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:1.8.1.4 (diaphorase)
2,754 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human platelets exposed in vitro to increasing amounts of BCNU rapidly develop a progressive, relatively selective, and almost complete deficiency of GSSG-R activity. Several other enzymes are not inhibited when intact platelets are exposed to the nitrosourea; lipoamide dehydrogenase was investigated because of the remarkable similarity of the structure of its active site with that of GSSG-R. BCNU inhibits lipoamide dehydrogenase and GSSG-R only when they are in the reduced state; in the intact platelet, lipoamide dehydrogenase (unlike GSSG-R) is oxidized and is therefore unaffected. This is the first documentation of lipoamide dehydrogenase activity in platelets. After BCNU exposure, there is a reduced release of 14C-serotonin in response to collagen; the cells become incapable of aggregating in response to even large doses of epinephrine, ADP, collagen, or arachidonic acid, with loss of both primary and secondary waves of aggregation. At higher doses of BCNU, there is also a diminished PF-3 activity of intact platelets; sonication of drug-treated platelets normalizes coagulant activity. The drug-induced functional abnormalities occur despite preservation of the number of platelets, their electron microscopic appearance, and their capacity to take up 14C-serotonin. BCNU induced GSSG-R deficiency precedes the development of the earliest evidence of platelet dysfunction, and almost all of the enzyme's activity must be abolished before any functional abnormality becomes detectable. A small fraction of GSSG-R activity is essential for platelet function, and BCNU provides a powerful new tool to investigate the role of the enzymatic reduction of glutathione in platelet physiology and pathology.
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PMID:Glutathione reductase deficiency and platelet dysfunction induced by 1,3-bis(2-chloroethyl)-1-nitrosourea. 668 96

Tendon tissue of eleven athletes suffering from insertion tendopathy and of two controls was examined. Part of the tissue was prepared for routine light microscopy, a part for enzyme histochemical staining of Nicotinamide-adenine-dinudeotide-diaphorase (NADP-diaphorase), lactate dehydrogenase (LDH), beta-glucuronidase and alkaline phosphatase. Small pieces of tissue were also prepared for electron microscopic examination. The removed tissue was edematous and mushy. The normally densely packed parallel or interwoven collagen bundles were loosened by edema, focal necrosis or hemorrhage. Infiltration of fatty tissue and granulation tissue was also present. The amount of acid mucopolysaccharides was markedly increased. The histochemical studies showed strong enzyme activity of NADP-diaphorase and LDH in normal tendon tissue as well as around areas of degeneration and in granulation tissue. beta-Glucuronidase and alkaline phosphatase was present, but in general with lesser activity than the above enzymes. The electron microscopic examination revealed marked degeneration of the fiber systems, focal necrosis, deposit of amorphous masses and mucopolysaccharides and focal mineralisation. The reparative zones showed proliferating capillaries, often with a collapsed lumen and prominent endothelial cells and basement membranes.
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PMID:Insertion tendopathy in athletes. A light microscopic, histochemical and electron microscopic examination. 712 23

Congenital esophageal stenosis (CES) is a rare disorder with narrowed esophageal lumen that presents as dysphagia from childhood and that is often associated with tracheobronchial remnants or webs. The pathogenesis of CES is unknown. The aim of this study was to examine the histological and immunohistochemical features of CES. Esophagi from 2 young adults with CES and 3 controls with no motility disorders underwent routine H&E staining, trichrome staining for collagen, and detailed immunocytochemical studies for general neuronal markers (protein gene product 9.5, neuron-specific enolase, and S-100) and neurotransmitters (vasoactive intestinal polypeptide, substance P, and galanin) and nitric oxide synthase by beta-nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase and a specific NO synthase antibody. Quantitative experiments compared the numbers of myenteric neurons and amounts of fibers at the circular muscle. CES esophagi showed infiltration of neutrophils in the myenteric plane, without any increase in collagen. NADPH-diaphorase histochemistry showed a significant reduction of myenteric nitrinergic neurons (7 +/- 3.4 vs. 2.7 +/- 1.8 neurons per high-power field) and fibers at the circular muscle. Other peptidergic neurons studied were not significantly reduced in CES. The specific total lack of NO inhibitory innervation may be an important mechanism in the pathogenesis of stenosis and aperistalsis of the esophagus in this disorder.
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PMID:Peptidergic and nitrinergic denervation in congenital esophageal stenosis. 754 Oct

The neurons of whole cardiac atria were stained using a NADH-diaphorase technique in young adult (3 months old) (GI) and aging rats (20 months old) (GII). Light microscopy revealed differences in the appearance of the neurons in the two groups. In GI, most ganglia contained 50-100 neurons while in GII, most ganglia usually contained 20 neurons. The mean total number of neurons in the atria of GII was 245+/-31, i.e. only 23% of the mean value in GI (1086+/-203). The mean size of the ganglionic neurons (area of maximum cell profile) was 702 microm2 in GI and 1065 microm2 in GII. Histological sections of the ganglia revealed that a capsule of collagen fibers sheaths each ganglion in both groups. In GII, the density of collagen fibers increases in the capsule and in the septa within the ganglia; yellow or red, type I collagen fibers predominate in this group. No elastic fibers were present in the cardiac ganglia of either group. It is suggested that in aging rats, structural changes and reorganization of the remnant neurons accompany neuron reduction.
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PMID:Fall in the number of intracardiac neurons in aging rats. 1057 31

We developed a rat model of traumatic arteriogenic erectile dysfunction (ED) for the study of vasculogenic ED. Bilateral ligation of the internal iliac artery was performed on 30 three-month old male Sprague-Dawley rats as an experimental group. The control group consisted of 12 rats which underwent dissection of the internal iliac artery without ligation. Before their euthanization at 3 days, 7 days, and 1 month (10 rats in the experimental group and four rats in the control group at each time point), erectile function was assessed by electrostimulation of the cavernous nerves. Penile tissues were collected for nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase staining, trichrome staining, electron microscopy and RT-PCR for transforming growth factor beta (TGF-beta1), insulin like growth factor-I (IGF-I) and fibroblast growth factors (FGF) mRNA expression. Electrostimulation of the cavernous nerves revealed a highly significant declining of the intracavernous pressure after 3 and 7 days. No significant recovery of erectile function was noted at 1 month. Histology showed degeneration of the dorsal nerve fibers in all experimental rats. There was little decrease in the bulk of intracavernous smooth muscle in the experimental rats euthanazed 7 and 30 days. NADPH diaphorase staining revealed a significant decrease in nitric oxide synthase (NOS) containing nerve fibers in the dorsal and intracavernosal nerves in all rats in the experimental group. Electron microscopy showed a variety of changes such as collapse of sinusoids, increased cell debris, fibroblast and myofibroblast loss, intracellular deposition of fat and collagen and fatty degeneration. RT-PCR revealed up-regulation of TGF-beta1 after 3 days but not after 7 days or 1 month. There is no significant difference in IGF-I or FGF expression between the experimental and control group. Bilateral ligation of internal iliac arteries produces a reliable animal model for traumatic arteriogenic ED. Further studies are needed to investigate the molecular mechanism of ED in this model.
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PMID:Traumatic arteriogenic erectile dysfunction: a rat model. 1152 15

Comparable pathological changes in the mitral valve have been described in dogs, pigs and human patients with myxomatous mitral valve disease (MMVD), i.e., primary mitral valve prolapse. The progressive myxomatous changes are probably a response to repeated impact on the leaflets, and endothelial stress or damage probably plays a central role in the pathogenesis. Little, however, is known about the vasoactive substances that mediate the subendothelial changes. The aim of this study was to investigate the expression of nitric oxide synthase (NOS) in canine mitral valve leaflets and to relate the findings to MMVD changes. The mitral valve was taken post mortem from 12 dogs (six males and six females) and a whole valve NADPH (the reduced form of nicotinamide-adenine dinucleotide phosphate) diaphorase (NADPH-d) reaction was performed. Macroscopical (semiquantitative) and microscopical (computer image analysis) evaluations of the staining due to NADPH-d activity were performed at four specific areas of the valve and related to microscopical signs of MMVD and gross signs of thickening or prolapse, or both. Macroscopically, the NADPH-d colour grade was correlated with the degree of MMVD (P=0.01). In addition, endothelial NADPH-d staining intensity was correlated with macroscopical signs of disease (P=0.004) as well as with collagen degeneration (P=0.008) and deposition of mucopolysaccharides (P=0.02). Age, gender and specific area of the valve did not seem to influence the NADPH-d activity. In conclusion, increased NADPH-d activity, suggesting increased NOS expression, was found in areas of the mitral valve with myxomatous changes. This indicates that nitric oxide (NO) may play a role in the pathogenesis of MMVD in dogs.
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PMID:Increased NADPH-diaphorase activity in canine myxomatous mitral valve leaflets. 1292 17

We investigated weight gain, the size of the small intestine and numbers and sizes of enteric neurons in rats whose mothers had been deprived of protein during pregnancy and who themselves were deprived postpartum. Postnatally, protein deprivation was for 42 days, or for 21 days with refeeding for a further 21 days. Control animals received normal nourishment. Neurons were located by nicotinamide adenine dinucleotide (NADH) diaphorase staining, by acetylcholinesterase (AChE) activity and immunoreactivity for choline acetyltransferase (ChAT). The collagen and elastic fibers in the myenteric ganglia were evaluated histologically. The myenteric ganglia were regular and uniform in the nourished and refed groups. In the undernourished group, the myenteric ganglia were irregularly arranged and the cytoplasm of most of the neurons showed less intense staining for NADH diaphorase, AChE and ChAT. AChE activity and ChAT immunoreactivity showed that most ganglionic neurons were stained in nourished and refed groups, but the neurons of undernourished rats were unstained or moderately stained. The distribution of the connective tissue of the ganglionic capsule was similar in the three groups. There was a decrease in weight of undernourished rats, which was restored in refed rats. The size of the small intestine of the undernourished group was smaller than in the normally fed group, by about 45%, but it was similar in nourished and refed rats. After 42 days of protein deprivation the numbers of neurons that were revealed by NADH diaphorase were fewer than in well nourished rats, but numbers were not different between nourished and refed rats. These observations indicate that protein deprivation alters histological features and acetylcholinesterase activity of neurons and also reduces body weight but these were restored by refeeding.
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PMID:Effects of pre- and postnatal protein deprivation and postnatal refeeding on myenteric neurons of the rat small intestine: a quantitative morphological study. 1671 68

This study aimed to evaluate the effects of regular physical activity on the morphology of the myenteric plexus of the duodenum in rats during the ageing process. To this end, 45 Wistar rats were divided into three groups: C (sedentary - 6 months old), S (sedentary - 12 months old) and T (trained - 12 months old). The animals of group S were given with a physical activity programme consisting of a 10-min-treadmill workout once a week. The animals of group T were submitted to the physical activity programme five times a week. Their duodenums were collected and submitted to the techniques of nicotinamide adenine dinucleotide (NADH)-diaphorase enzyme histochemistry for whole-mount preparations and transmission electron microscopy. No differences in the constitution of the myenteric plexuses were found when the sedentary and trained groups were compared with the control group. The ultrastructural features were similar for the three groups. However, it was verified that the physical activity of the trained animals resulted in a similar myenteric neuron morphology to that of the adult animals (6 months old), thereby confirming its beneficial effect, as the sedentary animals had larger alterations in the collagen fibrils and the basal membrane that occur through ageing. The quantitative analysis showed that the NADH-diaphorase positive neurons decreased with ageing and increased with physical activity (P > 0.05). No significant alteration (P > 0.05) in the neuronal profile area of the NADH-diaphorase positive neurons has been observed with ageing.
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PMID:Effects of exercise on the morphology of the myenteric neurons of the duodenum of Wistar rats during the ageing process. 1838 60

Calomys callosus is a wild, native forest rodent found in South America. In Brazil, this species has been reported to harbour the parasitic protozoan Trypanosoma cruzi. The ganglionated plexus of this species was studied using whole-mount preparations of trachea that were stained using histological and histochemical methods. The histological methods were used to determine the position of the ganglia with respect to the trachea muscle and to determine the presence of elastic and collagen fibers. The histochemical method of NADH-diaphorase was used for morphometric evaluations of the plexus. The tracheal plexus lies exclusively over the muscular part of the organ, dorsal to the muscle itself. It varies in pattern and extent between animals. The average number of neurons was 279 and the cellular profile area ranged from 38.37 microm2 to 805.89 microm2. Acetylcholinesterase (AChE) histochemistry verified that both ganglia and single neurons lie along nerve trunks and are reciprocally interconnected with the plexus. Intensely AChE-reactive neurons were found to be intermingled with poorly reactive ones. Two longitudinal AChE-positive nerve trunks were also observed and there was a diverse number of ganglia along the intricate network of nerves interconnecting the trunks. A ganglion capsule of collagen and elastic fibers surrounding the neurons was observed. Under polarized light, the capsule appeared to be formed by Type I collagen fibers.
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PMID:Morphological and quantitative study of ganglionated plexus of Calomys callosus trachea. 1882 17

Recently, there has been an increased interest in unravelling the molecular mechanisms and cellular pathways controlling the differentiation and proliferation of human stem cell lines. Proteome analysis has proven to be an effective approach to comprehensive analysis of the regulatory network of differentiation. In the present study we applied 2-DE combined with capillary-LC-MS/MS analysis to profile differentially regulated proteins upon differentiation of dental follicle precursor cells (DFPCs). Out of 115 differentially regulated proteins, glutamine synthetase, lysosomal proteinase cathepsin B proteins, plastin 3 T-isoform, beta-actin, superoxide dismutases, and transgelin were found to be highly up-regulated, whereas cofilin-1, pro-alpha 1 collagen, destrin, prolyl 4-hydrolase and dihydrolipoamide dehydrogenase were found to be highly down-regulated. The group of up-regulated proteins is associated with actin-bundling and defence against oxidative cellular stress, whereas down-regulated proteins were associated with collagen biosynthesis. Bioinformatic analyses of the entire data set confirmed these findings that represent significant steps towards the understanding of DFPC differentiation. The bioinformatic analyses suggest that proteins associated with cell cycle progression and protein metabolism were down-regulated and proteins involved in catabolism, cell motility and biological quality were up-regulated. These results display the general physiological state of DFPCs before and after osteogenic differentiation. We also identified regulatory proteins, such as the transcription factors TP53 and Sp-1, associated with the differentiation process. Further studies will investigate the impact of identified regulatory proteins for cell proliferation and osteogenic differentiation in DFPCs.
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PMID:Proteomic analysis of osteogenic differentiation of dental follicle precursor cells. 1928 89


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