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At least 19 recordsLinked to original sources
PubMed2025

Loss and recovery dynamics of mitochondria in laticifer vessels of the rubber tree under repeated latex harvesting.

Natural rubber is harvested by periodically incising the laticifer vessels in the bark of rubber trees to release latex, the cytoplasm of laticifers. Although mitochondria are suspended in the cytoplasm and were expected to leak out, some earlier studies failed to detect their presence. In this study, we identified mitochondria and plastids in expelled latex using molecular methods and confocal microscopy, quantifying their abundance at 13 850 ± 800 mitochondria per microliter latex. Each tapping event released approximately 746 ± 35 mtDNA copies and 113 ± 7 mitochondria per laticifer cell (mean cell volume: 0.008134 μl). Individual mitochondria contained 6.7 ± 0.6 genome copies (mean ± SD), a value significantly higher than the 1.5 ± 0.2 mtDNA copies per mitochondrion observed in leaves. This suggests that laticifer mitochondria are primed for proliferation. We further investigated mitochondrial dynamics during tapping cycles by measuring temporal changes in concentration. Initial latex flow exhibited the highest mitochondrial concentration (18 749 ± 954/μl), which progressively decreased to 40% of the initial level (7542 ± 940/μl) within 30 min, likely due to dilution from water influx. Following latex vessel plugging, the mitochondrial population rebounded rapidly, surpassing the initial concentration by 1.4-fold within 3 days. Subsequent tapping cycles (second and third) exhibited similar mitochondrial loss and recovery trends, though recovery kinetics shifted from a linear (first cycle) to a logarithmic pattern. These results indicate that tapping stimulates mitochondrial proliferation and that laticifer mitochondria lack protective mechanisms comparable to those of the nucleus, resulting in their expulsion with latex during harvesting.

Hevea↗
PubMedDate not supplied

[Effect of thymosine on oxidative phosphorylation in mitochondria of mouse liver in the dynamics of chemical carcinogenesis].

Oxidative phosphorylation in the mice liver mitochondria with chemical carcinogenesis was studied as affected by thymosine. It is found that under chemical carcinogenesis the energy metabolism (fraction III) lowered and administration of thymosine in the early periods of carcinogenesis favoured an increase in the indices up to the control level. In the late period of carcinogenesis the mentioned effect was not observed. The favourable effect of thymosine on the oxidative phosphorylation was associated with an increase in the immunological indices in the animals under experiment. It is supposed that the activity of thymosine as a hormonal factor includes participation in the energy metabolism regulation.

Animals↗
PubMed2026

Mitochondrial resilience: a convergent framework for pathogenesis and neuroprotection in Parkinson's disease.

Parkinson's disease (PD) is traditionally described as a dopaminergic neurodegenerative disorder driven by α-synuclein aggregation and selective neuronal loss in the substantia nigra pars compacta. While this characterization captures the core clinical and pathological features, it does not fully explain disease initiation and progression. Converging evidence from human genetics, cellular and structural biology, and systems neuroscience now supports a unified framework in which PD results from the progressive erosion of mitochondrial resilience. Here, mitochondrial resilience denotes the capacity of neuronal mitochondrial networks to withstand stress and recover bioenergetic and cellular homeostasis through coordinated quality control, metabolic adaptation, and organelle communication. Rare, high-impact monogenic mutations in PINK1, PRKN (encoding Parkin), PARK7 (DJ-1), LRRK2, and SNCA, along with common risk variants identified in genome-wide association studies, converge on interconnected pathways that govern mitochondrial quality control, bioenergetics, organelle dynamics, and cellular stress responses. These vulnerabilities are most pronounced in the highly energetic dopaminergic neurons of the substantia nigra, where sustained calcium cycling, high bioenergetic demand, and environmental stressors increase cellular susceptibility. Research has moved beyond early observations of respiratory chain impairment and oxidative stress to reveal context-specific disruptions in PINK1/Parkin-mediated mitophagy, lysosomal trafficking, mitochondrial-derived vesicle dynamics, and neuroimmune signaling. This integrated framework reframes PD as a disorder of impaired cellular maintenance rather than solely a consequence of late-stage degenerative processes. It provides a translational shift from mechanism-based biomarkers to early detection of mitochondrial failure and supports therapeutic strategies aimed at restoring mitochondrial function and resilience, offering a direct route to disease-modifying neuroprotection in PD and potentially other neurodegenerative disorders.

LRRK2↗
PubMed2026

Functional impact of Nth like DNA glycosylase 1 on mitochondrial dynamics.

Nth like DNA glycosylase 1 (NTHL1), a key base excision repair enzyme, has long been considered essential for nuclear and mitochondrial genome integrity. Combining in vitro biochemical assays, in cellulo molecular biology, and bioinformatic analyses, we investigated how NTHL1 loss affects mitochondrial DNA (mtDNA) stability and mitochondrial function. Contrary to the conventional view that mtDNA damage is solely detrimental, we find that NTHL1 loss confers a beneficial, mitochondria-initiated phenotype in human cells. Despite accumulating mtDNA lesions, NTHL1 loss unexpectedly increases mtDNA copy number, elevates oxidative phosphorylation protein levels, and enhances mitochondrial respiration. NTHL1-/- cells also show increased mitochondrial mass and higher levels of the biogenesis regulator PGC1α and the fusion protein OPA1, indicating an adaptive response that boosts mitochondrial function and capacity. Consequently, NTHL1-/- cells exhibit resistance to mitochondrial stress, accompanied by increased eIF2α phosphorylation and reduced MYC levels, converging on a broader transcriptional adaptive program. This phenotype depends on mitochondrial NTHL1 and reactive oxygen species (ROS) signaling, since treatment with ROS scavengers or mitochondria-specific reintroduction of NTHL1 rescues it. Together, these findings position NTHL1 as a key modulator of mtDNA stability and mitochondrial function, revealing that loss of this DNA repair enzyme shifts cellular metabolism toward a stress-adaptive state and enhances resilience to oxidative stress.

Humans↗
PubMedDate not supplied

[Effect of narcotics on the enzymatic activity of neuronal and synaptic mitochondria of rat brain].

The action of morphine (20 mg/kg) and phenobarbital (80 mg/kg) on the activity of acetylcholinesterase (ACS) and Mg2+-dependent ATP-ase in fractions of unpurified mitochondria and neuronal mitochondria of the rats brain was studied. It is shown that with prolonged introduction of both morphine and phenobarbital the dynamics of the Mg2+-dependent ATP-ase activity in fractions of neuronal mitochondria and synaptosomes is dissimilar, the synaptosomes fractions then displaying a specific influence of morphine and phenobarbital on the Mg2+-dependent ATP-ase activity, while in the neutronal mitochondria fraction changes occurring in the activity of this enzyme proved to be analogus to those taking place after administration of both morphine and phenobarbital. The ACS activity in the synaptosomes fraction following introduction of both morphine and phenobarbital did not differ from the control one.

Acetylcholinesterase↗
PubMed2025

Innovative strategies for mitochondrial dysfunction in myeloproliferative neoplasms a step toward precision medicine.

Myeloproliferative neoplasms (MPNs) are clonal disorders of hematopoietic stem cells characterized by aberrant proliferation of myeloid lineages, driven primarily by mutations in JAK2, CALR, and myeloproliferative leukemia, leading to constitutive activation of the JAK-STAT pathway. Emerging evidence highlights mitochondrial dysfunction as a key factor in MPN pathogenesis, contributing to increased reactive oxygen species production, mitochondrial DNA mutations, and dysregulated mitochondrial dynamics, which collectively promote clonal expansion and apoptosis resistance. Targeting mitochondrial pathways has gained attention as a therapeutic strategy, with approaches including mitochondria-targeted antioxidants, metabolic inhibitors, and modulation of mitophagy and mitochondrial fission/fusion dynamics. However, challenges such as drug delivery specificity, therapeutic resistance, and off-target effects remain significant. Recent advances in precision medicine, incorporating genomic, transcriptomic, and proteomic profiling, offer a more personalized approach to MPN treatment by tailoring interventions to individual mutation patterns. Additionally, novel therapeutic strategies, including gene editing technologies, RNA-based therapies, and nanoparticle-mediated drug delivery systems, hold promise for overcoming current treatment limitations. The integration of artificial intelligence in drug discovery and biomarker identification further enhances the potential for targeted therapies. Future research should focus on refining these strategies, developing reliable biomarkers for patient stratification, and exploring combination therapies that enhance treatment efficacy while minimizing adverse effects. By addressing mitochondrial dysfunction as an underlying driver of MPNs, these emerging approaches have the potential to improve disease management, extend patient survival, and enhance quality of life. Also, this new approach of precision medicine allows patient stratification and ensures that treatments are formed according to the individual disease biology of each patient, which results in overall better outcomes.

combination drug therapy↗
PubMed1979

[Oxidative phosphorylation in the intact and regenerating liver from a chronobiological viewpoint].

The dynamics of oxidative phosphorylation of the regenerating liver mitochondria on the endogenous and exogenous (glutamate, succinate, ascorbate) substrates in comparison with the normal diurnal and seasonal changes of this process was studied by the polarographical method. With the increase of its activity reflecting the deviation from the state of physiological rest (intact liver in spring, autumn, winter; regenerating liver), the range and synphasing of the oxidative phosphorylation indices were decreased, their bimodal distributions were transformed into the monomodal ones down to the full loss of diurnal periodicity. The degree of the process desynchronization depends, thus, directly on the degree of its activity.

Animals↗
PubMed1977

[Changes in rat liver mitochondria under conditions of bilateral subdiaphramatic vagotomy].

A study was made of the changes in the mitochondria of the rat liver under conditions of bilateral subphrenic vagotomy. Two stages in the dynamics of the response of the mitochondrial apparatus to denervation were distingished. During the first stage (0.5-3 days after vagotomy) there occurred reversible functional disturbances of the mitochondria caused by the postoperative stress. The second stage (7 to 60 days after the denervation) was charaterized by more marked structural-functional changes having a number od common features with those seen in hypoxia and being result of vagotomy proper.

Animals↗
PubMed1979

Oxidation-reduction ratio studies of mitochondria in freeze-trapped samples. NADH and flavoprotein fluorescence signals.

The recording of oxidation-reduction-related fluorescence signals of oxidized flavoprotein (Fp) and reduced pyridine nucleotide (PN) from isolated mitochondria at temperatures below -80 degrees C can be accompanished with a high degree of accuracy and a wide dynamic range. The specific low temperature enhancement of the fluorescence signals due to increased quantum yield and to multiple scattering affords increased accuracy and less interference due to screening pigments such as hemoglobin and myoglobin. Since the metabolic processes are arrested and the recording speed can be greatly diminished, the technique can operate with a much smaller concentration of mitochondria than is needed at room temperature, and the method is suitable for localized oxidation-reduction measurements. The Fp and PN signals originate from the mitochondrial matrix space in which they represent the major fluorochromes. Since Fp and PN are near oxidation-reduction equilibrium, the ratio of the two fluorescence intensities, suitably normalized, approximates the oxidation-reduction ratio of oxidized flavoprotein/reduced pyridine nucleotide. Thus, this technique affords a foundation for the resolution of oxidation-reduction states in two and three dimensions.

Animals↗
PubMed1979

Morphology of muscle fibres in amphibian submandibular muscle.

The microscopic organization and ultrastructure of the submandibular muscle of 10 species of Amphibia were compared. Among other fibre features the diameter of fibres, their content of mitochondria and fat, organization of sarcomeres: morphology of Z-line, M-band and sarcoplasmic reticulum were taken into consideration and 4 main types of muscle fibres were distinguished. They correspond to tonic (slow) and phasic (red, white and intermediate) ones. Slight variety of fibre morphology and of fibre elements among the examined species was found. Special attention to the variety of fibre morphology among the established types has been paid and the existence of continuous "spectrum" of fibres was suggested. The correlation of frequency of fibres of particular types with the body size, gular oscillation frequency, and some other characteristics of the submandibular muscle in the examined species was discussed. Also the zonal arrangement of muscle according to the fibre types, as well as possible dynamic nature of muscle fibres were emphasised.

Animals↗
PubMed1978

Evidence for a new mammalian organ. II. Calcium kinetics.

The calcium content and calcium kinetics of the fatty tissue complex comprising the renal sinus organ of the rat kidney are reported. A comparison is made to control brown and white fat in the same animal. The calcium content of the renal sinus tissue is significantly greater than controls. Calcium localization in the mitochondria of the sinus tissue complex is demonstrated. Radioactive isotope studies (45Ca, 85Sr and 99mTc) indicate a dynamic exchange of calcium between the systemic pool and the sinus organ. Active accumulation appears to be operative. Supporting evidence for the existence of a portal vascular system joining the renal sinus complex and the renal parenchyma is presented. The significance of a calcium sink in the renal sinus tissue of the rat kidney is discussed.

Adipose Tissue↗
PubMed1977

Evidence for a new mammalian organ. II. Calcium kinetics.

The calcium content and calcium kinetics of the fatty tissue complex comprising the renal sinus organ of the rat kidney are reported. A comparison is made to control brown and white fat in the same animal. The calcium content of the renal sinus tissue is significantly greater than controls. Calcium localization in the mitochondria of the sinus tissue complex is demonstrated. Radioactive iostope studies (45Ca, 85Sr and 99mTc) indicate a dynamic exchange of calcium between the systemic pool and the sinus organ. Active accumulation appears to be operative. Supporting evidence for the existence of a portal vascular system joining the renal sinus complex and the renal parenchyma is presented. The significance of a calcium sink in the renal sinus tissue of the rat kidney is discussed.

Adipose Tissue↗
PubMed2026

Mitochondrial homeodynamics in ageing: mechanisms, resilience, and interventions.

Mitochondria integrate bioenergetics, redox signalling, calcium handling, biosynthesis, apoptosis, and stress responses. Their contribution to ageing depends less on any single pathway than on the ability to sustain these functions through continuous maintenance, remodelling, and inter-organelle communication. This review proposes mitochondrial homeodynamics as a systems-level framework for that ability, which rests not on static preservation but on three linked capacities. Maintenance safeguards mitochondrial genome, proteome, and membrane integrity. Adaptation adjusts metabolism and remodels network and cristae architecture to match changing demand. Recovery restores function and reserve after challenge. These capacities emerge from mitochondrial quality control, network and cristae remodelling, biogenesis, mitophagy, retrograde stress signalling, and inter-organelle communication. So defined, mitochondrial dysfunction becomes a measurable loss of capacity rather than a descriptive category. Ageing erodes these capacities in tissue- and context-specific ways, which reduces physiological reserve, slows recovery after stress, and amplifies sterile inflammation. The mechanisms underlying these capacities, the biomarkers that report them, and the interventions proposed to preserve them are evaluated in turn. Exercise provides the strongest human evidence for coordinated mitochondrial and functional adaptation, whereas evidence for energy restriction, NAD+ precursors, mitophagy-supporting compounds, and mitochondria-targeted agents remains heterogeneous and endpoint-specific. No mitochondrial intervention has been shown to slow ageing or extend lifespan in healthy humans, and movement of a biomarker towards a younger reference value does not establish rejuvenation. Progress will require dynamic measures of maintenance, adaptation, and recovery, obtained in defined tissues and interpreted alongside clinically meaningful outcomes.

Humans↗
PubMed1978

Binding of cytochrome b5 to membranes of isolated subcellular organelles from rat liver.

The in vitro incorporation of a well-characterized integral protein cytochrome b5 into membranes of various subcellular organelles was investigated by biochemical and immunochemical methods. Microsomes, peroxisomes, and outer mitochondrial membranes, all containing endogenous cytochrome b5, incorporated large amounts of the hemoprotein in such a way that it was reducible by an inherent NADH cytochrome b5 reductase. Lysosomal membranes did not incorporate cytochrome b5. Inner mitochondrial and Golgi membranes, which do not naturally contain cytochrome b5, bound it in vitro but it was not reduced in the presence of NADH. These results show some discrepancies between the natural localization and the in vitro binding of cytochrome b5. They confirm one aspect of the fluid membrane theory and bring new elements to our understanding of the maintenance of the specific features of the membranes of subcellular organelles with respect to the cell dynamism.

Cytochrome Reductases↗
PubMed2026

Cardiac mitochondrial proteome of lean, healthy Ossabaw minipigs with predisposition to metabolic syndrome versus that of Göttingen minipigs.

Ossabaw minipigs differ from other (mini)pig strains by their genetic predisposition to develop full metabolic syndrome and their nonresponsiveness to cardioprotective interventions, even before developing the diseased phenotype. Previous DNA sequencing data revealed differences in a cluster of mitochondrial protein-coding genes between Ossabaw and Göttingen minipigs-a large animal model without such a genetic predisposition and a responsiveness to cardioprotection. Alterations in mitochondrial protein composition affect mitochondrial function, and mitochondria play a crucial role in the development of metabolic syndrome and for cardioprotection. Therefore, we aimed to compare the cardiac mitochondrial proteome between lean Ossabaw minipigs with a healthy phenotype and Göttingen minipigs to gain initial insights into potential differences in mitochondrial protein composition and function. Cardiac mitochondria (left ventricular tissue) of both minipig strains (male/female pigs) were isolated, and the proteome was analyzed by liquid chromatography-tandem mass spectrometry. An unbiased, nonhypothesis-driven proteome analysis identified 97% overlap in the proteome. Among the 3% of differentially expressed proteins, 19 were related to mitochondrial metabolism, 8 to transcription and translation, 3 to small molecule transport, 2 to oxidative phosphorylation, and 1 to dynamics and surveillance. These small differences in protein composition were associated with an altered mitochondrial energy turnover-ATP production was reduced by 49% in Ossabaw compared with Göttingen minipig mitochondria. This proteome analysis provides a broader basis to understand how genetic alterations result in changes of the mitochondrial proteome and function, which might be relevant for the development and progression of metabolic syndrome and/or the primordial nonresponsiveness to cardioprotection in Ossabaw minipigs.NEW & NOTEWORTHY Our comprehensive cardiac mitochondrial proteome of Ossabaw and Göttingen minipigs is a valuable resource for cardiac biomedical research. Moreover, our proteome analysis provides a broader basis for understanding how genetic alterations result in changes of the mitochondrial proteome and support a mechanistic link between subtle, strain-specific mitochondrial proteomic signatures and altered mitochondrial energy turnover. These changes may be relevant for the development and progression of metabolic syndrome and/or primordial nonresponsiveness to cardioprotection in Ossabaw minipigs.

Animals↗