 h to 26 days showed a positive correlation between metabolic rate and oxygen radicals production. At the same time, stored sperm showed a 37 per cent reduced metabolic rate, and 42 per cent reduced reactive oxygen species (ROS) production, compared with freshly ejaculated sperm. Rank differences between males in ROS production and metabolic rate observed in ejaculated sperm did not predict rank differences in stored sperm. Our method of simultaneously measuring ROS production and metabolic rate of the same sample has the advantage of providing data that are independent of sperm density and any extracellular antioxidants that are proteins. Our method also excludes effects owing to accumulated hydrogen peroxide. Our results unify aspects of competing theories of cellular ageing and suggest that reducing metabolic rate may be an important means of extending stored sperm lifespan and functionality in crickets. Our data also provide a possible explanation for why traits of ejaculates sampled from the male may be rather poor predictors of paternity in sexual selection studies and likelihood of pregnancy in reproductive medicine.

scholarly journals Another Facet to the Anticancer Response to Lamellarin D: Induction of Cellular Senescence through Inhibition of Topoisomerase I and Intracellular Ros Production

Marine Drugs ◽  
2014 ◽  
Vol 12 (2) ◽  
pp. 779-798 ◽  
Author(s):  
Caroline Ballot ◽  
Alain Martoriati ◽  
Manel Jendoubi ◽  
Sébastien Buche ◽  
Pierre Formstecher ◽  
...  
Keyword(s):  
Cellular Senescence ◽  
Topoisomerase I ◽  
Ros Production ◽  
Intracellular Ros ◽  
Anticancer Response

scholarly journals oxLDL-mediated cellular senescence is associated with increased NADPH oxidase p47phox recruitment to caveolae

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Jing Wang ◽  
Yuzhi Bai ◽  
Xia Zhao ◽  
Jing Ru ◽  
Ning Kang ◽  
...  
Keyword(s):  
Cellular Senescence ◽  
Clinical Intervention ◽  
Ros Generation ◽  
Ros Production ◽  
Caveolin 1 ◽  
Cellular Ageing ◽  
Vascular Endothelia ◽  
Membrane Target ◽  
High Degree ◽  
Atherosclerotic Changes

Atherosclerosis develops as a consequence of inflammation and cell senescence. In critical factors involved in the atherosclerotic changes, reactive oxygen species (ROS) generation is considered a leading cause. While NADPH oxidases, particularly NOX2, are the main sources of ROS, how they are regulated in the disease is incompletely understood. In addition, how caveolae, the membrane structure implicated in oxLDL deposition under vascular endothelia, is involved in the oxLDL-mediated ROS production remains mostly elusive. We report here that macrophages exposed to oxLDL up-regulate its caveolin-1 expression, and the latter in turn up-regulates NOX2 p47phox level. This combination effect results in increased cellular senescence. Interestingly, oxLDL treatment causes the p47phox residing in the cytosol to translocate to the caveolae. Immunoprecipitation assays confirms that cavelin-1 is in high degree association with p47phox. These results suggest caveolin-1 may serve as the membrane target for p47phox and as a switch for ROS production following oxLDL exposure. Our results reveal a previously unknown molecular event in oxLDL-mediated cellular ageing, and may provide a target for clinical intervention for atherosclerosis.

Metabolic Rate and Oxygen Radical Levels Increase But Radical Generation Rate Decreases with Male Age in Drosophila melanogaster Sperm

2020 ◽  
Vol 75 (12) ◽  
pp. 2278-2285 ◽  
Author(s):  
Biz R Turnell ◽  
Klaus Reinhardt
Keyword(s):  
Drosophila Melanogaster ◽  
Metabolic Rate ◽  
Cell Types ◽  
Somatic Tissue ◽  
Ros Production ◽  
Male Age ◽  
Fluorescent Lifetime Imaging Microscopy ◽  
Age Related ◽  
Mitochondrial Ros ◽  
Ros Accumulation

Abstract Oxidative damage increases with age in a variety of cell types, including sperm, which are particularly susceptible to attack by reactive oxygen species (ROS). While mitochondrial respiration is the main source of cellular ROS, the relationship between the rates of aerobic metabolism and ROS production, and how this relationship may be affected by age, both in sperm and in other cell types, is unclear. Here, we investigate in Drosophila melanogaster sperm, the effects of male age on (i) the level of hydrogen peroxide in the mitochondria, using a transgenic H2O2 reporter line; (ii) the in situ rate of non-H2O2 ROS production, using a novel biophysical method; and (iii) metabolic rate, using fluorescent lifetime imaging microscopy. Sperm from older males had higher mitochondrial ROS levels and a higher metabolic rate but produced ROS at a lower rate. In comparison, a somatic tissue, the gut epithelium, also showed an age-related increase in mitochondrial ROS levels but a decrease in metabolic rate. These results support the idea of a tissue-specific optimal rate of aerobic respiration balancing the production and removal of ROS, with aging causing a shift away from this optimum and leading to increased ROS accumulation. Our findings also support the view that pathways of germline and somatic aging can be uncoupled, which may have implications for male infertility treatments.

Protein Kinase C   Plays a Key Role in Cellular Senescence Programs of Human Normal Diploid Cells

2009 ◽  
Vol 146 (1) ◽  
pp. 87-93 ◽  
Author(s):  
Y. Katakura ◽  
M. Udono ◽  
K. Katsuki ◽  
H. Nishide ◽  
Y. Tabira ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cellular Senescence ◽  
Kinase C ◽  
Diploid Cells

Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence

2013 ◽  
Vol 305 (10) ◽  
pp. L737-L746 ◽  
Author(s):  
Hiromichi Hara ◽  
Jun Araya ◽  
Saburo Ito ◽  
Kenji Kobayashi ◽  
Naoki Takasaka ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Cellular Senescence ◽  
Fusion Proteins ◽  
Mitochondrial Dynamics ◽  
Bronchial Epithelial Cells ◽  
Ros Production ◽  
Mitochondrial Fragmentation ◽  
Bronchial Epithelial ◽  
Mitochondrial Ros

Mitochondria are dynamic organelles that continuously change their shape through fission and fusion. Disruption of mitochondrial dynamics is involved in disease pathology through excessive reactive oxygen species (ROS) production. Accelerated cellular senescence resulting from cigarette smoke exposure with excessive ROS production has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Hence, we investigated the involvement of mitochondrial dynamics and ROS production in terms of cigarette smoke extract (CSE)-induced cellular senescence in human bronchial epithelial cells (HBEC). Mitochondrial morphology was examined by electron microscopy and fluorescence microscopy. Senescence-associated β-galactosidase staining and p21 Western blotting of primary HBEC were performed to evaluate cellular senescence. Mitochondrial-specific superoxide production was measured by MitoSOX staining. Mitochondrial fragmentation was induced by knockdown of mitochondrial fusion proteins (OPA1 or Mitofusins) by small-interfering RNA transfection. N-acetylcysteine and Mito-TEMPO were used as antioxidants. Mitochondria in bronchial epithelial cells were prone to be more fragmented in COPD lung tissues. CSE induced mitochondrial fragmentation and mitochondrial ROS production, which were responsible for acceleration of cellular senescence in HBEC. Mitochondrial fragmentation induced by knockdown of fusion proteins also increased mitochondrial ROS production and percentages of senescent cells. HBEC senescence and mitochondria fragmentation in response to CSE treatment were inhibited in the presence of antioxidants. CSE-induced mitochondrial fragmentation is involved in cellular senescence through the mechanism of mitochondrial ROS production. Hence, disruption of mitochondrial dynamics may be a part of the pathogenic sequence of COPD development.

Pneumolysin induces cellular senescence by increasing ROS production and activation of MAPK/NF-κB signal pathway in glial cells

Toxicon ◽  
2017 ◽  
Vol 129 ◽  
pp. 100-112 ◽  
Author(s):  
Ii-Seul Kwon ◽  
Jinwook Kim ◽  
Dong-Kwon Rhee ◽  
Byung-Oh Kim ◽  
Suhkneung Pyo
Keyword(s):  
Glial Cells ◽  
Cellular Senescence ◽  
Signal Pathway ◽  
Ros Production

scholarly journals Clonal heterogeneity influences the fate of new adaptive mutations

2016 ◽  
Author(s):  
Ignacio Vázquez-García ◽  
Francisco Salinas ◽  
Jing Li ◽  
Andrej Fischer ◽  
Benjamin Barré ◽  
...  
Keyword(s):  
De Novo ◽  
Selective Inhibition ◽  
Relative Fitness ◽  
Cancer Therapies ◽  
Chemotherapeutic Drugs ◽  
Unique Haplotype ◽  
Time Resolved ◽  
Adaptive Mutations ◽  
Joint Contribution ◽  
Diploid Cells

The joint contribution of pre-existing and de novo genetic variation to clonal adaptation is poorly understood, but essential to design successful antimicrobial or cancer therapies. To address this, we evolve genetically diverse populations of budding yeast, S. cerevisiae , consisting of diploid cells with unique haplotype combinations. We study the asexual evolution of these populations under selective inhibition with chemotherapeutic drugs by time-resolved whole-genome sequencing and phenotyping. All populations undergo clonal expansions driven by de novo mutations, but remain genetically and phenotypically diverse. The clones exhibit widespread genomic instability, rendering recessive de novo mutations homozygous and refining pre-existing variation. Finally, we decompose the fitness contributions of pre-existing and de novo mutations by creating a large recombinant library of adaptive mutations in an ensemble of genetic backgrounds. Both pre-existing and de novo mutations substantially contribute to fitness, and the relative fitness of pre-existing variants sets a selective threshold for new adaptive mutations.

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