Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.1.1.27 (lactate dehydrogenase)
29,211 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of Salmonella abortus equi lipopolysaccharides (LPS) on pure cultures of rat Kupffer cells (Kc) were studied. In vitro, LPS is ingested by Kc and located in vacuoles and secondary lysosomes. Culture of Kc in the presence of 1-50 micrograms LPS/ml during 24 h did not affect the viability of the Kc as measured by trypan blue exclusion, neutral red uptake, lactate dehydrogenase leakage and cell survival and spreading. LPS treatment did not influence the ultrastructure of Kc. The exposure of Kc to LPS in vitro did not change the phagocytic activity. Several biochemical processes were stimulated: glucose consumption, MTT-tetrazolium salt reduction, total protein synthesis and secretion of proteins. LPS activated Kc to tumoricidal activity against L929 mouse fibrosarcoma cells. In the light of the above observations, it is concluded that purified LPS is not cytotoxic for pure Kc in culture. On the contrary, LPS stimulates several biochemical and functional processes.
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PMID:Response of cultured rat Kupffer cells to lipopolysaccharide. 324 96

Established renal epithelial cell lines of human, pig, and dog origin (293, LLC-PK1, MDCK) were examined in terms of nephrotoxicity and ability to biotransform cyclosporine A (CsA). All three cell lines exhibited a comparable concentration dependent cytotoxicity to CsA treatment. Alterations in cell function included a decreased transport of lysine, an inhibition of growth, and an activation of lysosomal and mitochondrial activity as indicated by the increased uptake of neutral red (NR) and increased reduction of the tetrazolium dye MTT at 1-6 microM CsA. Increased leakage of lactic dehydrogenase and activities of gamma-glutamyl transpeptidase (GGT) and N-acetyl-beta-D-hexosaminidase were observed at 48 h and 12 microM CsA. A discrimination between CsA and the less nephrotoxic cyclosporine-(CsH) was shown for DNA synthesis and NR uptake. The contribution of extrarenal parameters on kidney cell function was studied by the addition of medium from hepatocytes exposed to CsA to the kidney cell lines. A more potent inhibition of DNA synthesis and enhanced reduction of MTT resulted than by addition of equimolar CsA directly to the kidney cells. These data indicate that hepatocyte constituents present in the medium due to CsA treatment affect kidney cell function; additionally, the presence of CsA metabolites may contribute to the CsA-induced nephrotoxicity. The vascular nephrotoxicity induced by CsA, an increased deposition of platelets in the renal arterioles, was mimicked by cocultures of endothelial cell monolayers and platelets. CsA increased the aggregability and adherence of platelets to the endothelial cell monolayers, whereas CsH had no effect.
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PMID:Cyclosporine A nephrotoxicity studied by the combined application of kidney cell lines, hepatocytes, and endothelial-platelet cocultures. 350 90

The influence of auto-oxidized phospholipids on the reduction of the tetrazolium salt MTT coupled to the NAD+-dependent lactate dehydrogenase reaction was studied. The following results were obtained: (1) peroxidized phosphatidylcholine interfered in the time-course of the lactate dehydrogenase-mediated MTT reduction; (2) there was a time-dependent decrease in the hydroperoxide content of phosphatidylcholine vesicles during the incubation; (3) the diminution of phosphatidylcholine hydroperoxides required the presence of all the components of the system except MTT; (4) hydroperoxide diminution and MTT reduction were mediated by the superoxide radical O2-, since both processes were inhibited by superoxide dismutase; (5) EDTA inhibited the hydroperoxide decrease and abolished the interference of peroxidized phosphatidylcholine with MTT reduction. It was concluded that hydroperoxides compete with MTT for the electrons coming from substrate oxidation. The superoxide radical O2- and traces of some contaminating metal ion are involved in the process. This is a potential complication in the study of the effect of lipids on enzymatic activities assayed by the tetrazolium salt method.
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PMID:Effect of auto-oxidized phospholipids on oxidative enzyme assays based on tetrazolium salt reduction. 641 Nov 23

The activities of lactate dehydrogenase, succinate dehydrogenase and glutamate dehydrogenase, originating from rat hippocampus were determined 3, 10, 20 and 40 days post partum. Hemispheric asymmetry was tested using tetrazolium salt MTT-bromide and the elution technique. It could be revealed that significant differences between enzymatic activities occur between both hemispheres of the hippocampus. The greatest difference observed was 14%. Our dates show that a predominantly left-side dominance takes place in the hippocampus.
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PMID:[The activity of several dehydrogenases in both hemispheres of the hippocampus from rats during some phases of postnatal development (author's transl)]. 728 91

Alteration of calcium homeostasis has been proposed to play a major role in cell necrosis induced by a variety of chemical agents such as acetaminophen (APAP). In this study, a potential protective effect of the dihydropyridine calcium channel blocking agent, nifedipine, was investigated in vitro on acetaminophen-induced hepatocyte damage. Rat hepatocytes were exposed during 20 hours to various concentrations of APAP (0.50 to 4.00 mM). The following metabolic and functional parameters were investigated: -lactate dehydrogenase (LDH) release as an indicator of plasma membrane integrity, -cell viability evaluated by the colorimetric MTT assay, and intracellular calcium concentration as evaluated by two fluorimetric methods: a scanning laser cytometer using indo-1-AM as fluorescent probe and a fluorescence plate reader using fluo-3-AM as calcium indicator. Incubation of hepatocytes with APAP alone in the range 0.50 to 4.00mM resulted in a dose-response relationship with regard to LDH release (243% to 750% of control) and to the loss of cell viability (0 to 67% of control). Moreover these results were correlated with a significant increase in cytosolic calcium content (189 to 406 nM). Nifedipine treatment prior to APAP exposure, partially prevented LDH release, the plasma membrane blebbing, and thereby the loss of viability. In addition, intracellular calcium level progressively returned within the limits of the control values with increasing concentrations of nifedipine. It can be concluded that, in vitro conditions, nifedipine pretreatment exhibits a preventive effect against acetaminophen hepatocyte injury.
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PMID:Protective effect of nifedipine against cytotoxicity and intracellular calcium alterations induced by acetaminophen in rat hepatocyte cultures. 749 6

The cytotoxic effect caused by the hypomethylating agent S-adenosyl-L- homocysteine (SAH) was compared with that of two drugs commonly used to induce DNA hypomethylation, 5-azacytidine and 5-aza-2'-deoxycytidine. Two in vitro cytotoxicity tests, the tetrazolium MTT assay and the intracellular lactate dehydrogenase (LDH) activity test, suggest that SAH induces hypomethylation without causing any cytotoxic effect. We propose the use of SAH as a non-cytotoxic agent which may be more suitable for inducing experimental DNA hypomethylation.
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PMID:S-adenosyl-L-homocysteine: a non-cytotoxic hypomethylating agent. 751 95

1. A human dermal equivalent (HDE) gel was constructed from rat tail tendon collagen (type 1) and human dermal fibroblasts (HFs). Histological studies revealed that the HFs within the HDE gel matrix assumed the shape of differentiated dermal fibroblasts and were metabolically viable as determined by the MTT assay. 2. The HDE system was developed to determine if viable, differentiated HFs have the potential to contribute to tissue damage by releasing the proteolytic enzyme elastase following exposure to sulphur mustard (HD). Elastase was measured, using the substrate suc-ala-ala-val-p-nitroanilide (SAAVNA), because of its association with various human pathological bullous skin diseases. An additional elastase substrate (suc-ala-ala-ala-p-nitroanilide; SAAANA) was also used. A miniaturised assay was employed to measure lactate dehydrogenase (LDH), a cytosolic enzyme released following damage to the cell membrane. 3. Elastase levels (measured with SAAVNA) increased to over 740% of those in control culture medium at 24 h after exposure of the HDE to HD (2 mM) and may therefore be part of the mechanism associated with dermo-epidermal separation and blistering in humans following exposure of skin to HD. LDH was released from the HDE after exposure to HD in a time dependent fashion, suggesting a steady leakage of cytosolic constituents after the initial exposure. 4. The results suggest that differentiated human dermal fibroblasts have the potential to contribute to the development of the vesication response by releasing proteases such as elastase extracellularly after HD exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The generation of a human dermal equivalent to assess the potential contribution of human dermal fibroblasts to the sulphur mustard-induced vesication response. 757 18

The detection of lactate dehydrogenase (LDH) can be used to evaluate efficiently anti-influenza A virus agents. LDH levels in the virus-infected Madin-Darby canine kidney cell cultures were significantly higher than in controls, were in proportion to the degree of virus infection, and corresponded to a decrease in mitochondrial dehydrogenase activity as assayed using a tetrazolium colorimetric assay (MTT method). The EC50 value and cytotoxicity of ribavirin, 3-deazaguanine, pyrazofurin, and carbodine against influenza A virus as measured by the LDH detection method was equivalent to that derived by the MTT method.
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PMID:Use of lactate dehydrogenase to evaluate the anti-viral activity against influenza A virus. 773 38

Velnacrine maleate (Mentane) is an aminoacridine drug developed for the treatment of Alzheimer's disease. Although velnacrine maleate has not been observed to cause prominent cytotoxicity in in vitro hepatocyte cultures, this drug was associated with elevated serum levels of hepatic enzymes in clinical trials. The purpose of the present study was to manipulate cultures of rat hepatocytes in an attempt to elicit a cytotoxic response from this drug and to better understand the in vitro mechanisms of action. Cytotoxicity was evaluated by measuring lactate dehydrogenase (LDH) leakage, neutral red (NR) uptake, and 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide (MTT) reduction. Preliminary studies with fluorescent probes did not indicate a role for calcium influx or the formation of reactive oxygen species in the cytotoxicity of velnacrine maleate. However, depletion of cellular glutathione (GSH) by diamide (DA) pretreatment resulted in a cytotoxic response at concentrations of velnacrine maleate (1 and 10 micrograms/ml) which were approximately 25-fold lower than those in the absence of DA. Similarly, pretreatment with velnacrine maleate enhanced the cytotoxicity of DA. Pre-exposure of cells to a mixture of DA and t-butyl hydroperoxide (t-BHP) at non-toxic concentrations resulted in significant cytotoxicity of the hepatocyte cultures by velnacrine maleate. Results from these studies indicate that oxidative stress and GSH depletion may enhance Alzheimer patients' susceptibility to the hepatotoxic potential of aminoacridine drugs.
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PMID:Effect of glutathione depletion and oxidative stress on the in vitro cytotoxicity of velnacrine maleate. 776 13

Exposure of renal proximal tubular epithelial cells (LLC-PK1) to the nephrotoxicants 2-bromo-6-(glutathion-S-yl)hydroquinone, 2-bromo-3-(glutathion-S-yl)-hydroquinone, and 2-bromo-(diglutathion-S-yl)hydroquinone caused DNA fragmentation and cytotoxicity. Viability measured by lysosomal neutral red accumulation was the most sensitive parameter of cytotoxicity, and preceded toxicity determined by either the mitochondrial MTT assay or by measuring intracellular lactate dehydrogenase activity. DNA fragmentation was detected as early as 15 min after exposure to 2-bromo-6-(glutathion-S-yl)hydroquinone (100 microM), 2-bromo-3-(glutathion-S-yl)hydroquinone (200 microM), and 2-bromo-(diglutathion-S-yl)hydroquinone (400 microM) and prior to other indices of toxicity. The ability of the cells to repair DNA damage was evident by the decrease in the extent of single strand breaks following removal of 2-bromo-3-(glutathion-S-yl)hydroquinone from the incubation medium. Moreover, inhibition of poly(ADP-ribose)polymerase with 3-amino-benzamide (10 mM), following exposure of LLC-PK1 cells to 0.5 mM 2-bromo-6-(glutathion-S-yl)hydroquinone or 2-bromo-(diglutathion-S-yl)hydroquinone, decreased cytotoxicity, indicating that DNA repair processes, activated in response to DNA damage, exacerbate toxicity. Treatment with the endonuclease inhibitor, aurintricarboxylic acid did not decrease cytotoxicity. A decrease in the cytotoxicity caused by 2-bromo-6-(glutathion-S-yl)hydroquinone and 2-bromo-(diglutathion-S-yl)hydroquinone was observed when cells were incubated with catalase or pretreated with deferoxamine (10 mM). The data suggest a mechanism whereby the conjugates generate hydrogen peroxide, and the subsequent iron-catalyzed generation of hydroxyl radicals causes DNA fragmentation and cytotoxicity.
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PMID:Reactive oxygen species and DNA damage in 2-bromo-(glutathion-S-yl) hydroquinone-mediated cytotoxicity. 779 84


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