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Mitochondria AND NAD ratio

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https://www.readbyqxmd.com/read/27867097/mitochondrial-remodeling-in-the-liver-following-chronic-alcohol-feeding-to-rats
#1
Derick Han, Heather S Johnson, Madhuri P Rao, Gary Martin, Harsh Sancheti, Kai H Silkwood, Carl W Decker, Kim Tho Nguyen, Joseph G Casian, Enrique Cadenas, Neil Kaplowitz
The feeding of alcohol orally (Lieber-DeCarli diet) to rats has been shown to cause declines in mitochondrial respiration (state III), decreased expression of respiratory complexes, and decreased respiratory control ratios (RCR) in liver mitochondria. These declines and other mitochondrial alterations have led to the hypothesis that alcohol feeding causes "mitochondrial dysfunction" in the liver. If oral alcohol feeding leads to mitochondrial dysfunction, one would predict that increasing alcohol delivery by intragastric (IG) alcohol feeding to rats would cause greater declines in mitochondrial bioenergetics in the liver...
November 17, 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27793977/acute-stimulation-of-glucose-influx-upon-mitoenergetic-dysfunction-requires-lkb1-ampk-sirt2-and-mtor-raptor
#2
Dania C Liemburg-Apers, Jori A L Wagenaars, Jan A M Smeitink, Peter H G M Willems, Werner J H Koopman
Mitochondria play a central role in cellular energy production, and their dysfunction can trigger a compensatory increase in glycolytic flux to sustain cellular ATP levels. Here, we studied the mechanism of this homeostatic phenomenon in C2C12 myoblasts. Acute (30 min) mitoenergetic dysfunction induced by the mitochondrial inhibitors piericidin A and antimycin A stimulated Glut1-mediated glucose uptake without altering Glut1 (also known as SLC2A1) mRNA or plasma membrane levels. The serine/threonine liver kinase B1 (LKB1; also known as STK11) and AMP-activated protein kinase (AMPK) played a central role in this stimulation...
December 1, 2016: Journal of Cell Science
https://www.readbyqxmd.com/read/27634671/pharmacological-inhibition-of-nox4-ameliorates-alcohol-induced-liver-injury-in-mice-through-improving-oxidative-stress-and-mitochondrial-function
#3
Qian Sun, Wenliang Zhang, Wei Zhong, Xinguo Sun, Zhanxiang Zhou
BACKGROUND: Oxidative stress plays a crucial role in the development of alcoholic liver disease (ALD), however effective pharmacological treatment for oxidative injury is still lacking. The objective of this study was to determine whether inhibition of NADPH oxidase activity could reverse alcohol-induced liver injury via protecting mitochondrial functions. METHODS: C57BL/6J mice were pair-fed with Lieber-DeCarli control or ethanol diet for four week with or without administration with 30mg/kg/d GKT137831, a NOX4 inhibitor for the last two weeks...
September 12, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27558544/hyperammonaemia-induced-skeletal-muscle-mitochondrial-dysfunction-results-in-cataplerosis-and-oxidative-stress
#4
Gangarao Davuluri, Allawy Allawy, Samjhana Thapaliya, Julie H Rennison, Dharmvir Singh, Avinash Kumar, Yana Sandlers, David R Van Wagoner, Chris A Flask, Charles Hoppel, Takhar Kasumov, Srinivasan Dasarathy
KEY POINTS: Hyperammonaemia occurs in hepatic, cardiac and pulmonary diseases with increased muscle concentration of ammonia. We found that ammonia results in reduced skeletal muscle mitochondrial respiration, electron transport chain complex I dysfunction, as well as lower NAD(+) /NADH ratio and ATP content. During hyperammonaemia, leak of electrons from complex III results in oxidative modification of proteins and lipids. Tricarboxylic acid cycle intermediates are decreased during hyperammonaemia, and providing a cell-permeable ester of αKG reversed the lower TCA cycle intermediate concentrations and increased ATP content...
August 25, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/27551320/moderately-decreased-maternal-dietary-energy-intake-during-pregnancy-reduces-fetal-skeletal-muscle-mitochondrial-biogenesis-in-the-pigs
#5
Tiande Zou, Bing Yu, Jie Yu, Xiangbing Mao, Ping Zheng, Jun He, Zhiqing Huang, Yue Liu, Daiwen Chen
BACKGROUND: Mitochondria are of major importance in oocyte and early embryo, playing a key role in maintaining energy homeostasis. Epidemiological findings indicate that maternal undernutrition-induced mitochondrial dysfunction during pregnancy is associated with the development of metabolic disorders in offspring. Here, we investigated the effects of moderately decreased maternal energy intake during pregnancy on skeletal muscle mitochondrial biogenesis in fetal offspring with pig as a model...
2016: Genes & Nutrition
https://www.readbyqxmd.com/read/27489254/normalization-of-nad-redox-balance-as-a-therapy-for-heart-failure
#6
Chi Fung Lee, Juan D Chavez, Lorena Garcia-Menendez, Yongseon Choi, Nathan D Roe, Ying Ann Chiao, John S Edgar, Young Ah Goo, David R Goodlett, James E Bruce, Rong Tian
BACKGROUND: Impairments of mitochondrial function in the heart are linked intricately to the development of heart failure, but there is no therapy for mitochondrial dysfunction. METHODS: We assessed the reduced/oxidized ratio of nicotinamide adenine dinucleotide (NADH/NAD(+) ratio) and protein acetylation in the failing heart. Proteome and acetylome analyses were followed by docking calculation, mutagenesis, and mitochondrial calcium uptake assays to determine the functional role of specific acetylation sites...
September 20, 2016: Circulation
https://www.readbyqxmd.com/read/27474736/the-contribution-of-nicotinamide-nucleotide-transhydrogenase-to-peroxide-detoxification-is-dependent-on-the-respiratory-state-and-counterbalanced-by-other-sources-of-nadph-in-liver-mitochondria
#7
Juliana Aparecida Ronchi, Annelise Francisco, Luiz Augusto Correa Passos, Tiago Rezende Figueira, Roger Frigério Castilho
The forward reaction of nicotinamide nucleotide transhydrogenase (NNT) reduces NADP(+) at the expense of NADH oxidation and H(+) movement down the electrochemical potential across the inner mitochondrial membrane, establishing an NADPH/NADP(+) ratio severalfold higher than the NADH/NAD(+) ratio in the matrix. In turn, NADPH drives processes, such as peroxide detoxification and reductive biosynthesis. In this study, we generated a congenic mouse model carrying a mutated Nnt(C57BL/6J) allele from the C57BL/6J substrain...
September 16, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27337687/autophagy-deficiency-in-myeloid-cells-increases-susceptibility-to-obesity-induced-diabetes-and-experimental-colitis
#8
Hae-Youn Lee, Jinyoung Kim, Wenying Quan, June-Chul Lee, Min-Soo Kim, Seok-Hyung Kim, Jin-Woo Bae, Kyu Yeon Hur, Myung-Shik Lee
Autophagy, which is critical for the proper turnover of organelles such as endoplasmic reticulum and mitochondria, affects diverse aspects of metabolism, and its dysregulation has been incriminated in various metabolic disorders. However, the role of autophagy of myeloid cells in adipose tissue inflammation and type 2 diabetes has not been addressed. We produced mice with myeloid cell-specific deletion of Atg7 (autophagy-related 7), an essential autophagy gene (Atg7 conditional knockout [cKO] mice). While Atg7 cKO mice were metabolically indistinguishable from control mice, they developed diabetes when bred to ob/w mice (Atg7 cKO-ob/ob mice), accompanied by increases in the crown-like structure, inflammatory cytokine expression and inflammasome activation in adipose tissue...
August 2, 2016: Autophagy
https://www.readbyqxmd.com/read/27298826/oxidative-stress-and-liver-morphology-in-experimental-cyclosporine-a-induced-hepatotoxicity
#9
Agnieszka Korolczuk, Kinga Caban, Magdalena Amarowicz, Grażyna Czechowska, Joanna Irla-Miduch
Cyclosporine A is an immunosuppressive drug used after organ's transplantation. The adverse effects on such organs as kidney or liver may limit its use. Oxidative stress is proposed as one of the mechanisms of organs injury. The study was designed to elucidate CsA-induced changes in liver function, morphology, oxidative stress parameters, and mitochondria in rat's hepatocytes. Male Wistar rats were used: group A (control) receiving physiological saline, group B cyclosporine A in a dose of 15 mg/kg/day subcutaneously, and group C the CsA-vehicle (olive oil)...
2016: BioMed Research International
https://www.readbyqxmd.com/read/27183225/cyclophilin-d-knock-out-mice-show-enhanced-resistance-to-osteoporosis-and-to-metabolic-changes-observed-in-aging-bone
#10
Laura C Shum, Noelle S White, Sergiy M Nadtochiy, Karen L de Mesy Bentley, Paul S Brookes, Jennifer H Jonason, Roman A Eliseev
Pathogenic factors associated with aging, such as oxidative stress and hormone depletion converge on mitochondria and impair their function via opening of the mitochondrial permeability transition pore (MPTP). The MPTP is a large non-selective pore regulated by cyclophilin D (CypD) that disrupts mitochondrial membrane integrity. MPTP involvement has been firmly established in degenerative processes in heart, brain, and muscle. Bone has high energy demands and is therefore expected to be highly sensitive to mitochondrial dysfunction...
2016: PloS One
https://www.readbyqxmd.com/read/27157912/malate-aspartate-shuttle-inhibitor-aminooxyacetic-acid-leads-to-decreased-intracellular-atp-levels-and-altered-cell-cycle-of-c6-glioma-cells-by-inhibiting-glycolysis
#11
Caixia Wang, Heyu Chen, Mingchao Zhang, Jie Zhang, Xunbin Wei, Weihai Ying
NADH shuttles, including malate-aspartate shuttle (MAS) and glycerol-3-phosphate shuttle, can shuttle the reducing equivalents of cytosolic NADH into mitochondria. It is widely accepted that the major function of NADH shuttles is to increase mitochondrial energy production. Our study tested the hypothesis that the novel major function of NADH shuttles in cancer cells is to maintain glycolysis by decreasing cytosolic NADH/NAD(+) ratios. We found that AOAA, a widely used MAS inhibitor, led to decreased intracellular ATP levels, altered cell cycle and increased apoptosis and necrosis of C6 glioma cells, without affecting the survival of primary astrocyte cultures...
August 1, 2016: Cancer Letters
https://www.readbyqxmd.com/read/27155879/the-non-apoptotic-action-of-bcl-xl-regulating-ca-2-signaling-and-bioenergetics-at-the-er-mitochondrion-interface
#12
Abasha Williams, Teruo Hayashi, Daniel Wolozny, Bojiao Yin, Tzu-Chieh Su, Michael J Betenbaugh, Tsung-Ping Su
Bcl-2 family proteins are known to competitively regulate Ca(2+); however, the specific inter-organelle signaling pathways and related cellular functions are not fully elucidated. In this study, a portion of Bcl-xL was detected at the ER-mitochondrion interface or MAM (mitochondria-associated ER membrane) in association with type 3 inositol 1,4,5-trisphosphate receptors (IP3R3); an association facilitated by the BH4 and transmembrane domains of Bcl-xL. Moreover, increasing Bcl-xL expression enhanced transient mitochondrial Ca(2+) levels upon ER Ca(2+) depletion induced by short-term, non-apoptotic incubation with thapsigargin (Tg), while concomitantly reducing cytosolic Ca(2+) release...
June 2016: Journal of Bioenergetics and Biomembranes
https://www.readbyqxmd.com/read/27124460/complementation-of-mitochondrial-electron-transport-chain-by-manipulation-of-the-nad-nadh-ratio
#13
Denis V Titov, Valentin Cracan, Russell P Goodman, Jun Peng, Zenon Grabarek, Vamsi K Mootha
A decline in electron transport chain (ETC) activity is associated with many human diseases. Although diminished mitochondrial adenosine triphosphate production is recognized as a source of pathology, the contribution of the associated reduction in the ratio of the amount of oxidized nicotinamide adenine dinucleotide (NAD(+)) to that of its reduced form (NADH) is less clear. We used a water-forming NADH oxidase from Lactobacillus brevis (LbNOX) as a genetic tool for inducing a compartment-specific increase of the NAD(+)/NADH ratio in human cells...
April 8, 2016: Science
https://www.readbyqxmd.com/read/27068062/reactive-oxygen-species-production-in-cardiac-mitochondria-after-complex-i-inhibition-modulation-by-substrate-dependent-regulation-of-the-nadh-nad-ratio
#14
Paavo Korge, Guillaume Calmettes, James N Weiss
Reactive oxygen species (ROS) production by isolated complex I is steeply dependent on the NADH/NAD(+) ratio. We used alamethicin-permeabilized mitochondria to study the substrate-dependence of matrix NADH and ROS production when complex I is inhibited by piericidin or rotenone. When complex I was inhibited in the presence of malate/glutamate, membrane permeabilization accelerated O2 consumption and ROS production due to a rapid increase in NADH generation that was not limited by matrix NAD(H) efflux. In the presence of inhibitor, both malate and glutamate were required to generate a high enough NADH/NAD(+) ratio to support ROS production through the coordinated activity of malate dehydrogenase (MDH) and aspartate aminotransferase (AST)...
July 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/26712469/concurrent-acetylation-of-foxo1-3a-and-p53-due-to-sirtuins-inhibition-elicit-bim-puma-mediated-mitochondrial-dysfunction-and-apoptosis-in-berberine-treated-hepg2-cells
#15
Shatrunajay Shukla, Ankita Sharma, Vivek Kumar Pandey, Sheikh Raisuddin, Poonam Kakkar
Post-translational modifications i.e. phosphorylation and acetylation are pivotal requirements for proper functioning of eukaryotic proteins. The current study aimed to decode the impact of acetylation/deacetylation of non-histone targets i.e. FoxO1/3a and p53 of sirtuins (NAD(+) dependent enzymes with lysine deacetylase activity) in berberine treated human hepatoma cells. Berberine (100 μM) inhibited sirtuins significantly (P<0.05) at transcriptional level as well as at translational level. Combination of nicotinamide (sirtuin inhibitor) with berberine potentiated sirtuins inhibition and increased the expression of FoxO1/3a and phosphorylation of p53 tumor suppressor protein...
January 15, 2016: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/26708453/production-of-superoxide-hydrogen-peroxide-by-the-mitochondrial-2-oxoadipate-dehydrogenase-complex
#16
Renata L S Goncalves, Victoria I Bunik, Martin D Brand
In humans, mutations in dehydrogenase E1 and transketolase domain containing 1 (DHTKD1) are associated with neurological abnormalities and accumulation of 2-oxoadipate, 2-aminoadipate, and reactive oxygen species. The protein encoded by DHTKD1 has sequence and structural similarities to 2-oxoglutarate dehydrogenase, and the 2-oxoglutarate dehydrogenase complex can produce superoxide/H2O2 at high rates. The DHTKD1 enzyme is hypothesized to catalyze the oxidative decarboxylation of 2-oxoadipate, a shared intermediate of the degradative pathways for tryptophan, lysine and hydroxylysine...
February 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/26629314/modulation-of-the-matrix-redox-signaling-by-mitochondrial-ca-2
#17
REVIEW
Jaime Santo-Domingo, Andreas Wiederkehr, Umberto De Marchi
Mitochondria sense, shape and integrate signals, and thus function as central players in cellular signal transduction. Ca(2+) waves and redox reactions are two such intracellular signals modulated by mitochondria. Mitochondrial Ca(2+) transport is of utmost physio-pathological relevance with a strong impact on metabolism and cell fate. Despite its importance, the molecular nature of the proteins involved in mitochondrial Ca(2+) transport has been revealed only recently. Mitochondrial Ca(2+) promotes energy metabolism through the activation of matrix dehydrogenases and down-stream stimulation of the respiratory chain...
November 26, 2015: World Journal of Biological Chemistry
https://www.readbyqxmd.com/read/26475290/impaired-energy-metabolism-of-the-taurine%C3%A2-deficient-heart
#18
Stephen W Schaffer, Kayoko Shimada-Takaura, Chian Ju Jong, Takashi Ito, Kyoko Takahashi
Taurine is a β-amino acid found in high concentrations in excitable tissues, including the heart. A significant reduction in myocardial taurine content leads to the development of a unique dilated, atrophic cardiomyopathy. One of the major functions of taurine in the heart is the regulation of the respiratory chain. Hence, we tested the hypothesis that taurine deficiency-mediated defects in respiratory chain function lead to impaired energy metabolism and reduced ATP generation. We found that while the rate of glycolysis was significantly enhanced in the taurine-deficient heart, glucose oxidation was diminished...
February 2016: Amino Acids
https://www.readbyqxmd.com/read/26278015/curcumin-treatment-enhances-the-effect-of-exercise-on-mitochondrial-biogenesis-in-skeletal-muscle-by-increasing-camp-levels
#19
Ronald D Ray Hamidie, Tatsuya Yamada, Rie Ishizawa, Yoko Saito, Kazumi Masuda
BACKGROUND: In response to physiologic stressors, skeletal muscle has the potential to elicit wide variety of adaptive responses, such as biogenesis of mitochondria and clearance of damaged mitochondria to promote healthy muscle. The polyphenol curcumin, derived from the rhizome Curcuma longa L., is a natural antioxidant that exhibits various pharmacological activities and therapeutic properties. However, the effect of curcumin on the regulation of mitochondrial biogenesis in skeletal muscle remains unknown...
October 2015: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/26263161/protective-effect-of-sevoflurane-postconditioning-against-cardiac-ischemia-reperfusion-injury-via-ameliorating-mitochondrial-impairment-oxidative-stress-and-rescuing-autophagic-clearance
#20
Peng Yu, Jing Zhang, Shuchun Yu, Zhenzhong Luo, Fuzhou Hua, Linhui Yuan, Zhidong Zhou, Qin Liu, Xiaohong Du, Sisi Chen, Lieliang Zhang, Guohai Xu
BACKGROUND AND PURPOSE: Myocardial infarction leads to heart failure. Autophagy is excessively activated in myocardial ischemia/reperfusion (I/R) in rats. The aim of this study is to investigate whether the protection of sevoflurane postconditioning (SPC) in myocardial I/R is through restored impaired autophagic flux. METHODS: Except for the sham control (SHAM) group, each rat underwent 30 min occlusion of the left anterior descending coronary (LAD) followed by 2 h reperfusion...
2015: PloS One
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