Methane biogenesis during sodium azide-induced chemical hypoxia in rats

2013 ◽  
Vol 304 (2) ◽  
pp. C207-C214 ◽  
Author(s):  
Eszter Tuboly ◽  
Andrea Szabó ◽  
Dénes Garab ◽  
Gábor Bartha ◽  
Ágnes Janovszky ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Sodium Azide ◽  
Methane Production ◽  
Structural Damage ◽  
Bacterial Flora ◽  
Laser Scanning Microscopy ◽  
Whole Body ◽  
Oral Antibiotic ◽  
Methane Generation ◽  
Chemical Hypoxia

Previous studies demonstrated methane generation in aerobic cells. Our aims were to investigate the methanogenic features of sodium azide (NaN3)-induced chemical hypoxia in the whole animal and to study the effects of l-α-glycerylphosphorylcholine (GPC) on endogenous methane production and inflammatory events as indicators of a NaN3-elicited mitochondrial dysfunction. Group 1 of Sprague-Dawley rats served as the sham-operated control; in group 2, the animals were treated with NaN3 (14 mg·kg−1·day−1 sc) for 8 days. In group 3, the chronic NaN3 administration was supplemented with daily oral GPC treatment. Group 4 served as an oral antibiotic-treated control (rifaximin, 10 mg·kg−1·day−1) targeting the intestinal bacterial flora, while group 5 received this antibiotic in parallel with NaN3 treatment. The whole body methane production of the rats was measured by means of a newly developed method based on photoacoustic spectroscopy, the microcirculation of the liver was observed by intravital videomicroscopy, and structural changes were assessed via in vivo fluorescent confocal laser-scanning microscopy. NaN3 administration induced a significant inflammatory reaction and methane generation independently of the methanogenic flora. After 8 days, the hepatic microcirculation was disturbed and the ATP content was decreased, without major structural damage. Methane generation, the hepatic microcirculatory changes, and the increased tissue myeloperoxidase and xanthine oxidoreductase activities were reduced by GPC treatment. In conclusion, the results suggest that methane production in mammals is connected with hypoxic events associated with a mitochondrial dysfunction. GPC is protective against the inflammatory consequences of a hypoxic reaction that might involve cellular or mitochondrial methane generation.

scholarly journals The Interplay between Mitochondrial Morphology and Myomitokines in Aging Sarcopenia

2020 ◽  
Vol 22 (1) ◽  
pp. 91
Author(s):  
Vanina Romanello
Keyword(s):  
Mitochondrial Dysfunction ◽  
Poor Quality ◽  
Whole Body ◽  
Fibroblast Growth Factor 21 ◽  
Mitochondrial Morphology ◽  
Mass Force ◽  
Major Mechanism ◽  
Muscle Aging ◽  
And Function

Sarcopenia is a chronic disease characterized by the progressive loss of skeletal muscle mass, force, and function during aging. It is an emerging public problem associated with poor quality of life, disability, frailty, and high mortality. A decline in mitochondria quality control pathways constitutes a major mechanism driving aging sarcopenia, causing abnormal organelle accumulation over a lifetime. The resulting mitochondrial dysfunction in sarcopenic muscles feedbacks systemically by releasing the myomitokines fibroblast growth factor 21 (FGF21) and growth and differentiation factor 15 (GDF15), influencing the whole-body homeostasis and dictating healthy or unhealthy aging. This review describes the principal pathways controlling mitochondrial quality, many of which are potential therapeutic targets against muscle aging, and the connection between mitochondrial dysfunction and the myomitokines FGF21 and GDF15 in the pathogenesis of aging sarcopenia.

scholarly journals Lipid, fatty acid, carnitine- and choline derivative profiles in rheumatoid arthritis outpatients with different degrees of periodontal inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kathrin Beyer ◽  
Stein Atle Lie ◽  
Bodil Bjørndal ◽  
Rolf K. Berge ◽  
Asbjørn Svardal ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Fatty Acid ◽  
Mitochondrial Dysfunction ◽  
Inflammatory Diseases ◽  
Whole Body ◽  
Cross Sectional ◽  
Chronic Inflammatory Diseases ◽  
Periodontal Inflammation ◽  
Inflammatory Status ◽  
Lipid Fatty Acid

AbstractRheumatoid arthritis (RA) and periodontitis are chronic inflammatory diseases with several pathogenic pathways in common. Evidence supports an association between the diseases, but the exact underlying mechanisms behind the connection are still under investigation. Lipid, fatty acid (FA) and metabolic profile alterations have been associated with several chronic inflammatory diseases, including RA and periodontitis. Mitochondria have a central role in regulating cellular bioenergetic and whole-body metabolic homeostasis, and mitochondrial dysfunction has been proposed as a possible link between the two disorders. The aim of this cross-sectional study was to explore whole-blood FA, serum lipid composition, and carnitine- and choline derivatives in 78 RA outpatients with different degrees of periodontal inflammation. The main findings were alterations in lipid, FA, and carnitine- and choline derivative profiles. More specifically, higher total FA and total cholesterol concentrations were found in active RA. Elevated phospholipid concentrations with concomitant lower choline, elevated medium-chain acylcarnitines (MC-AC), and decreased ratios of MC-AC and long-chain (LC)-AC were associated with prednisolone medication. This may indicate an altered mitochondrial function in relation to the increased inflammatory status in RA disease. Our findings may support the need for interdisciplinary collaboration within the field of medicine and dentistry in patient stratification to improve personalized treatment. Longitudinal studies should be conducted to further assess the potential impact of mitochondrial dysfunction on RA and periodontitis.

scholarly journals Ursodeoxycholic Acid Regulates Hepatic Energy Homeostasis and White Adipose Tissue Macrophages Polarization in Leptin-Deficiency Obese Mice

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 253 ◽  
Author(s):  
Yu-Sheng Chen ◽  
Hsuan-Miao Liu ◽  
Tzung-Yan Lee
Keyword(s):  
Adipose Tissue ◽  
Mitochondrial Dysfunction ◽  
Ursodeoxycholic Acid ◽  
White Adipose Tissue ◽  
Whole Body ◽  
Bile Acid Metabolism ◽  
Obese Mice ◽  
Alcoholic Fatty Liver ◽  
Tissue Macrophage ◽  
Stat3 Phosphorylation

Obesity has been shown to play a role in the pathogenesis of several forms of metabolic syndrome, including non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes. Ursodeoxycholic acid (UDCA) has been shown to possess antioxidant and anti-inflammatory properties and prevents mitochondrial dysfunction in the progression of obesity-associated diseases. The aim of the study was to evaluate the mechanisms of UDCA during obesity-linked hepatic mitochondrial dysfunction and obesity-associated adipose tissue macrophage-induced inflammation in obese mice. UDCA significantly decreased lipid droplets, reduced free fatty acids (FFA) and triglycerides (TG), improved mitochondrial function, and enhanced white adipose tissue browning in ob/ob mice. This is associated with increased hepatic energy expenditure, mitochondria biogenesis, and incorporation of bile acid metabolism (Abca1, Abcg1 mRNA and BSEP, FGFR4, and TGR5 protein). In addition, UDCA downregulated NF-κB and STAT3 phosphorylation by negative regulation of the expression of SOCS1 and SOCS3 signaling. These changes were accompanied by decreased angiogenesis, as shown by the downregulation of VEGF, VCAM, and TGF-βRII expression. Importantly, UDCA is equally effective in reducing whole body adiposity. This is associated with decreased adipose tissue expression of macrophage infiltration (CD11b, CD163, and CD206) and lipogenic capacity markers (lipofuscin, SREBP-1, and CD36). Furthermore, UDCA significantly upregulated adipose browning in association with upregulation of SIRT-1-PGC1-α signaling in epididymis adipose tissue (EWAT). These results suggest that multi-targeted therapies modulate glucose and lipid biosynthesis fluxes, inflammatory response, angiogenesis, and macrophage differentiation. Therefore, it may be suggested that UDCA treatment may be a novel therapeutic agent for obesity.

Depression and neuroprogression: Sirtuins and mitochondria as crucial hubs

2019 ◽  
pp. 77-106
Author(s):  
George Anderson ◽  
Michael Maes
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Mitochondrial Dysfunction ◽  
Nitrosative Stress ◽  
Whole Body ◽  
Oxidative And Nitrosative Stress ◽  
Psychiatric Classification ◽  
Biochemical Alterations ◽  
Tryptophan Catabolites ◽  
Early Developmental

Neuroprogressive processes in major depressive disorder (MDD) can occur in association with recurrent episodes. The primary biological underpinnings are mediated by increases in the levels of immune-inflammation, tryptophan catabolites, mitochondrial dysfunction, and oxidative and nitrosative stress. Such biochemical alterations may be driven by changes in many peripheral and central sites, including in the gut, as well as by early developmental priming, such as prenatal stressors and breastfeeding consequences. As such, the conceptualization of MDD is shifted from simple psychological and central biochemical models to one that includes whole body processes over a developmental timescale. This provides a model that better integrates wider bodies of data relevant to the aetiology and course of MDD, and which therefore underpins the neuroprogressive processes that can occur over the course of MDD. This also significantly challenges current MDD (and wider psychiatric) classification by shifting classification to one based on biological processes rather than one based on subjective phenomenology.

Comparison of methane production by co-digesting fruit and vegetable waste with first stage and second stage anaerobic digester sludge from a two stage digester

2012 ◽  
Vol 65 (7) ◽  
pp. 1252-1257 ◽  
Author(s):  
Nathan D. Park ◽  
Ronald W. Thring ◽  
Steve S. Helle
Keyword(s):  
Methane Production ◽  
Anaerobic Digester ◽  
Batch Reactors ◽  
Vegetable Waste ◽  
Fruit And Vegetable ◽  
Methane Generation ◽  
Second Stage ◽  
Substrate Ratio ◽  
Sewer Sludge ◽  
Anaerobic Digester Sludge

Fruit and vegetable waste (FVW) was co-digested with first stage (FSS) and second stage anaerobic digester sludge (SSS) separately, over the course of 10 days, in batch reactors. Addition of FVW significantly increased the methane production in both sludges. After 10 days of digestion FSS + FVW produced 514 ± 57 L CH4 kg VS−1added compared with 392 ± 16 L CH4 for the SSS + FVW. The increased methane yield was most likely due to the higher inoculum substrate ratio of the FSS. The final VS and COD contents of the sewer sludge and FVW mixtures were not significantly different from the control values suggesting that all of the FVW added was degraded within 10 days. It is recommended that FVW be added to the first stage of the anaerobic digester in order to maximize methane generation.

scholarly journals Activation of the Nrf2-ARE Pathway Ameliorates Hyperglycemia-Mediated Mitochondrial Dysfunction in Podocytes Partly Through Sirt1

2018 ◽  
Vol 48 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Qunzi Zhang ◽  
Qiongxia Deng ◽  
Jun Zhang ◽  
JianTing Ke ◽  
Ye Zhu ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Structural Damage ◽  
Antioxidant Response ◽  
Sirtuin 1 ◽  
Small Interfering Rnas ◽  
Matrix Deposition ◽  
Mitochondrial Superoxide ◽  
Study Results ◽  
Oxidative Pathway ◽  
Nrf2 Expression

Background/Aims: Previously we have shown that activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-antioxidant response element (ARE) attenuated hyperglycemia-induced damage in podocytes, but the molecular mechanism remains unknown. Methods: Tert-butylhydroquinone (t-BHQ) and small interfering RNAs (siRNAs) were used to regulate Nrf2 expression, while nicotinamide and siRNAs were used to regulate sirtuin 1 (Sirt1) activity and expression, respectively. Mitochondrial superoxide, membrane potential and ATP levels were measured to assess changes in mitochondrial function. Nephrin and synaptopodin expression were measured by western blot analysis. Human podocytes and db/db diabetic mice were used in this study. Results: t-BHQ pretreatment of human podocytes exposed to high glucose (HG) alleviated mitochondrial dysfunction, enhanced the expression of Sirt1, nephrin and synaptopodin and lowered BSA permeability compared with podocytes exposed to HG without t-BHQ pretreatment (p< 0.05). Human podocytes exposed to HG had more severe mitochondrial dysfunction, lower expression of Sirt1, synaptopodin and nephrin and higher BSA permeability than podocytes exposed to HG when Nrf2 expression was downregulated by siRNAs (p< 0.05). The protection provided by activation of the Nrf-ARE pathway in podocytes exposed to HG was partially diminished when Sirt1 expression or activity was decreased by siRNAs or inhibitor compared with podocytes exposed to HG and pretreated with t-BHQ (p< 0.05). When nicotinamide and t-BHQ were both administered to db/db mice, we observed higher levels of urinary albumin/creatinine, lower nephrin and synaptopodin expression, more severe mesangial matrix deposition, collagen deposition on pathological slides and mitochondrial structural damage in podocytes compared to db/db mice treated only with t-BHQ. Conclusions: Our findings suggest that crosstalk between Sirt1 and the Nrf2-ARE anti-oxidative pathway forms a positive feedback loop and that protection provided by t-BHQ activation of the Nrf2-ARE pathway in db/db mice is partly dependent on Sirt1.

scholarly journals Testosterone Decreases Placental Mitochondrial Content and Cellular Bioenergetics

Biology ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 176 ◽  
Author(s):  
Jay S. Mishra ◽  
Chellakkan S. Blesson ◽  
Sathish Kumar
Keyword(s):  
Mitochondrial Dysfunction ◽  
Copy Number ◽  
Structural Damage ◽  
Plasma Testosterone ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Testosterone Levels ◽  
Mitochondrial Copy Number ◽  
Maternal Testosterone

Placental mitochondrial dysfunction plays a central role in the pathogenesis of preeclampsia. Since preeclampsia is a hyperandrogenic state, we hypothesized that elevated maternal testosterone levels induce damage to placental mitochondria and decrease bioenergetic profiles. To test this hypothesis, pregnant Sprague–Dawley rats were injected with vehicle or testosterone propionate (0.5 mg/kg/day) from gestation day (GD) 15 to 19. On GD20, the placentas were isolated to assess mitochondrial structure, copy number, ATP/ADP ratio, and biogenesis (Pgc-1α and Nrf1). In addition, in vitro cultures of human trophoblasts (HTR-8/SVneo) were treated with dihydrotestosterone (0.3, 1.0, and 3.0 nM), and bioenergetic profiles using seahorse analyzer were assessed. Testosterone exposure in pregnant rats led to a 2-fold increase in plasma testosterone levels with an associated decrease in placental and fetal weights compared with controls. Elevated maternal testosterone levels induced structural damage to the placental mitochondria and decreased mitochondrial copy number. The ATP/ADP ratio was reduced with a parallel decrease in the mRNA and protein expression of Pgc-1α and Nrf1 in the placenta of testosterone-treated rats compared with controls. In cultured trophoblasts, dihydrotestosterone decreased the mitochondrial copy number and reduced PGC-1α, NRF1 mRNA, and protein levels without altering the expression of mitochondrial fission/fusion genes. Dihydrotestosterone exposure induced significant mitochondrial energy deficits with a dose-dependent decrease in basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. In summary, our study suggests that the placental mitochondrial dysfunction induced by elevated maternal testosterone might be a potential mechanism linking preeclampsia to feto-placental growth restriction.

scholarly journals Oxidative Stress in the Healthy and Wounded Hepatocyte: A Cellular Organelles Perspective

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Tommaso Mello ◽  
Francesca Zanieri ◽  
Elisabetta Ceni ◽  
Andrea Galli
Keyword(s):  
Oxidative Stress ◽  
Structural Damage ◽  
Redox State ◽  
Iron Homeostasis ◽  
Structural Integrity ◽  
Whole Body ◽  
Metabolic Demand ◽  
Research Activity ◽  
Cellular Compartments ◽  
Cellular Organelles

Accurate control of the cell redox state is mandatory for maintaining the structural integrity and physiological functions. This control is achieved both by a fine-tuned balance between prooxidant and anti-oxidant molecules and by spatial and temporal confinement of the oxidative species. The diverse cellular compartments each, although structurally and functionally related, actively maintain their own redox balance, which is necessary to fulfill specialized tasks. Many fundamental cellular processes such as insulin signaling, cell proliferation and differentiation and cell migration and adhesion, rely on localized changes in the redox state of signal transducers, which is mainly mediated by hydrogen peroxide (H2O2). Therefore, oxidative stress can also occur long before direct structural damage to cellular components, by disruption of the redox circuits that regulate the cellular organelles homeostasis. The hepatocyte is a systemic hub integrating the whole body metabolic demand, iron homeostasis and detoxification processes, all of which are redox-regulated processes. Imbalance of the hepatocyte’s organelles redox homeostasis underlies virtually any liver disease and is a field of intense research activity. This review recapitulates the evolving concept of oxidative stress in the diverse cellular compartments, highlighting the principle mechanisms of oxidative stress occurring in the healthy and wounded hepatocyte.

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