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mitochondria damage

Hao Wu, Fang Zeng, Hang Zhang, Jiangsheng Xu, Jianrong Qiu, Shuizhu Wu
The applications of photodynamic therapy (PDT) are usually limited by photosensitizers' side effects and singlet oxygen's short half-life. Herein, a mitochondria-targeted nanosystem is demonstrated to enhance the PDT efficacy by releasing a bio-precursor of photosensitizer under two-photon irradiation. A phototriggerable coumarin derivative is first synthesized by linking 5-aminolevulinic acid (5-ALA, the bio-precursor) to coumarin; and the nanosystem (CD-ALA-TPP) is then fabricated by covalently incorporating this coumarin derivative and a mitochondria-targeting compound triphenylphosphonium (TPP) onto carbon dots (CDs)...
February 2016: Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
Waleska K Martins, Andreza B Gomide, Érico T Costa, Helena C Junqueira, Beatriz S Stolf, Rosangela Itri, Maurício S Baptista
BACKGROUND: Cell senescence is a process of central importance to the understanding of aging as well as to the development of new drugs. It is related with genomic instability, which has been shown to occur in the presence of autophagy deficiency. Yet, the mechanism that triggers genomic instability and senescence from a condition of autophagy deficiency remains unknown. By analyzing the consequences of treating human keratinocytes (HaCaT) with the pentacyclic triterpenoid Betulinic Acid (BA) we were able to propose that cell senescence can develop as a response to parallel damage in the membranes of mitochondria and lysosome...
October 20, 2016: Biochimica et Biophysica Acta
Madhusudanarao Vuda, Ashwin Kamath
Several commonly used medications impair mitochondrial function resulting in adverse effects or toxicities. Drug induced mitochondrial dysfunction may be a consequence of increased production of reactive oxygen species, altered mitochondrial permeability transition, impaired mitochondrial respiration, mitochondrial DNA damage or inhibition of beta-oxidation of fatty acids. The clinical manifestation depends on the specific drug and its effect on mitochondria. Given the ubiquitous presence of mitochondria and its central role in cellular metabolism, drug-mitochondrial interactions may manifest clinically as hepatotoxicity, enteropathy, myelosuppression, lipodystrophy syndrome or neuropsychiatric adverse effects, to name a few...
October 19, 2016: Mitochondrion
Aaron Wilson, Vasily A Yakovlev
Cancer development and progression have been linked to oxidative stress, a condition characterized by unbalanced increase in ROS and RNS production. The main endogenous initiators of the redox imbalance in cancer cells are defective mitochondria, elevated NOX activity, and uncoupled NOS3. Traditionally, most attention has been paid to direct oxidative damage to DNA by certain ROS. However, increase in oxidative DNA lesions does not always lead to malignancy. Hence, additional ROS-dependent, pro-carcinogenic mechanisms must be important...
October 19, 2016: Free Radical Biology & Medicine
Timothy M Brenza, Shivani Ghaisas, Julia E Vela Ramirez, Dilshan Harischandra, Vellareddy Anantharam, Balaraman Kalyanaraman, Anumantha G Kanthasamy, Balaji Narasimhan
A progressive loss of neuronal structure and function is a signature of many neurodegenerative conditions including chronic traumatic encephalopathy, Parkinson's, Huntington's and Alzheimer's diseases. Mitochondrial dysfunction and oxidative and nitrative stress have been implicated as key pathological mechanisms underlying the neurodegenerative processes. However, current therapeutic approaches targeting oxidative damage are ineffective in preventing the progression of neurodegeneration. Mitochondria-targeted antioxidants were recently shown to alleviate oxidative damage...
October 19, 2016: Nanomedicine: Nanotechnology, Biology, and Medicine
Xia Cong, Qian Zhang, Huatao Li, Zhongling Jiang, Rongfeng Cao, Shansong Gao, Wenru Tian
Puerarin, a bioactive isoflavone glucoside extracted from radix Puerariae, has been proven to possess many biological activities. However, the role of puerarin in protecting bovine Sertoli cells (bSCs) under heat stress conditions remains to be clarified. The present study aimed to explore the possible protective mechanism of puerarin for primary cultured bSCs subjected to heat stress. Bovine Sertoli cells were treated with 15 μM of puerarin before they were exposed to 42 °C for 1 hour. The dose of puerarin (15 μM) was determined on the basis of cell viability...
September 21, 2016: Theriogenology
Qian Cai, Prasad Tammineni
Alzheimer's disease (AD) is characterized by brain deposition of amyloid plaques and tau neurofibrillary tangles along with steady cognitive decline. Synaptic damage, an early pathological event, correlates strongly with cognitive deficits and memory loss. Mitochondria are essential organelles for synaptic function. Neurons utilize specialized mechanisms to drive mitochondrial trafficking to synapses in which mitochondria buffer Ca2+ and serve as local energy sources by supplying ATP to sustain neurotransmitter release...
October 20, 2016: Journal of Alzheimer's Disease: JAD
Jewel L Podratz, Han Lee, Patrizia Knorr, Stephanie Koehler, Steven Forsythe, Kelsey Lambrecht, Suzette Arias, Kiley Schmidt, Gabrielle Steinhoff, Georgiy Yudintsev, Amy Yang, Eugenia Trushina, Anthony Windebank
Cisplatin is an effective chemotherapy drug that induces peripheral neuropathy in cancer patients. In rodent dorsal root ganglion neurons, cisplatin binds nuclear and mitochondrial DNA (mtDNA) inducing DNA damage and apoptosis. Platinum-mtDNA adducts inhibit mtDNA replication and transcription leading to mitochondrial degradation. Cisplatin also induces climbing deficiencies associated with neuronal apoptosis in adult Drosophila melanogaster. Here we used Drosophila larvae that express green fluorescent protein in the mitochondria of motor neurons to observe the effects of cisplatin on mitochondrial dynamics and function...
October 17, 2016: Neurobiology of Disease
Zuriñe Antón, Ane Landajuela, Javier H Hervás, L Ruth Montes, Sonia Hernández-Tiedra, Guillermo Velasco, Felix M Goñi, Alicia Alonso
The phospholipid cardiolipin (CL) has been proposed to play a role in selective mitochondrial autophagy, or mitophagy. CL externalization to the outer mitochondrial membrane would act as a signal for the human Atg8 ortholog subfamily, MAP1LC3 (LC3). The latter would mediate both mitochondrial recognition and autophagosome formation, ultimately leading to removal of damaged mitochondria. We have applied quantitative biophysical techniques to the study of CL interaction with various Atg8 human orthologs, namely LC3B, GABARAPL2 and GABARAP...
October 20, 2016: Autophagy
Grazyna Nowak, Diana Takacsova Bakajsova, Judit Megyesi
Previously, we documented that activation of protein kinase C-ε (PKC-ε) mediates mitochondrial dysfunction in cultured renal proximal tubule cells (RPTC). This study tested whether deletion of the PKC-ε decreases dysfunction of renal cortical mitochondria and improves kidney function after renal ischemia. PKC-ε levels in mitochondria of ischemic kidneys increased 24h after ischemia. Complex I- and complex II-coupled state 3 respirations were reduced 44% and 27%, respectively, in wild-type (WT) but unchanged and increased in PKC-ε-deficient (KO) mice after ischemia...
October 19, 2016: American Journal of Physiology. Renal Physiology
Darius Ebrahimi-Fakhari, Afshin Saffari, Lara Wahlster, Alessia Di Nardo, Daria Turner, Tommy L Lewis, Christopher Conrad, Jonathan M Rothberg, Jonathan O Lipton, Stefan Kölker, Georg F Hoffmann, Min-Joon Han, Franck Polleux, Mustafa Sahin
Tuberous sclerosis complex (TSC) is a neurodevelopmental disease caused by TSC1 or TSC2 mutations and subsequent activation of the mTORC1 kinase. Upon mTORC1 activation, anabolic metabolism, which requires mitochondria, is induced, yet at the same time the principal pathway for mitochondrial turnover, autophagy, is compromised. How mTORC1 activation impacts mitochondrial turnover in neurons remains unknown. Here, we demonstrate impaired mitochondrial homeostasis in neuronal in vitro and in vivo models of TSC...
October 18, 2016: Cell Reports
Ahmad Alodaib, Nara Sobreira, Wendy A Gold, Lisa G Riley, Nicole J Van Bergen, Meredith J Wilson, Bruce Bennetts, David R Thorburn, Corinne Boehm, John Christodoulou
Recent advances in next-generation sequencing strategies have led to the discovery of many novel disease genes. We describe here a non-consanguineous family with two affected boys presenting with early onset of severe axonal neuropathy, optic atrophy, intellectual disability, auditory neuropathy and chronic respiratory and gut disturbances. Whole-exome sequencing (WES) was performed on all family members and we identified compound heterozygous variants (c.[760C>A];[1528G>C];p.[(Gln254Lys);(Ala510Pro)] in the polyribonucleotide nucleotidyltransferase 1 (PNPT1) gene in both affected individuals...
October 19, 2016: European Journal of Human Genetics: EJHG
Elena V Galitsyna, Andrey V Zhelankin, Igor A Sobenin, Alexander N Orekhov
In addition to external factors, such as exercise, food and the environment, genetic predisposition makes great contribution to the development of metabolic disorders and cardiovascular disease. This review is aimed to examine the genetic basis of complex metabolic disorders conventionally described as "metabolic syndrome" (MetS), with the special focus on currently known mutations in the nuclear and mitochondrial genomes, which are associated both with the individual components of MetS and combinations thereof, and also on the studies of the relationship of MetS phenotype as a binary trait...
October 18, 2016: Current Pharmaceutical Design
Hani N Sabbah
Introduction Heart failure (HF) has reached epidemic proportions worldwide. Despite the availability of drugs that reduce mortality and afford good symptom relief, HF continues to exact a considerable clinical and economic burden. Current HF therapies elicit benefit by reducing cardiac workload by lowering heart rate and loading conditions, thereby reducing myocardial energy demands. Areas covered Recent recognition that the failing heart is "energy deprived" and its primary energy source, the mitochondria, is dysfunctional, has focused attention on mitochondria as a worthy therapeutic target...
October 19, 2016: Expert Review of Cardiovascular Therapy
Mei-Mei Gu, Jing-Rong Kong, Di-Huang, Ting Peng, Chen-Ying Xie, Kai-Yuan Yang, Yuan Liu, Wei-Na Wang
Prohibitin2 (PHB2), a potential tumor suppressor protein, plays important roles in inhibition of cell cycle progression, transcriptional regulation, apoptosis and the mitochondrial respiratory chain. To explore its potential roles in crustaceans' immune responses we have identified and characterized LvPHB2, a 891 bp gene encoding a 297 amino acids protein in the shrimp Litopenaeus vannamei. Expression analyses showed that LvPHB2 is expressed in all examined tissues, and largely present in cytoplasm, correlating with its known anti-oxidation function in mitochondria...
October 15, 2016: Developmental and Comparative Immunology
Franziska Ertmer, Harriëtte Oldenhof, Saskia Schütze, Karl Rohn, Willem F Wolkers, Harald Sieme
If the physiological balance between production and scavenging of reactive oxygen species (ROS) is shifted towards production of ROS this may result in accumulation of cell damage over time. In this study stallion spermatozoa were incubated with xanthine and xanthine oxidase (X-XO) to artificially generate defined levels of superoxide and hydrogen peroxide resulting in sub-lethal oxidative damage. The effects of X-XO treatment on various sperm characteristics were studied. Special emphasis was placed on sperm osmotic tolerance pre-freeze and its correlation with cryosurvival, given that cryopreservation exposes cells to osmotic stress...
October 19, 2016: Reproduction, Fertility, and Development
Javier Prieto, Marian León, Xavier Ponsoda, Francisco García-García, Roque Bort, Eva Serna, Manuela Barneo-Muñoz, Francesc Palau, Joaquín Dopazo, Carlos López-García, Josema Torres
We have recently shown that mitochondrial fission is induced early in reprogramming in a Drp1-dependent manner; however, the identity of the factors controlling Drp1 recruitment to mitochondria was unexplored. To investigate this, we used a panel of RNAi targeting factors involved in the regulation of mitochondrial dynamics and we observed that MiD51, Gdap1 and, to a lesser extent, Mff were found to play key roles in this process. Cells derived from Gdap1-null mice were used to further explore the role of this factor in cell reprogramming...
October 18, 2016: Cell Cycle
Jia Shi, Jian-Bo Yu, Wei Liu, Dan Wang, Yuan Zhang, Li-Rong Gong, Shu-An Dong, Da-Quan Liu
Acute respiratory distress syndrome (ARDS) is one of the most devastating complications of sepsis lacking of effective therapy. Mitochondrial dynamics undergoing continuous fusion and fission play a crucial role in mitochondrial structure and function. Fis1, as a small protein located on the outer membrane of mitochondria, has been thought to be an important protein mediated mitochondrial fission. During ARDS, alveolar macrophages suffer from increased oxidative stress and apoptosis, and also accompanied by disrupted mitochondrial dynamics...
October 14, 2016: Experimental Cell Research
Xi Ling, Guowei Zhang, Lei Sun, Zhi Wang, Peng Zou, Jianfang Gao, Kaige Peng, Qing Chen, Huan Yang, Niya Zhou, Zhihong Cui, Ziyuan Zhou, Jinyi Liu, Jia Cao, Lin Ao
Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants that have adverse effects on the male reproductive function. Many studies have confirmed that PAHs preferentially accumulate in mitochondria DNA relative to nuclear DNA and disrupt mitochondrial functions. However, it is rare whether exposure to PAHs is associated with mitochondrial damage and dysfunction in sperm. To evaluate the effects of PAHs on sperm mitochondria, we measured mitochondrial membrane potential (MMP), mitochondrial DNA copy number (mtDNAcn) and mtDNA integrity in 666 individuals from the Male Reproductive Health in Chongqing College Students (MARHCS) study...
October 14, 2016: Environmental Pollution
John E Cebak, Indrapal N Singh, Rachel L Hill, Juan Wang, Edward D Hall
Lipid peroxidation is a key contributor to the pathophysiology of traumatic brain injury (TBI). Traditional antioxidant therapies are intended to scavenge the free radicals responsible for either the initiation or the propagation of lipid peroxidation (LP). A more recently explored approach involves scavenging the terminal LP breakdown products that are highly reactive and neurotoxic carbonyl compounds 4-hydroxynonenal (4-HNE) and acrolein to prevent their covalent modification and rendering of cellular proteins non-functional leading to loss of ionic homeostasis, mitochondrial failure, and subsequent neuronal death...
October 18, 2016: Journal of Neurotrauma
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