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https://www.readbyqxmd.com/read/28738262/systematic-review-of-community-health-impacts-of-mountaintop-removal-mining
#1
REVIEW
Abee L Boyles, Robyn B Blain, Johanna R Rochester, Raghavendhran Avanasi, Susan B Goldhaber, Sofie McComb, Stephanie D Holmgren, Scott A Masten, Kristina A Thayer
BACKGROUND: The objective of this evaluation is to understand the human health impacts of mountaintop removal (MTR) mining, the major method of coal mining in and around Central Appalachia. MTR mining impacts the air, water, and soil and raises concerns about potential adverse health effects in neighboring communities; exposures associated with MTR mining include particulate matter (PM), polycyclic aromatic hydrocarbons (PAHs), metals, hydrogen sulfide, and other recognized harmful substances...
July 21, 2017: Environment International
https://www.readbyqxmd.com/read/28734981/apigenin-attenuates-patulin-induced-apoptosis-in-hek293-cells-by-modulating-ros-mediated-mitochondrial-dysfunction-and-caspase-signal-pathway
#2
Yujie Zhong, Chengni Jin, Jing Gan, Xiaorui Wang, Zhenqiang Shi, Xiaodong Xia, Xiaoli Peng
Mycotoxins like patulin (PAT) are among the most significant food contaminant with regard to public health. This study aimed to evaluate the protective effect of apigenin (API), one of the most bioactive flavonoids in plant-derived food, on PAT-induced apoptosis in HEK293 cells. Cells were treated under basic conditions, 8 μM PAT without or with API (2.5, 5 and 10 μM) concomitantly for 10 h. API exerted renoprotective effect by inhibiting intracellular reactive oxygen species (ROS) accumulation, modulating oxidative phosphorylation especially elevating the expression of ATP synthase, re-establishing mitochondrial membrane potential (MMP) and maintaining higher intracellular ATP level, accompanied by p53, Bax downregulation and Bcl-2 upregulation...
July 19, 2017: Toxicon: Official Journal of the International Society on Toxinology
https://www.readbyqxmd.com/read/28733449/mitochondrial-function-in-engineered-cardiac-tissues-is-co-regulated-by-extracellular-matrix-elasticity-and-tissue-alignment
#3
Davi Marco Lyra-Leite, Allen Mariano Andres, Andrew Patrick Petersen, Nethika Ruvini Ariyasinghe, Nathan Cho, Jezell Athena Lee, Roberta A Gottlieb, Megan L McCain
Mitochondria in cardiac myocytes are critical for generating ATP to meet the high metabolic demands associated with sarcomere shortening. Distinct remodeling of mitochondrial structure and function occur in cardiac myocytes in both developmental and pathological settings. However, the factors that underlie these changes are poorly understood. Because remodeling of tissue architecture and extracellular matrix (ECM) elasticity are also hallmarks of ventricular development and disease, we hypothesize that these environmental factors regulate mitochondrial function in cardiac myocytes...
July 21, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28732339/aryl-and-alkyl-phosphorus-containing-flame-retardants-induced-mitochondrial-impairment-and-cell-death-in-chinese-hamster-ovary-cho-k1-cells
#4
Chao Huang, Na Li, Shengwu Yuan, Xiaoya Ji, Mei Ma, Kaifeng Rao, Zijian Wang
Phosphorus-containing flame retardants (PFRs) are increasingly in demand worldwide as replacements for brominated flame retardants (BFRs), but insufficient available toxicological information on PFRs makes assessing their health risks challenging. Mitochondria are important targets of various environmental pollutants, and mitochondrial dysfunction may lead to many common diseases. In the present study, mitochondria impairment-related endpoints were measured by a high content screening (HCS) assay for 11 selected non-halogen PFRs in Chinese hamster ovary (CHO-k1) cells...
July 18, 2017: Environmental Pollution
https://www.readbyqxmd.com/read/28726269/previous-physical-exercise-alters-hepatic-profile-of-oxidative-inflammatory-status-and-limits-the-secondary-brain-damage-induced-by-severe-tbi-in-rats
#5
Mauro Robson Torres de Castro, Ana Paula de Oliveira Ferreira, Guilherme Lago Busanello, Luís Roberto Hart da Silva, Mauro Eduardo Porto da Silveira Junior, Fernando Fiorin, Gabriela Arrifano, Maria Elena Crespo López, Rômulo Pillon Barcelos, María J Cuevas, Guilherme Bresciani, Javier González-Gallego, Michele Rechia Fighera, Luiz Fernando Freire Royes
Although systemic responses have been described after traumatic brain injury (TBI), little is known regarding potential interactions between brain and peripheral organs after neuronal injury. In this sense, we decided to investigate whether peripheral oxidative/inflammatory response contributes to the neuronal dysfunction after TBI as well as prophylactic role of exercise training. Animals were submitted to fluid percussion injury (FPI) after 6 weeks of swimming training. Previous exercise training increased mRNA expression of X receptor alpha (LXR-α), ATP-binding cassette transporter (ABCA1), and decreased inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α) and interleukin (IL)-6 expression per se in liver...
July 20, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28720899/p32-heterozygosity-protects-against-age-and-diet-induced-obesity-by-increasing-energy-expenditure
#6
Yong Liu, Patrick L Leslie, Aiwen Jin, Koji Itahana, Lee M Graves, Yanping Zhang
Obesity is increasing in prevalence and has become a global public health problem. The main cause of obesity is a perturbation in energy homeostasis, whereby energy intake exceeds energy expenditure. Although mitochondrial dysfunction has been linked to the deregulation of energy homeostasis, the precise mechanism is poorly understood. Here, we identify mitochondrial p32 (also known as C1QBP) as an important regulator of lipid homeostasis that regulates both aerobic and anaerobic energy metabolism. We show that while whole-body deletion of the p32 results in an embryonic lethal phenotype, mice heterozygous for p32 are resistant to age- and high-fat diet-induced ailments, including obesity, hyperglycemia, and hepatosteatosis...
July 18, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28720712/regulation-of-the-autophagy-system-during-chronic-contractile-activity-induced-muscle-adaptations
#7
Yuho Kim, David A Hood
Skeletal muscle is adaptable to exercise stimuli via the upregulation of mitochondrial biogenesis, and recent studies have suggested that autophagy also plays a role in exercise-induced muscle adaptations. However, it is still obscure how muscle regulates autophagy over the time course of training adaptations. This study examined the expression of autophagic proteins in skeletal muscle of rats exposed to chronic contractile activity (CCA; 6 h/day, 9V, 10 Hz continuous, 0.1 msec pulse duration) for 1, 3, and 7 days (n = 8/group)...
July 2017: Physiological Reports
https://www.readbyqxmd.com/read/28719878/the-effects-of-fluoride-on-neuronal-function-occurs-via-cytoskeleton-damage-and-decreased-signal-transmission
#8
Lingli Chen, Hongmei Ning, Zhihong Yin, Xiaochao Song, Yongchao Feng, Hao Qin, Yi Li, Jundong Wang, Yaming Ge, Wenkui Wang
It has been reported that fluoride exposure may cause serious public health problems, particularly neurotoxicity. However, the underlying mechanisms remain unclear. This study used Neuro-2A cells to investigate the effects of fluoride on the cytoskeleton. The Neuro-2A cells were exposed to 0, 1, 2, 4 and 6 mM sodium fluoride (NaF) for 24 h. Cell viability and lactate dehydrogenase (LDH) release were examined. It was observed that exposure to NaF reduced cell viability, disrupted cellular membrane integrity, and high levels of LDH were released...
June 30, 2017: Chemosphere
https://www.readbyqxmd.com/read/28719865/antioxidant-effect-of-exercise-exploring-the-role-of-the-mitochondrial-complex-i-superassembly
#9
J R Huertas, S Al Fazazi, A Hidalgo-Gutierrez, L C López, R A Casuso
Mitochondrial respiratory complexes become assembled into supercomplexes (SC) under physiological conditions. One of the functional roles of these entities is the limitation of reactive oxygen species (ROS) produced by complex I (CI) of the respiratory chain. We sought to determine whether the systemic antioxidant effect of exercise is mediated by the assembly of mitochondrial CIs into SCs in rats. Male Wistar rats were exercise trained or remained sedentary for ten weeks; then, blood samples were collected, and the gastrocnemius muscle was isolated...
July 11, 2017: Redox Biology
https://www.readbyqxmd.com/read/28713289/mitochondrial-vdac1-a-key-gatekeeper-as-potential-therapeutic-target
#10
REVIEW
Amadou K S Camara, YiFan Zhou, Po-Chao Wen, Emad Tajkhorshid, Wai-Meng Kwok
Mitochondria are the key source of ATP that fuels cellular functions, and they are also central in cellular signaling, cell division and apoptosis. Dysfunction of mitochondria has been implicated in a wide range of diseases, including neurodegenerative and cardiac diseases, and various types of cancer. One of the key proteins that regulate mitochondrial function is the voltage-dependent anion channel 1 (VDAC1), the most abundant protein on the outer membrane of mitochondria. VDAC1 is the gatekeeper for the passages of metabolites, nucleotides, and ions; it plays a crucial role in regulating apoptosis due to its interaction with apoptotic and anti-apoptotic proteins, namely members of the Bcl-2 family of proteins and hexokinase...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28712506/vdac1-functions-in-ca-2-homeostasis-and-cell-life-and-death-in-health-and-disease
#11
REVIEW
Varda Shoshan-Barmatz, Yakov Krelin, Anna Shteinfer-Kuzmine
In the outer mitochondrial membrane (OMM), the voltage-dependent anion channel 1 (VDAC1) serves as a mitochondrial gatekeeper, controlling the metabolic and energy cross-talk between mitochondria and the rest of the cell. VDAC1 also functions in cellular Ca(2+) homeostasis by transporting Ca(2+) in and out of mitochondria. VDAC1 has also been recognized as a key protein in mitochondria-mediated apoptosis, contributing to the release of apoptotic proteins located in the inter-membranal space (IMS) and regulating apoptosis via association with pro- and anti-apoptotic members of the Bcl-2 family of proteins and hexokinase...
June 23, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28711655/ubiquitination-at-the-mitochondria-in-neuronal-health-and-disease
#12
REVIEW
Christian Covill-Cooke, Jack Howden, Nicol Birsa, Josef Kittler
The preservation of mitochondrial function is of particular importance in neurons given the high energy requirements of action potential propagation and synaptic transmission. Indeed, disruptions in mitochondrial dynamics and quality control are linked to cellular pathology in neurodegenerative diseases, such as Alzheimer's and Parkinson's disease. Here, we will discuss the role of ubiquitination by the E3 ligases: Parkin, MARCH5 and Mul1, and how they regulate mitochondrial homeostasis. Furthermore, given the role of Parkin and Mul1 in the formation of mitochondria-derived vesicles we give an overview of this area of mitochondrial homeostasis...
July 12, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28711444/mitochondrial-membrane-potential
#13
Ljubava D Zorova, Vasily A Popkov, Egor Y Plotnikov, Denis N Silachev, Irina B Pevzner, Stanislovas S Jankauskas, Valentina A Babenko, Savva D Zorov, Anastasia V Balakireva, Magdalena Juhaszova, Steven J Sollott, Dmitry B Zorov
The mitochondrial membrane potential (ΔΨm) generated by proton pumps (Complexes I, III and IV) is an essential component in the process of energy storage during oxidative phosphorylation. Together with the proton gradient (ΔpH), ΔΨm forms the transmembrane potential of hydrogen ions which is harnessed to make ATP. The levels of ΔΨm and ATP in the cell are kept relatively stable although there are limited fluctuations of both these factors that can occur reflecting normal physiological activity. However, sustained changes in both factors may be deleterious...
July 12, 2017: Analytical Biochemistry
https://www.readbyqxmd.com/read/28709131/tiron-ameliorates-oxidative-stress-and-inflammation-in-titanium-dioxide-nanoparticles-induced-nephrotoxicity-of-male-rats
#14
Ashraf Morgan, Mona K Galal, Hanan A Ogaly, Marwa A Ibrahim, Reham M Abd-Elsalam, Peter Noshy
Although the widespread use of titanium dioxide nanoparticles (TiO2 NPs), few studies were conducted on its hazard influence on human health. Tiron a synthetic vitamin E analog was proven to be a mitochondrial targeting antioxidant. The current investigation was performed to assess the efficacy of tiron against TiO2 NPs induced nephrotoxicity. Eighty adult male rats divided into four different groups were used: group I was the control, group II received TiO2 NPs (100mg\Kg BW), group III received TiO2 NPs plus tiron (470mg\kg BW), and group IV received tiron alone...
July 11, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28707667/-the-activity-of-proapoptotic-genes-increases-after-renal-ischemia-reperfusion
#15
O I Kit, D I Vodolazhsky, S N Dimitriadi, D S Kutilin, N N Timoshkina, E N Gudueva, E M Frantsiyants
According to the World Health Organization, pathologies associated with ischemia/reperfusion occupy the leading position in the structure of mortality. The efficiency of localized kidney cancer surgery is limited by the damaging effects of prolonged warm ischemia and reperfusion. Ischemia/reperfusion damage to renal tissue may be related to changes in the expression profiles of pro- and antiapoptotic genes. Here, we have presented the longitudinal expression profiles of apoptosis-related genes in tissues of left and right (intact) kidneys of male rats exposed to unilateral ischemia followed by reperfusion...
May 2017: Molekuliarnaia Biologiia
https://www.readbyqxmd.com/read/28707399/neuroglobin-and-friends
#16
REVIEW
Marco Fiocchetti, Manuela Cipolletti, Valentina Brandi, Fabio Polticelli, Paolo Ascenzi
In the year 2000, the third member of the globin family was discovered in human and mouse brain and named neuroglobin (Ngb). Neuroglobin overexpression significantly protects both heart and brain from hypoxic/ischemic and oxidative stress-related insults, whereas decreased Ngb levels lead to an exacerbation of tissue injuries. Moreover, Ngb overexpression protects neurons from mitochondrial dysfunctions and neurodegenerative disorders such as Alzheimer disease; however, it facilitates the survival of cancer cells...
July 14, 2017: Journal of Molecular Recognition: JMR
https://www.readbyqxmd.com/read/28706150/potential-genotoxic-and-cytotoxicity-of-emamectin-benzoate-in-human-normal-liver-cells
#17
Zhijie Zhang, Xinyu Zhao, Xiaosong Qin
Pesticide residue inducing cancer-related health problems draw people more attention recently. Emamectin benzoate (EMB) has been widely used in agriculture around the world based on its specificity targets. Although potential risk and the molecular mechanism of EMB toxicity to human liver has not been well-characterized. Unlike well-reported toxicity upon central nervous system, potential genotoxic and cytotoxicity of EMB in human liver cell was ignored and very limited. In this study, we identify genotoxicity and cytotoxicity of EMB to human normal liver cells (QSG7701 cell line) in vitro...
July 4, 2017: Oncotarget
https://www.readbyqxmd.com/read/28705993/effects-of-%C3%AE-hydroxy-%C3%AE-methylbutyrate-hmb-on-skeletal-muscle-mitochondrial-content-and-dynamics-and-lipids-after-10-days-of-bed-rest-in-older-adults
#18
Robert A Standley, Giovanna Distefano, Suzette L Pereira, Min Tian, Owen J Kelly, Paul M Coen, Nicolaas E P Deutz, Robert R Wolfe, Bret H Goodpaster
Loss of muscle mass during periods of disuse likely has negative health consequences for older adults. We have previously shown that β-hydroxy-β-methylbutyrate (HMB) supplementation during 10 days of strict bed rest (BR) attenuates the loss of lean mass in older adults. To elucidate potential molecular mechanisms of HMB effects on muscle during bed rest and resistance training rehabilitation (RT), we examined mediators of skeletal muscle mitochondrial dynamics, autophagy and atrophy, and intramyocellular lipids...
July 13, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28705612/cardiac-mitochondrial-dynamics-mir-mediated-regulation-during-cardiac-injury
#19
Anusha Sivakumar, Ramasamy Subbiah, Rekha Balakrishnan, Jeyaprakash Rajendhran
Mitochondrial integrity is indispensable for cardiac health. With the advent of modern imaging technologies, mitochondrial motility and dynamics within the cell are extensively studied. Terminally differentiated and well-structured cardiomyocytes depict little mitochondrial division and fusion, questioning the contribution of mitochondrial fusion proteins (Mitofusin 1/2 and Optic Atrophy 1 protein) and fission factors (Dynamin-like protein 1 and mitochondrial fission 1 protein) in cardiomyocyte homeostasis...
July 10, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28704930/mitochondrial-dysfunction-mediated-by-poly-adp-ribose-polymerase-1-activation-contributes-to-hippocampal-neuronal-damage-following-status-epilepticus
#20
Yi-Chen Lai, J Scott Baker, Taraka Donti, Brett H Graham, William J Craigen, Anne E Anderson
Mitochondrial dysfunction plays a central role in the neuropathology associated with status epilepticus (SE) and is implicated in the development of epilepsy. While excitotoxic mechanisms are well-known mediators affecting mitochondrial health following SE, whether hyperactivation of poly(ADP-ribose) polymerase-1 (PARP-1) also contributes to SE-induced mitochondrial dysfunction remains to be examined. Here we first evaluated the temporal evolution of poly-ADP-ribosylated protein levels in hippocampus following kainic acid-induced SE as a marker for PARP-1 activity, and found that PARP-1 was hyperactive at 24 h following SE...
July 12, 2017: International Journal of Molecular Sciences
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