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:1.3.5.1 (succinate dehydrogenase)
8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gemfibrozil is a lipid-regulating agent widely used in patients at risk of coronary disease. Pharmaceutical products, such as gemfibrozil, are found in municipal effluents and represent a major source of contamination. To date, there is little available information about the adverse effects of gemfibrozil in aquatic organisms. For this reason, the toxic effects were investigated using model systems from four trophic levels. The most sensitive system was the immobilization of Daphnia magna, with a non-observed adverse effect level of 30 microM and a mean effective concentration of 120 microM after 72 h, followed by the inhibition of bioluminescence of Vibrio fischeri, the hepatoma fish cell line PLHC-1 line and the inhibition of the growth of Chlorella vulgaris. Although protein content, neutral red uptake, methylthiazol metabolization and lysosomal function were reduced in PLHC-1 cells, stimulations were observed for lysosomal function, metallothionein levels and succinate dehydrogenase, glucose-6-phosphate dehydrogenase and acetylcholinesterase activities. No changes were observed in ethoxyresorufin-O-deethylase activity. The main morphological alterations were hydropic degeneration and loss of cells. Modulation studies on gemfibrozil toxicity were also carried out. General antioxidants and calcium chelators did not modify the toxicity of gemfibrozil, whereas a Fe(III) chelator, a membrane permeable sulphydryl-protecting compound and glutathione level modifying agents did change the toxicity. One of the possible mechanisms of gemfibrozil toxicity seems to be the binding to sulphydryl groups, including those of glutathione. According to the result, gemfibrozil should be classified as harmful to aquatic organisms. However, comparing the concentrations in water and the toxicity quantified in the assayed systems, gemfibrozil is not expected to represent acute risk to the aquatic biota.
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PMID:Toxicological effects of the lipid regulator gemfibrozil in four aquatic systems. 1716 44

The enzyme histochemical reactions for acetylcholinesterase, lactic dehydrogenase, succinic dehydrogenase and nitroxide synthase are currently the gold standards for the diagnosis of gastrointestinal motility disorders. The acetylcholinesterase staining reaction shows the cholinergic nerve fibre network of the muscularis mucosae and muscularis propria, and correlates with their acetylcholinesterase activity. Lactic dehydrogenase, succinic dehydrogenase and nitroxide synthase selectively demonstrate the nerve cells of the myenteric and submucous plexus. These enzyme histochemical techniques require fresh, native tissue. Consequently, the transport of biopsies from gastroenterology or surgery to pathology must be well organized and feasible without time loss. Alternatively, biopsies may be mailed on dry ice to more distant pathology institutes. The enzyme histochemical laboratory technique has been optimized and refined over four decades. The optimized reactions are highly reliable and reproducible. In particular, a standardized methodology is a prerequisite for the interinstitutional comparability of results. This laboratory manual provides a detailed methodological description of the most important enzyme histochemical reactions for the diagnosis of gastrointestinal motility disorders.
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PMID:[Enzyme histochemical diagnosis of gastrointestinal motility disorders. A laboratory guide]. 1730 9

Propyl gallate is an antioxidant widely used in foods, cosmetics and pharmaceuticals. The occurrence and fate of additives in the aquatic environment is an emerging issue in environmental chemistry. To date, there is little available information about the adverse effects of propyl gallate on aquatic organisms. Therefore, the toxic effects were investigated, using five model systems from four trophic levels. The most sensitive system was the hepatoma fish cell line PLHC-1 according to total protein content, with an EC(50) of 10 microM and a NOAEL of 1 microM at 72 h, followed by the immobilization of Daphnia magna, the inhibition of bioluminescence of Vibrio fischeri, the salmonid fish cell line RTG-2 and the inhibition of the growth of Chlorella vulgaris. Although protein content, neutral red uptake, methylthiazol metabolization and acetylcholinesterase activity were reduced in PLHC-1 cells, stimulations were observed for lysosomal function, succinate dehydrogenase, glucose-6-phosphate dehydrogenase and ethoxyresorufin-O-deethylase activities. No changes were observed in metallothionein levels. The main morphological observations were the loss of cells and the induction of cell death mainly by necrosis but also by apoptosis. The protective and toxic effects of propyl gallate were evaluated. General antioxidants and calcium chelators did not modify the toxicity of propyl gallate, but an iron-dependent lipid peroxidation inhibitor gave 22% protection. The results also suggest that propyl gallate cytotoxicity is dependent on glutathione levels, which were modulated by malic acid diethyl ester and 2-oxothiazolidine-4-carboxylic acid. According to the results, propyl gallate should be classified as toxic to aquatic organisms.
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PMID:Ecotoxicological effects of the antioxidant additive propyl gallate in five aquatic systems. 1738 89

Indium nitrate is mainly used as a semiconductor in batteries, for plating and other chemical and medical applications. There is a lack of available information about the adverse effects of indium compounds on aquatic organisms. Therefore, the toxic effects on systems from four trophic levels of the aquatic ecosystem were investigated. Firstly, the bacterium Vibrio fischeri, the alga Chlorella vulgaris and the cladoceran Daphnia magna were used in the toxicological evaluation of indium nitrate. The most sensitive model was V. fischeri, with a NOAEL of 0.02 and an EC(50) of 0.04 mM at 15 min. Although indium nitrate should be classified as harmful to aquatic organisms, it is not expected to represent acute risk to the aquatic biota. Secondly, PLHC-1 fish cell line was employed to investigate the effects and mechanisms of toxicity. Although protein content, neutral red uptake, methylthiazol metabolization, lysosomal function and acetylcholinesterase activity were reduced in cells, stimulations were observed for metallothionein levels and succinate dehydrogenase and glucose-6-phosphate dehydrogenase activities. No changes were observed in ethoxyresorufin-O-deethylase activity. To clarify the main events in PLHC-1 cell death induced by indium nitrate, nine modulators were applied. They were related to oxidative stress (alpha-tocopherol succinate, mannitol and sodium benzoate), disruption of calcium homeostasis (BAPTA-AM and EGTA), thiol protection (1,4-dithiotreitol), iron chelation (deferoxiamine) or regulation of glutathione levels (2-oxothiazolidine-4-carboxylic acid and malic acid diethyl ester). The main morphological alterations were hydropic degeneration and loss of cells. At least, in partly, toxicity seems to be mediated by oxidative stress, and particularly by NADPH-dependent lipid peroxidation.
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PMID:Toxicological assessment of indium nitrate on aquatic organisms and investigation of the effects on the PLHC-1 fish cell line. 1780 41

Repeated low-dose exposure to carbofuran exerts its neurotoxic effects by non-cholinergic mechanisms. Emerging evidence indicates that oxidative stress plays an important role in carbofuran neurotoxicity after sub-chronic exposure. The purpose of the present study is to evaluate the role of mitochondrial oxidative stress and dysfunction as a primary event responsible for neurotoxic effects observed after sub-chronic carbofuran exposure. Carbofuran was administered to rats at a dose of 1 mg/kg orally for a period of 28 days. There was a significant inhibition in the activity of acetylcholinesterase (66.6%) in brain samples after 28 days of carbofuran exposure. Mitochondrial respiratory chain functions were assessed in terms of MTT (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) reduction and activity of succinate dehydrogenase in isolated mitochondria. It was observed that carbofuran exposure significantly inhibited MTT reduction (31%) and succinate dehydrogenase activity (57%). This was accompanied by decrease in low-molecular weight thiols (66.6%) and total thiols (37.4%) and an increase in lipid peroxidation (43.7%) in the mitochondria isolated from carbofuran-exposed rat brain. The changes in mitochondrial oxidative stress and functions were associated with impaired cognitive and motor functions in the animals exposed to carbofuran as compared to the control animals. Based on these results, it is clear that carbofuran exerts its neurotoxicity by impairing mitochondrial functions leading to oxidative stress and neurobehavioral deficits.
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PMID:Mitochondrial oxidative stress and dysfunction in rat brain induced by carbofuran exposure. 1834 May 26

To compare the effects of cobalt at different cellular levels, cultured mouse neuroblastoma cells (Neuro-2a) were exposed for 24 hr to cobalt(II) chloride. The following toxicity indicators were assessed: cell proliferation by quantification of total protein content; cytoplasmic membrane integrity to cytosolic lactate dehydrogenase leakage; lysosomal hexosaminidase release; lactate dehydrogenase activity (LDH); mitochondrial succinate dehydrogenase activity (SDH); relative neutral red uptake by lysosomes (RNRU); lysosomal hexosaminidase activity (HEX), and acetylcholinesterase activity (AChE). The effect of cobalt on the various indicators differed. Cobalt was not very toxic to neuroblastoma cell proliferation (EC(50) = 200 mum). Cytoplasmic membrane permeability was not specifically increased, and LDH leakage occurred only at high concentrations, prior to the stimulation of HEX activity, an enzyme involved in sphingolipid degradation. In contrast, cobalt was lysosomotropic, with HEX release. The effects on lysosomal function were also studied with the RNRU, showing stimulation at low concentrations and inhibition at high concentrations. Neural AChE was decreased after an initial stimulation at low concentrations. LDH and SDH intracellular activities were both stimulated from low concentrations, mitochondrial SDH activity being the most sensitive marker studied. Metabolic stimulatory effects induced by cobalt were, therefore, more marked than changes in cytoplasmic and lysosomal membrane permeability.
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PMID:Effects of cobalt on mouse neuroblastoma cells cultured in vitro. 2065 Jan 2

In order to compare the effects of cocaine at morphological, basal cytotoxicity, biochemical and molecular levels, cultured mouse neuroblastoma cells (Neuro-2a) were exposed to a range of concentrations of cocaine hydrochloride. Neuroblastoma cell proliferation, evaluated by quantification of total protein content, was very sensitive to cocaine, being increasingly inhibited from 12 to 72 hr of exposure (EC(50) = 3.1 mm at 24 hr). Cytoplasmic membrane permeability to lactate dehydrogenase was not particularly increased and lysosomal function was stimulated from 0.05 to 1.5 mm, and inhibited from 2.5 mm. A shift to anaerobiosis was detected as intracellular lactate dehydrogenase (LDH) activity was increased and mitochondrial succinate dehydrogenase (SDH) activity decreased. Hexosaminidase (HEX), a lysosomal enzyme involved in sphingolipid degradation, was stimulated only at 1 mm and neural acetylcholinesterase (AChE) activity was stimulated from 2.5 mm. Morphological examination of exposed cultures revealed that most cells became bipolar and multipolar neurons by extension of neurites, but also suffered cytoplasmic vacuolization, hydropic degeneration and nuclear pyknosis. Although cells developing apoptosis were observed, no DNA oligonucleosomal fragmentation was detected by agarose gel electrophoresis of DNA from cells exposed to cocaine. In conclusion, in addition to predominance of anaerobiosis, little disruption of membranes and severe morphologic injury, biochemical and morphological differentiation-like effects were the most prominent alterations produced by cocaine on mouse neuroblastoma cells.
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PMID:Morphological, biochemical and molecular effects of cocaine on mouse neuroblastoma cells culture in vitro. 2065 45

To compare the effects of thallium at different cellular levels, cultured mouse neuroblastoma cells (Neuro-2A) were exposed for 24 hr to thallium(I) acetate. The following toxic indicators were assessed in the in vitro test system: cell proliferation by quantification of total protein content of the culture; cytoplasmic membrane integrity to cytosolic lactate dehydrogenase (LDH) leakage; lysosomal hexosaminidase release; lactate dehydrogenase activity; mitochondrial succinate dehydrogenase activity; relative neutral red uptake by lysosomes; lysosomal hexosaminidase sphingolipid degradation activity; acetylcholinesterase activity. The effects of thallium on the various indicators differed. Neural acetylcholinesterase activity was extremely sensitive to T1 inhibition. In contrast, hexosaminidase, an enzyme involved in glycosphingolipid degradation, was stimulated prior to cytoplasmic membrane disruption detected as LDH leakage. Relative neutral red uptake was slightly more sensitive than cell growth inhibition and the reduction in hexosaminidase release suggests an interaction with lysosomes. The low degree of sensitivity of cell proliferation, as judged by the protein content of the cultures, may reflect inhibition of protein degradation. LDH glycolytic activity was severely inhibited, but succinate dehydrogenase activity in the citric acid cycle was increased, probably owing to the mitochondrial accumulation of thallium.
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PMID:In vitro effects of thallium on mouse neuroblastoma cells. 2069 72

An in vitro model system has been developed to establish dose-response relationships of mercuric chloride (HgCl(2)) and methylmercuric chloride (HgCH(3)Cl). Mouse neuroblastoma cell cultures (Neuro-2a) were exposed for 24 hr and cytotoxic effects evaluated with eight different endpoints. Toxic indicators assessed in the in vitro test system were as follows: cell proliferation by quantification of total protein content; cytoplasmic membrane integrity by cytosolic lactate dehydrogenase leakage; lysosomal membrane stability by hexosaminidase release; lactate dehydrogenase activity; mitochondrial succinate dehydrogenase activity; relative neutral red uptake by lysosomes; lysosomal hexosaminidase sphingolipid degradation activity; acetylcholinesterase activity. The toxicity of the two chemical species of mercury on neuroblastoma cells differed. HgCl(2) inhibited LDH activity specifically and very potently. Gross disruption of cytoplasmic membrane was accompanied by stimulation of hexosaminidase. HgCH(3)Cl was 50 times more toxic than HgCl(2) to cell proliferation and also caused important alterations in both membrane stability and metabolic activities over a narrow range of doses. The data suggest that HgCl(2) acts mainly on cell membranes and LDH, whereas, although HgCH(3)Cl is more cytotoxic, it does not affect any of the above-mentioned endpoints as specifically.
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PMID:In vitro effects of mercuric chloride and methylmercury chloride on neuroblastoma cells. 2073 14

Mitochondrial alterations are believed to play a critical role in the pathophysiology of neurodegenerative diseases and in some well-described myopathies. In the present study, we evaluated muscle changes in vivo after blocking the mitochondrial complex II of the respiratory chain by using 3-nitropropionic acid (3-NP). This neurotoxin has been used as a pharmacological tool in animal models to address some of the metabolic modifications that might underlie central neurodegeneration; however, changes in peripheral musculature have not been documented. We believe that skeletal muscles must be affected because their integrity highly depends on oxidative metabolism. Therefore, histochemical, ultrastructural, and biochemical changes were studied in the muscles of mice treated with low doses of 3-NP (15 mg/kg, i.p., for 5 days). 3-NP-treated mice displayed changes in alkaline phosphatase (APase), succinic dehydrogenase (SDH), and cytochrome c oxidase (COX) levels in the gracilis and gastrocnemius muscles. These changes were statistically significant for APase and SDH in both muscles and for COX only in the gastrocnemius. No significant alterations in acetylcholinesterase (AChE) expression were observed in either muscle. Analysis of the muscle ultrastructure revealed mitochondrial atrophy as well as sarcomere and nuclei disorganization. At the biochemical level, nitric oxide (NO) and lipid peroxidation (LPO) changed in the muscles of 3-NP-treated mice, suggesting metabolic alterations due to oxidative stress. Early damage in the striatal tissue and behavioral modifications are also documented.
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PMID:Low doses of 3-nitropropionic acid in vivo induce damage in mouse skeletal muscle. 2073 97


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