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1

Ali Mutashar, Sara, Dr Wasan Taha Saadoon, and Prof Dr Abdul Hameed A. M. Al Qaseer. "Evaluation of Serum Levels of Lactate Dehydrogenase Isoenzymes in COVID- 19 Patients." Journal of University of Shanghai for Science and Technology 23, no. 08 (2021): 443–50. http://dx.doi.org/10.51201/jusst/21/08395.

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Background: This study aimed to determine the serum levels of lactate dehydrogenase isoenzymes (LDH1, LDH2, LDH3, LDH4, and LDH5) and their contribution to the total lactate dehydrogenase enzyme elevation observed in COVID-19 patients. Design of study: This study was conducted in collaboration between Al-Nahrain University/College of Medicine/Chemistry and Biochemistry Department and Al- Yarmouk Teaching Hospital, Baghdad, Iraq. The study included 90 patients with confirmed COVID-19 infection: 45 with severe symptoms, and 45 with mild symptoms during the period from February 2021 to June 2021.
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2

Miyada, D. S., A. Fagin, H. Pirkle, J. Ocariz, and N. D. Vaziri. "Lactate dehydrogenase isoenzyme composition of human platelets." Clinical Chemistry 35, no. 12 (1989): 2325–26. http://dx.doi.org/10.1093/clinchem/35.12.2325.

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Abstract The LDH isoenzyme composition of 12 platelet preparations was determined by electrophoresis. The mean (+/- SD) percentages of LDH-1, LDH-2, LDH-3, LDH-4, and LDH-5 were 16.6 +/- 1.7, 30.1 +/- 1.0, 34.2 +/- 1.3, 18.2 +/- 1.3, and 0.9 +/- 1.1, respectively. In comparison with previous data, these data show identical ranking of the prevalence of each isoenzyme but significantly different percentages, particularly of LDH-1 and LDH-4. The release of platelet LDH by freezing and thawing differed little from that by homogenization.
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3

Triyono, Teguh, Umi Solekhah Intansari, and Caesar Haryo Bimoseno. "LACTATE DEHYDROGENASE (LDH) SELAMA PENYIMPANAN." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 19, no. 3 (2016): 174. http://dx.doi.org/10.24293/ijcpml.v19i3.416.

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During storage, erythrocytes suffered from biomechanical alterations called the “storage lesion”, which may caused hemolysis. The hemolysis released LDH into the plasma. The LDH that was released during hemolysis made it an adequate instrument to assess the quality of in vitro blood products. The aims of this study were to analyse the alteration of LDH level at day 1, 3, 7, 14, and 28 in the WB and PRC, to analyse the correlation between LDH level with storage duration, and also to analyse enhancement differences of LDH level between WB and PRC.This research was an observational study with a c
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4

Osis, Gunars, Amie M. Traylor, Laurence M. Black, et al. "Expression of lactate dehydrogenase A and B isoforms in the mouse kidney." American Journal of Physiology-Renal Physiology 320, no. 5 (2021): F706—F718. http://dx.doi.org/10.1152/ajprenal.00628.2020.

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Cellular release of lactate dehydrogenase (LDH) is being used as an injury marker; however, the exact localization of LDH within the nephron remains unclear. We show that LDH isoform A is expressed proximally, whereas isoform B is expressed distally. Both subunit expressions were significantly altered in models of acute kidney injury and chronic kidney disease. Our study provides new insights into basal and postinjury renal lactate metabolism.
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5

Kamalak, Hakan. "The Cell Viability of Dental Materials by The Lactate Dehydrogenase Assay." International Journal of Health Sciences and Research 14, no. 5 (2024): 160–67. http://dx.doi.org/10.52403/ijhsr.20240518.

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Objectives: the objective of this study is to search the cell membrane damage of resin composite materials on cultures of human gingival fibroblasts and neuron cells by the lactate dehydrogenase (LDH) test method. Methods: A range of thirteen resin composites sterilized under UV light for 2 hours were added to the culture medium of human gingival fibroblasts and neuron for 24 h and 72h. The samples were moved to 48- well-plates in a sterile cabin, one by one, in direct contact with the cells. After 24- and 72-hours incubation period, in the incubator at 37 oC with 5% CO2; Cell membrane damage
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6

Vork, Michaël M., Jan F. C. Glatz, Don A. M. Surtel, and Ger J. Van der Vusse. "Release of fatty acid binding protein and lactate dehydrogenase from isolated rat heart during normoxia, low-flow ischemia, and reperfusion." Canadian Journal of Physiology and Pharmacology 71, no. 12 (1993): 952–58. http://dx.doi.org/10.1139/y93-144.

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The present study was performed to monitor the effect of low-flow ischemia and reperfusion on changes in the protein permeability of the cardiomyocyte cell membrane and the endothelial cell layer for two cytoplasmic proteins, i.e., fatty acid binding protein (FABP) and lactate dehydrogenase (LDH), which differ appreciably with respect to physicochemica¡ characteristics. To accomplish this, isolated rat hearts were Langendorff perfused with separate collection of vascular and interstitial effluents. Control hearts were perfused normoxically for 300 min, whereas experimental hearts were subjecte
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7

Qhobosheane, Monde, Xiaojing Liu, Yunrong Gu, Donghai Wu, and Weihong Tan. "Two-Dimensional Imaging Biosensor for the Monitoring of Lactate Released from Brain Slices." Applied Spectroscopy 57, no. 6 (2003): 689–96. http://dx.doi.org/10.1366/000370203322005391.

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Real-time monitoring of lactate release from brain slices has been studied with an optical two-dimensional (2D) imaging biosensor. The 2D biosensor is prepared by direct immobilization of lactate dehydrogenase (LDH) molecules onto a flat silica glass surface through a covalent binding mechanism. The biosensor is able to spatially differentiate lactate concentration variations with conventional optical microscopic spatial resolution. This biosensor has the capability to effectively detect lactate down to a concentration of 100 nM. The 2D biosensor responds uniformly with 2.5% RSD from pixel to
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8

Zaib, Sumera, Aqsa Hayyat, Naba Ali, Asma Gul, Muhammad Naveed, and Imtiaz Khan. "Role of Mitochondrial Membrane Potential and Lactate Dehydrogenase A in Apoptosis." Anti-Cancer Agents in Medicinal Chemistry 22, no. 11 (2022): 2048. http://dx.doi.org/10.2174/1871520621666211126090906.

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: Apoptosis is a programmed cell death that occurs due to the production of several catabolic enzymes. During this process, several morphological and biochemical changes occur in mitochondria, the main organelle in the cell that participates in apoptosis and controls apoptotic pathways. During apoptosis, cytochrome c is released from mitochondria, and different proteins activate caspase cascades that carry out the cell towards the death process. Apoptosis mainly occurs due to p53 protein that allows the abnormal cells to proliferate. Bcl-2 and Bcl-xl are two anti-apoptotic members of the prote
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9

Anundi, I., J. King, D. A. Owen, H. Schneider, J. J. Lemasters, and R. G. Thurman. "Fructose prevents hypoxic cell death in liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 253, no. 3 (1987): G390—G396. http://dx.doi.org/10.1152/ajpgi.1987.253.3.g390.

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Perfusion of livers from fasted rats with nitrogen-saturated buffer caused hepatocellular damage within 30 min. Lactate dehydrogenase (LDH) was released at maximal rates of approximately 300 U . g-1 . h-1 under these conditions, and virtually all cells in periportal and pericentral regions of the liver lobule were stained with trypan blue. Infusion of glucose, xylitol, sorbitol, or mannitol (20 mM) did not appreciably change the time course or extent of damage due to perfusion with nitrogen-saturated perfusate. However, fructose (20 mM) completely prevented damage assessed by LDH release, tryp
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10

ALCAZAR, Oscar, Markus TIEDGE, and Sigurd LENZEN. "Importance of lactate dehydrogenase for the regulation of glycolytic flux and insulin secretion in insulin-producing cells." Biochemical Journal 352, no. 2 (2000): 373–80. http://dx.doi.org/10.1042/bj3520373.

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The role of lactate dehydrogenase (LDH) in the generation of the metabolic signal for insulin secretion was studied after stable overexpression in INS-1 and RINm5F insulin-producing cells. INS-1 cells with a 25-fold overexpression of LDH-A, the highest level achieved, showed a 20–30% decrease in the glucose oxidation rate at glucose concentrations above 5mM when compared with control cells, whereas values were unchanged at lower glucose concentrations. Lactate release increased in parallel with a decrease in the glucose oxidation rate. However, the INS-1 cell glucose-induced insulin secretory
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11

Abdel-Latif, Lubna, Byron K. Murray, Rebecca L. Renberg, et al. "Cell death in bovine parvovirus-infected embryonic bovine tracheal cells is mediated by necrosis rather than apoptosis." Journal of General Virology 87, no. 9 (2006): 2539–48. http://dx.doi.org/10.1099/vir.0.81915-0.

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The helper-independent bovine parvovirus (BPV) was studied to determine its effect on host embryonic bovine tracheal (EBTr) cells: whether the ultimate outcome of infection results in apoptotic cell death or cell death by necrosis. Infected cells were observed for changes marking apoptosis. Observations of alterations in nuclear morphology, membrane changes, apoptotic body formation, membrane phosphatidylserine inversions, caspase activation and cell DNA laddering in infected cells were not indicative of apoptosis. On the other hand, at the end of the virus replication cycle, infected cells re
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12

Klein, Robert, Oskar Nagy, Csilla Tóthová, and Frederika Chovanová. "Clinical and Diagnostic Significance of Lactate Dehydrogenase and Its Isoenzymes in Animals." Veterinary Medicine International 2020 (June 15, 2020): 1–11. http://dx.doi.org/10.1155/2020/5346483.

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Lactate dehydrogenase (LDH) is widely distributed enzyme in cells of various living systems where it is involved in carbohydrate metabolism catalyzing interconversion of lactate and pyruvate with NAD+/NADH coenzyme system. Cells of tissues are direct source of lactate dehydrogenase isoenzymes that are naturally distributed in blood plasma/serum of animals and humans producing characteristic profile. This profile depends on intracellular isoenzyme concentration in all tissues that contribute to the common pool of lactate dehydrogenases in plasma/serum as a consequence of natural cell degradatio
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13

Cui, Ai-Ling, Jian-Zhong Li, Zhi-Bo Feng, et al. "Humanin Rescues Cultured Rat Cortical Neurons from NMDA-Induced Toxicity Not by NMDA Receptor." Scientific World Journal 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/341529.

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Excitatory neurotoxicity has been implicated in many pathological situations and there is no effective treatment available. Humanin is a 24-aa peptide cloned from the brain of patients with Alzheimer’s disease (AD). In the present study, excitatory toxicity was induced by N-methyl-D-aspartate (NMDA) in primarily cultured rat cortical neurons. MTT assessment, lactate dehydrogenase (LDH) release, and calcein staining were employed to evaluate the protective activity of humanin on NMDA induced toxicity. The results suggested that NMDA (100 μmol/L, 2.5 hr) triggered neuronal morphological changes,
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14

Auclair, Joelle, and François Gagné. "Crowding Effects of Polystyrene Nanoparticles on Lactate Dehydrogenase Activity in Hydra Attenuata." Journal of Xenobiotics 10, no. 1 (2020): 2–10. http://dx.doi.org/10.3390/jox10010002.

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Plastics pervade our environment and potentially release important quantities of plastic nanoparticles (NPs) from degradation in the environment. The purpose of this study was to examine the crowding effects of polystyrene NPs on lactate dehydrogenase (LDH) in vitro and following exposure to Hydra attenuata. First, LDH activity was measured in vitro in the presence of filamentous (F-)actin and NPs (50 and 100 nm diameter) to determine changes in viscosity and the fractal kinetics of LDH. The fractal dimension (fD) was also determined using the rescaled range analysis procedure. Secondly, these
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15

Clinkenbeard, Kenneth D., Derek A. Mosier, Andrea L. Timko, and Anthony W. Confer. "Effects of Pasteurella haemolytica leukotoxin on cultured bovine lymphoma cells." American Journal of Veterinary Research 50, no. 2 (1989): 271–75. https://doi.org/10.2460/ajvr.1989.50.02.271.

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SUMMARY Leukotoxin activity from culture supernatants of Pasteurella, haemolytion serotype 1 in logarithmic growth phase caused rapid « 5 min) release of intracellular K+, uptake of extracellular Ca2+, and swelling of cultured bovine lymphoma cells (BL3 cells). Release of 51CrO42- and lactate dehydrogenase (LDH) from BL3 cells began after 15 minutes of incubation with leukotoxin at 37 C and was completed between 60 and 120 minutes of incubation. In addition, leukotoxin exposure of BL3 cells resulted in cell aggregation and adherence to glass surfaces. Scanning electron microscopy indicated tha
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16

Borle, A. B., and R. T. Stanko. "Pyruvate reduces anoxic injury and free radical formation in perfused rat hepatocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 3 (1996): G535—G540. http://dx.doi.org/10.1152/ajpgi.1996.270.3.g535.

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The effects of 5 mM pyruvate on anoxic injury, superoxide (O2-.) and hydrogen peroxide (H2O2) generation, and lactate dehydrogenase (LDH) release during reoxygenation after 2.5 h anoxia were studied in perfused rat hepatocytes. When pyruvate was present during anoxia and reoxygenation, there was little anoxic injury, and the generation of free radicals and LDH release during reoxygenation were reduced 50-60%. When Pyruvate was added during reoxygenation, there was no decrease in O2-. or LDH release, although H2O2 formation was depressed. Free radical formation and anoxic/reperfusion injury wer
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17

Vaglio-Garro, Annette, Andrea Halasz, Ema Nováková, et al. "Interplay between Energy Supply and Glutamate Toxicity in the Primary Cortical Culture." Biomolecules 14, no. 5 (2024): 543. http://dx.doi.org/10.3390/biom14050543.

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Limited substrate availability because of the blood–brain barrier (BBB) has made the brain develop specific molecular mechanisms to survive, using lactate synthesized by astrocytes as a source of energy in neurons. To understand if lactate improves cellular viability and susceptibility to glutamate toxicity, primary cortical cells were incubated in glucose- or lactate-containing media and toxic concentrations of glutamate for 24 h. Cell death was determined by immunostaining and lactate dehydrogenase (LDH) release. Mitochondrial membrane potential and nitric oxide (NO) levels were measured usi
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18

Masini, E., E. Giannella, S. Bianchi, and P. F. Mannaioni. "Histamine and lactate dehydrogenase (LDH) release in ischemic myocardium of the guinea-pig." Agents and Actions 20, no. 3-4 (1987): 281–83. http://dx.doi.org/10.1007/bf02074691.

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19

Vidya, P. V., and K. C. Chitra. "Induction of Cytotoxicity by Selected Nanoparticles in Chinese Hamster Ovary-K1 Cells." International Journal of Applied Sciences and Biotechnology 5, no. 2 (2017): 203–7. http://dx.doi.org/10.3126/ijasbt.v5i2.17619.

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The aim of the present study is to analyze the cytotoxicity of selected nanoparticles on Chinese Hamster Ovary-K1 (CHO-K1) cells using methyl tetrazolium (MTT) assay and lactate dehydrogenase (LDH) release assay. Four different metal oxide nanoparticles namely silicon dioxide (SiO2-NPs, 1 nm), aluminium oxide (Al2O3-NPs, 16.7 nm), titanium dioxide (TiO2-NPs, 11.4 nm) and iron oxide (Fe3O4-NPs, 15.65 nm) were exposed to CHO-K1 cells at 25, 50, 75 and 100 µg/ml concentrations for 24 h maintaining the control group. The percentage of cell viability using methyl tetrazolium (MTT) assay showed sign
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20

Fantini, Elisabeth, Pierre Athias, Martine Courtois, Shorheh Khatami, Alain Grynberg, and Annick Chevalier. "Oxygen and substrate deprivation on isolated rat cardiac myocytes: temporal relationship between electromechanical and biochemical consequences." Canadian Journal of Physiology and Pharmacology 68, no. 8 (1990): 1148–56. http://dx.doi.org/10.1139/y90-172.

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The effects of hypoxia and reoxygenation on action potentials (AP), contractions, and certain biochemical parameters were studied in isolated rat ventricular myocytes in monolayer culture in the presence and absence of glucose. Substrate deprivation alone had no influence on the basal properties. In the presence of glucose, a 4-h hypoxic treatment caused only a moderate decrease in AP amplitude and rate. In substrate-free conditions, hypoxia induced a gradual decline in plateau potential level and in AP duration and rate, followed by rhythm abnormalities and a failure of the electromechanical
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21

Naito, Eiji, Roka Shimada, and Masashi Yuki. "Diagnostic utility of measuring lactate dehydrogenase levels and its isoenzyme activities for the evaluation of malignancy in feline pleural effusion and ascitic fluid." Open Veterinary Journal 12, no. 5 (2022): 735. http://dx.doi.org/10.5455/ovj.2022.v12.i5.19.

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Background: Lactate dehydrogenase (LDH) isoenzymes may be useful in the differential diagnosis of pleural effusion (PE) and ascitic fluid (AF) aetiologies in cats since tissue damage induces their release, changing the pattern of their activity. Aim: The present study aimed to determine the diagnostic utility of measuring lactate dehydrogenase levels and isoenzyme activities in PE or AF in cats with malignancy. Materials and Methods: The results of LDH levels and isoenzyme activities in the serum, PE and AF of 29 cats were compared among malignant group, infectious group, and non-malignant, no
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22

Caraceni, P., D. H. Van Thiel, and A. B. Borle. "Dual effect of deferoxamine on free radical formation and reoxygenation injury in isolated hepatocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 1 (1995): G132—G137. http://dx.doi.org/10.1152/ajpgi.1995.269.1.g132.

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The effects of low concentrations (10 and 100 microM) and high concentrations (1, 10, and 20 mM) of deferoxamine (DFO) on superoxide (O2-.) formation, lipid peroxidation, and cell injury were studied in freshly isolated perfused rat hepatocytes during a 2-h reoxygenation period after 2.5 h of anoxia. O2-. production was measured by lucigenin-enhanced chemiluminescence, lipid peroxidation by malondialdehyde (MDA) formation, and cell injury by lactate dehydrogenase (LDH) release. On reoxygenation and in the absence of DFO, O2-. generation increased 11-fold, MDA increased 3.7-fold, and LDH releas
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23

Zhong, Hong, Mengting Liu, Yaya Ji, et al. "Genipin Reverses HFD-Induced Liver Damage and Inhibits UCP2-Mediated Pyroptosis in Mice." Cellular Physiology and Biochemistry 49, no. 5 (2018): 1885–97. http://dx.doi.org/10.1159/000493651.

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Background/Aims: Liver damage is a typical manifestation of nonalcoholic fatty liver disease (NAFLD). It originates from excessive fat accumulation, leading to hepatocyte death, inflammation, and fibrosis. Nonalcoholic steatohepatitis (NASH) is a type of NAFLD with a prevalence of 49% in morbidly obese patients. Pyroptosis plays an important role in the development of NASH; thus, it is important to elucidate the effect of lipid accumulation on pyroptosis. Genipin (GNP), a natural water-soluble cross-linking agent, has hepatoprotective effects and decreases lipid accumulation in the liver; howe
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24

Caraceni, P., A. Gasbarrini, D. H. Van Thiel, and A. B. Borle. "Oxygen free radical formation by rat hepatocytes during postanoxic reoxygenation: scavenging effect of albumin." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 3 (1994): G451—G458. http://dx.doi.org/10.1152/ajpgi.1994.266.3.g451.

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Free radical formation and reoxygenation injury were studied in rat hepatocytes perfused with Krebs-Henseleit bicarbonate buffer containing 1% or no albumin. After 2, 2.5, or 3 h of anoxia followed by 1 h reoxygenation in the absence of albumin, free radical formation assessed by low-level chemiluminescence and cell injury measured by lactate dehydrogenase (LDH) release and by trypan blue uptake increased proportionately. Chemiluminescence increased 4- to 7-fold, LDH release and trypan blue uptake increased 1.5- to 2-fold, compared with the end of anoxia. With 1% albumin, there was no increase
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25

Mäkelä, Jan-Henrik, and Boris Isomaa. "The Use of Several Leakage Markers which Enable Platelet Membrane Damage and Platelet Activation to be Distinguished." Alternatives to Laboratory Animals 21, no. 2 (1993): 187–90. http://dx.doi.org/10.1177/026119299302100211.

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We have studied the effects of four differently charged detergents and sphingosine on platelet membrane integrity and platelet activation, using the leakage of pre-loaded 43K+, pre-loaded [14C]-serotonin ([14C]-5-HT) and lactate dehydrogenase (LDH) as markers. Sphingosine, at a concentration of 20μM, induced a release of [14C]-5-HT as well as 43K+, without releasing LDH. The [14C]-5-HT743K+ ratio was about 1.5. A similar leakage pattern and the same [14C]-5-HT/43K+ ratio was also induced by thrombin, a potent platelet agonist, indicating that the release induced by sphingosine is due to platel
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26

Dubouchaud, Hervé, Gail E. Butterfield, Eugene E. Wolfel, Bryan C. Bergman, and George A. Brooks. "Endurance training, expression, and physiology of LDH, MCT1, and MCT4 in human skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 278, no. 4 (2000): E571—E579. http://dx.doi.org/10.1152/ajpendo.2000.278.4.e571.

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To evaluate the effects of endurance training on the expression of monocarboxylate transporters (MCT) in human vastus lateralis muscle, we compared the amounts of MCT1 and MCT4 in total muscle preparations (MU) and sarcolemma-enriched (SL) and mitochondria-enriched (MI) fractions before and after training. To determine if changes in muscle lactate release and oxidation were associated with training-induced changes in MCT expression, we correlated band densities in Western blots to lactate kinetics determined in vivo. Nine weeks of leg cycle endurance training [75% peak oxygen consumption (V˙o
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27

Greene, E. L., and M. S. Paller. "Xanthine oxidase produces O2-. in posthypoxic injury of renal epithelial cells." American Journal of Physiology-Renal Physiology 263, no. 2 (1992): F251—F255. http://dx.doi.org/10.1152/ajprenal.1992.263.2.f251.

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The hypothesis that posthypoxic renal injury is mediated by xanthine oxidase-derived oxygen free radical production was tested in an in vitro model of rat proximal tubule epithelial cells in primary culture subjected to 60 min of hypoxia and 30 min of reoxygenation. Hypoxia-reoxygenation-induced injury, measured as lactate dehydrogenase (LDH) release, was 54.0 +/- 7.1%. Inhibition of xanthine oxidase by 10(-4) M allopurinol attenuated injury (LDH release = 35.5 +/- 3.7%; P less than 0.01). Oxypurinol was similarly effective. Alternatively, cells were treated with 50 or 100 microM tungsten to i
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28

Jagetia, Ganesh Chandra, and Shaival Kamalaksha Rao. "Evaluation of Cytotoxic Effects of Dichloromethane Extract of Guduchi (Tinospora cordifolia Miers ex Hook F & THOMS) on Cultured HeLa Cells." Evidence-Based Complementary and Alternative Medicine 3, no. 2 (2006): 267–72. http://dx.doi.org/10.1093/ecam/nel011.

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Extracts ofTinospora cordifolia(TCE) have been shown to possess anti-tumor properties, but the mechanism of the anti-tumor function of TCE is poorly understood. This investigation elucidates the possible mechanism underlying the cytotoxic effects of dichlormethane extracts of TCE, after selecting optimal duration and concentration for treatment. HeLa cells were exposed to various concentrations of TCE, which has resulted in a concentration-dependent decline in the clonogenicity, glutathione-S-transferase (GST) activity and a concentration-dependent increase in lipid peroxidation (TBARS) with a
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29

TURCU, ELENA, CARMEN ARDELEANU, and GRIGORE MIHAESCU. "The role of lactate dehydrogenase of the pleural liquid in the cytopathological diagnosis." Romanian Biotechnological Letters 28, no. 2/2023 (2023): 3893–99. http://dx.doi.org/10.25083/rbl/28.2/3893.3899.

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Elevated serum or pleural fluid lactate dehydrogenase (LDH)enzyme levels can be associated with various conditions, including neoplasia, reticuloendothelial tumors, and leukemia. These conditions can lead to cell damage or death, causing LDH to be released into the bloodstream and pleural fluid. An increase in LDH levels may prompt further investigation into the underlying cause, which could include malignancies or other diseases. Elevated LDH levels in pleural fluid are often associated with certain conditions, and our study seeks to establish a quantitative assessment of LDH in conjunction w
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30

Gissel, Hanne, and Torben Clausen. "Ca2+ uptake and cellular integrity in rat EDL muscle exposed to electrostimulation, electroporation, or A23187." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 1 (2003): R132—R142. http://dx.doi.org/10.1152/ajpregu.00196.2002.

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We tested the hypothesis that increased Ca2+ uptake in rat extensor digitorum longus (EDL) muscle elicits cell membrane damage as assessed from release of the intracellular enzyme lactate dehydrogenase (LDH). This was done by using 1) electrostimulation, 2) electroporation, and 3) the Ca2+ ionophore A23187. Stimulation at 1 Hz for 120–240 min caused an increase in 45Ca uptake that was closely correlated to LDH release. This LDH release increased markedly with temperature. After 120 min of stimulation at 1 Hz, resting 45Ca uptake was increased 5.6-fold compared with unstimulated muscles. This w
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31

Byler, R. M., N. A. Sherman, J. S. Wallner, and L. D. Horwitz. "Hydrogen peroxide cytotoxicity in cultured cardiac myocytes is iron dependent." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 1 (1994): H121—H127. http://dx.doi.org/10.1152/ajpheart.1994.266.1.h121.

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Because of its potential importance in injury during myocardial ischemia and reperfusion, we assessed mechanisms of hydrogen peroxide (H2O2) cytotoxicity in cultured chick embryo cardiac myocytes. Injury was quantitated by release of lactate dehydrogenase (LDH) or 51Cr, both of which correlated with loss of cell viability assessed by trypan blue exclusion. The iron chelator deferoxamine (0.25–2 mM), but not equimolar iron-loaded deferoxamine, markedly reduced LDH and 51Cr release. Injury was also prevented or attenuated by the diffusible reactive oxygen metabolite scavengers dimethylthiourea (
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32

Liu, Wen, Zu Yong Wang, Pei Yin, Lei Ren, and Qi Qing Zhang. "Near-IR Sensitive Au-Au2S Nanoparticles with Biocompatibility for Drug Delivery." Advanced Materials Research 47-50 (June 2008): 1315–18. http://dx.doi.org/10.4028/www.scientific.net/amr.47-50.1315.

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The near-infrared (NIR) sensitive Au-Au2S nanoparticles (NPs) have shown many advantages as potential drug delivery systems. To further investigate biological safety of Au-Au2S NPs, cytotoxicity was estimated by calcein AM/EthD-1 fluorescence staining and the lactate dehydrogenase (LDH) release. The effects of NPs on apoptosis of CHL cells were determined by flow cytometry with Annexin V-FITC/PI double staining. It is evident that the Au-Au2S NPs are non-cytotoxic below IC50 dosage.
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33

Kiser, Zachary Monroe, Jacqueline Monroe Hibbert, and Alexander Quarshie. "Effect of Quercetin on Lipopolysaccharide and Hydroxyurea Induced Lactate Dehydrogenase Release from Immortalize Mouse Aortic Endothelial Cells." Blood 128, no. 22 (2016): 4846. http://dx.doi.org/10.1182/blood.v128.22.4846.4846.

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Abstract Background: A higher than normal basal inflammatory state is characteristic of sickle cell disease (SCD). Hydroxyurea (HU) is the only FDA approved drug for SCD. However, HU is a chemotherapy drug and is therefore naturally cytotoxic, often inducing apoptosis. Chronic inflammation in sickle cell patients is invariably associated with injury to the vascular endothelium. Quercetin is a dietary flavonoid found ubiquitously in plants and foods that have anti-oxidative and anti-inflammatory characteristics. Hypothesis: The dietary flavonoid quercetin will decrease cytotoxic effects of Lipo
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Murphy, E., A. LeFurgey, and M. Lieberman. "Biochemical and structural changes in cultured heart cells induced by metabolic inhibition." American Journal of Physiology-Cell Physiology 253, no. 5 (1987): C700—C706. http://dx.doi.org/10.1152/ajpcell.1987.253.5.c700.

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We examined the relationship between ionic homeostasis, ATP, and irreversible cell injury in cultured embryonic chick heart cells treated with rotenone (10(-4) M) alone or in combination with iodoacetate (IAA) (10(-3) M), in the presence of extracellular calcium (Ca0) (2.7 mM) and its nominal absence. Changes in Na, K, and total cell Ca content did not correlate with parameters indicative of irreversible injury, i.e., ultrastructural damage or lactate dehydrogenase (LDH) release. Because structural defects in the plasma membrane occurred without a significant release of LDH after exposure to r
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35

Mirabet, Maribel, David Garcia-Dorado, Javier Inserte, et al. "Platelets activated by transient coronary occlusion exacerbate ischemia-reperfusion injury in rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 3 (2002): H1134—H1141. http://dx.doi.org/10.1152/ajpheart.00065.2002.

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Platelets (Plt) accumulate in reperfused myocardium but their effect on myocardial necrosis has not been established. We tested the hypothesis that the effect of Plt depends on their activation status. Pig Plt were obtained before 48 min of coronary occlusion (pre-CO-Plt), 10 min after reperfusion (R-Plt), or after a 60-min sham operation (sham-Plt). Plt were infused into isolated rat hearts ( n = 124) and subsequently submitted to 60 min of ischemia and 60 min of reperfusion. P-selectin expression was higher ( P = 0.02) in R-Plt than in pre-CO-Plt or sham-Plt. Lactate dehydrogenase (LDH) rele
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36

Koyama, S., S. I. Rennard, L. Claassen, and R. A. Robbins. "Dibutyryl cAMP, prostaglandin E2, and antioxidants protect cultured bovine bronchial epithelial cells from endotoxin." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 2 (1991): L126—L132. http://dx.doi.org/10.1152/ajplung.1991.261.2.l126.

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Acute bronchitis secondary to bacterial infection in the airway is accompanied by an acute inflammatory response composed predominantly of neutrophils. Mucosal injury with denudation of the airway epithelium to basement membrane frequently occurs. We postulated that endotoxin might explain this cytotoxicity and neutrophil influx. To test this hypothesis, bovine bronchial epithelial cells were cultured, and the culture supernatant fluids were evaluated for neutrophil chemotactic activity (NCA) and lactate dehydrogenase (LDH) after exposure to endotoxin. Escherichia coli endotoxin stimulated the
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37

Bunnachak, D., A. R. Almeida, J. F. Wetzels, et al. "Ca2+ uptake, fatty acid, and LDH release during proximal tubule hypoxia: effects of mepacrine and dibucaine." American Journal of Physiology-Renal Physiology 266, no. 2 (1994): F196—F201. http://dx.doi.org/10.1152/ajprenal.1994.266.2.f196.

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In freshly isolated hypoxic rat proximal tubules, Ca2+ uptake rate increases promptly, within 1 min, and remains significantly elevated throughout a 20-min period of hypoxia. Lactate dehydrogenase (LDH) release, a sign of membrane injury, increases only after 5 min of hypoxia and thereafter rises progressively. The potential effect of increased Ca2+ uptake rate to activate phospholipases, which would then initiate membrane injury, was evaluated by treating hypoxic tubules with three dissimilar phospholipase inhibitors, i.e., mepacrine, dibucaine, or p-bromophenacyl bromide (PBPB). LDH release
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38

Seidenstuecker, Michael, Julia Weber, Sergio H. Latorre, et al. "Alendronate Release from UHMWPE-Based Biomaterials in Relation to Particle Size of the GUR Powder for Manufacturing." Materials 12, no. 11 (2019): 1832. http://dx.doi.org/10.3390/ma12111832.

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Ultra-high molecular weight polyethylene (UHMWPE) is widely used in endoprosthetics and has been the subject of countless studies. This project investigates the dependence of alendronate (AL) release on the molecular weight of the UHMWPE used (GUR1020 and GUR1050). A 0.5 wt% AL was added to the UHMWPE during the production of the moldings. In addition to the 14-day release tests, biocompatibility tests such as live dead assay, cell proliferation assay (WST) and Lactate dehydrogenase test (LDH) with MG-63 cells as well as a tensile test according to DIN EN ISO 527 were carried out. The released
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39

Hiebl, Bernhard, Sinem Peters, Ole Gemeinhardt, Stefan M. Niehues, and Friedrich Jung. "Impact of serum in cell culture media on in vitro lactate dehydrogenase (LDH) release determination." Journal of Cellular Biotechnology 3, no. 1 (2017): 9–13. http://dx.doi.org/10.3233/jcb-179002.

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40

Dickman, K. G., and L. J. Mandel. "Differential effects of respiratory inhibitors on glycolysis in proximal tubules." American Journal of Physiology-Renal Physiology 258, no. 6 (1990): F1608—F1615. http://dx.doi.org/10.1152/ajprenal.1990.258.6.f1608.

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The effects of inhibition of mitochondrial energy production at various points along the respiratory chain on glycolytic lactate production and transport function were examined in a suspension of purified rabbit renal proximal tubules. Paradoxically, partial blockage at site 3 by hypoxia (1% O2) induced lactate production, whereas total site 3 blockage by anoxia (0% O2) failed to stimulate glycolysis. Compared with anoxia, hypoxic tubules exhibited greater preservation of ATP and K+ contents during O2 deprivation and more fully recovered oxidative metabolism and transport function during reoxy
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41

Kragten, Johannes A., Wim Th Hermens, and Marja P. van Dieijen-Visser. "Cardiac Troponin T Release into Plasma after Acute Myocardial Infarction: Only Fractional Recovery Compared with Enzymes." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 33, no. 4 (1996): 314–23. http://dx.doi.org/10.1177/000456329603300406.

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After acute myocardial infarction (AMI) cardiac enzymes and proteins are released into plasma and are used as biochemical markers of cardiac muscle injury. We studied the completeness of the release of troponin T, a cardiac protein that is largely bound to myofibrillar structures and compared it with the release of cytoplasmic cardiac enzymes in 22 patients with AMI, who were treated with thrombolytic therapy. Creatine kinase (CK; EC 2.7.3.2), hydroxybutyrate dehydrogenase (HBDH), lactate dehydrogenase (LDH; EC 1.1.1.27) and troponin T were assayed serially in plasma samples obtained frequentl
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Pawlak, Justyna, Agata Trzcionka, Anna Mertas, Arkadiusz Dziedzic, Tomasz Hildebrandt, and Marta Tanasiewicz. "The Cytotoxicity Assessment of Novel Formulation Developed to Reduce Dentin Hypersensitivity Utilizing Dehydrogenase Assay." Coatings 11, no. 2 (2021): 217. http://dx.doi.org/10.3390/coatings11020217.

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The problem of real treatment of teeth hypersensitivity is still important and unsolved. The main goal of the experiment was to calculate the possible toxic effects on the fibroblasts cells CCL-1™ (NCTC clone 929) caused by original preparation to reduce tooth surfaces’ hypersensitivity, compared to the marketable preparation Seal & Protect (Dentsply). The assessment was made through measuring lactate dehydrogenase (LDH assay). Lactate dehydrogenase releases from the cell’s cytoplasm to the culture medium as a result of cell membrane damage and lysis of the cells. The measurement is based
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43

Buderus, S., B. Siegmund, R. Spahr, A. Krutzfeldt, and H. M. Piper. "Resistance of endothelial cells to anoxia-reoxygenation in isolated guinea pig hearts." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 2 (1989): H488—H493. http://dx.doi.org/10.1152/ajpheart.1989.257.2.h488.

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The release of cytosolic enzymes from myocardial and endothelial cells in the anoxic-reoxygenated guinea pig heart was investigated. Isolated hearts were perfused with Tyrode solution in the Langendorff mode. Sixty-minute anoxic perfusion with or without glucose (5 mM) was followed by 15-min normoxic perfusion with glucose. The losses of purine-nucleoside phosphorylase (PNP) from endothelial cells and of lactate dehydrogenase (LDH) and creatine kinase (CK) from the mass of myocardial cells were determined. After 30-min anoxia, the release of LDH and CK but not of PNP increased. Reoxygenation a
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44

Chiou, S. H., H. J. Lee та G. G. Chang. "Kinetic analysis of duck ε-crystallin, a lens structural protein with lactate dehydrogenase activity". Biochemical Journal 267, № 1 (1990): 51–58. http://dx.doi.org/10.1042/bj2670051.

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Biochemical characterization and kinetic analysis of epsilon-crystallin from the lenses of common ducks were undertaken to elucidate the enzyme mechanism of this unique crystallin with lactate dehydrogenase (LDH) activity. Despite the structural similarities between epsilon-crystallin and chicken heart LDH, differences in charge and kinetic properties were revealed by isoenzyme electrophoresis and kinetic studies. Bi-substrate kinetic analysis examined by initial-velocity and product-inhibition studies suggested a compulsory ordered Bi Bi sequential mechanism with NADH as the leading substrate
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45

Wei, Li, Li Li, Bin Zhang, and Lin Ma. "Propranolol Suppresses Cobalt Chloride-Induced Hypoxic Proliferation in Human Umbilical Vein Endothelial Cells in vitro." Pharmacology 103, no. 1-2 (2018): 61–67. http://dx.doi.org/10.1159/000494762.

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Background/Aims: To investigate the effect of propranolol on cobalt chloride (CoCl2)-induced hypoxic proliferation in human umbilical vein endothelial cells (HUVECs). Methods: CoCl2 was administrated to HUVECs to mimic hypoxic proliferation in infantile hemangioma. The proliferation of HUVECs was detected by Cell Counting Kit-8. Effects of propranolol on apoptosis and expressions of cell cycle-related genes, CDK4 and cyclin D1, were detected by flow cytometry and RT-PCR respectively. The release of vascular endothelial growth factor (VEGF) and lactate dehydrogenase (LDH) was measured by enzyme
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46

Wetzels, J. F., X. Wang, P. E. Gengaro, R. A. Nemenoff, T. J. Burke, and R. W. Schrier. "Glycine protection against hypoxic but not phospholipase A2-induced injury in rat proximal tubules." American Journal of Physiology-Renal Physiology 264, no. 1 (1993): F94—F99. http://dx.doi.org/10.1152/ajprenal.1993.264.1.f94.

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We studied the effects of glycine (2 mM) on hypoxia-induced changes in phospholipids and fatty acids in isolated rat proximal tubules. In this preparation, 25 min of hypoxia caused cell injury, as reflected by the release of lactate dehydrogenase (LDH) (13.1 +/- 0.8 vs. 43.5 +/- 3.2%; P < 0.01). Hypoxia caused increases in fatty acids and in lysophospholipids. Glycine prevented the hypoxia-induced cell injury (LDH 13.1 +/- 0.8 vs. 11 +/- 0.7%; not significant) but did not attenuate the increases in fatty acids or lysophospholipids. In additional experiments, the effects of glycine on phosph
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47

Kizaki, H., H. Shimada, F. Ohsaka, and T. Sakurada. "Adenosine, deoxyadenosine, and deoxyguanosine induce DNA cleavage in mouse thymocytes." Journal of Immunology 141, no. 5 (1988): 1652–57. http://dx.doi.org/10.4049/jimmunol.141.5.1652.

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Abstract When thymocytes were cultured with adenosine, deoxyadenosine, or deoxyguanosine at 1 mM for 24 h, DNA cleavage at internucleosomal sites with multiples of approximately 180 bp was induced, followed by lactate dehydrogenase release into the medium. In the presence of coformycin, an adenosine deaminase inhibitor, or formycin B, a purine nucleoside phosphorylase inhibitor, DNA cleavage was induced by these nucleosides at concentrations of less than 50 microM. Other purine and pyrimidine ribo- and deoxyribonucleosides did not induce DNA cleavage or LDH release. Because thymocyte nuclei co
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48

Vijayakumar, S., and S. Ganesan. "In VitroCytotoxicity Assay on Gold Nanoparticles with Different Stabilizing Agents." Journal of Nanomaterials 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/734398.

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Noble gold nanoparticles (AuNps) are generally nontoxic due to their inert nature. The gold nanoparticles are easily tagged with various proteins and biomolecules rich in aminoacid leading to important biomedical applications including targeted drug delivery, cellular imaging, and biosensing. In this study, three cytotoxicity detection assays 3-(4,5-dimethylthiozol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), neutral red cell, and lactate dehydrogenase (LDH) on gold nanoparticles stabilized with citrate, starch, and gum arabic are used. The assays used are based on different mode of detection
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Smedowski, Adrian, Marita Pietrucha-Dutczak, Ruchi Maniar, Michael Ajeleti, Iwona Matuszek, and Joanna Lewin-Kowalik. "FluoroGold-Labeled Organotypic Retinal Explant Culture for Neurotoxicity Screening Studies." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/2487473.

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Preclinical toxicity screening of the new retinal compounds is an absolute requirement in the pathway of further drug development. Since retinal neuron cultivation and in vivo studies are relatively expensive and time consuming, we aimed to create a fast and reproducible ex vivo system for retinal toxicity screening. For this purpose, we used rat retinal explant culture that was retrogradely labeled with the FluoroGold before the isolation. Explants were exposed to a toxic concentration of gentamicin and ciliary neurotrophic factor (CNTF), a known neuroprotective agent. The measured outcomes s
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Yun, Bogeon, HeeJung Lee, Moumita Ghosh, et al. "Serine Hydrolase Inhibitors Block Necrotic Cell Death by Preventing Calcium Overload of the Mitochondria and Permeability Transition Pore Formation." Journal of Biological Chemistry 289, no. 3 (2013): 1491–504. http://dx.doi.org/10.1074/jbc.m113.497651.

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Perturbation of calcium signaling that occurs during cell injury and disease, promotes cell death. In mouse lung fibroblasts A23187 triggered mitochondrial permeability transition pore (MPTP) formation, lactate dehydrogenase (LDH) release, and necrotic cell death that were blocked by cyclosporin A (CsA) and EGTA. LDH release temporally correlated with arachidonic acid release but did not involve cytosolic phospholipase A2α (cPLA2α) or calcium-independent PLA2. Surprisingly, release of arachidonic acid and LDH from cPLA2α-deficient fibroblasts was inhibited by the cPLA2α inhibitor pyrrophenone,
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