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:1.6.5.2 (NQO1)
6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper describes the development of the rat vomeronasal organ from the stage of anlage until adulthood. Groups of four rats were sacrificed daily from prenatal day 13 (E13) until birth; at days 2, 4, 7, 10, 14 and 16 after birth; weekly from day P21 to P42 plus an additional group of adults. The vomeronasal organs were processed for light microscopy, including alcian blue-PAS and NADH-diaphorase reactions, and also for electron microscopy. For summarizing our results we propose the following developmental stages: 1. Anlage (E13). 2. Early morphogenesis (E14-16). 3. Late morphogenesis (E17 to birth). 4. Initiation of secretory activity (First postnatal week). 5. Cytoarchitectural maturity (2nd postnatal week). 6. Complete maturity (From 3rd postnatal week onwards). Our results on the maturation of the histological structure and the histochemical reactions, indicate that there may be some functional activity at birth but the development of the organ still continues during the first three postnatal weeks to acquire its full functional capability.
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PMID:Developmental stages of the vomeronasal organ in the rat: a light and electron microscopic study. 144 18

First nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d)-positive perikarya in rat prefrontal cortex (PFC) are present at birth. On postnatal day (P) 1, there is an increase of NADPH-d-positive neurons in all developing layers of PFC. From P1 to P7, a further increase in the overall number of positive neurons is observed. First laminar and area shifts are noted on P21, while morphological maturation of NADPH-d-positive neurons is finished around P30. In conclusion, the postnatal development of NADPH-d neurons in PFC is in concordance with other developmental events in rat cerebral cortex.
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PMID:Postnatal development of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) positive neurons in rat prefrontal cortex. 805 91

Nitric oxide may serve as a retrograde messenger to refine or stabilize synapses in the developing nervous system. Whether this action is dependent upon glutamate and the N-methyl-D-aspartate receptor is not yet established. We have used the patch-cluster system in the intermediate gray layer (IGL) of the rat superior colliculus (SC), a system receiving both glutamatergic and cholinergic input, to study this question. The normal distribution and development of nitric oxide synthase (NOS) in SC was examined using nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry in Sprague-Dawley rats aged P4 to adulthood. Fibers containing acetylcholine (ACh) were identified using choline acetyltransferase (ChAT) immunocytochemistry. In addition, N omega-nitro-L-arginine, an inhibitor of NOS, was injected intraperitoneally from birth until P10, P14, P18, or P21-22 to determine if NOS inhibition would disrupt the formation of the ACh patches. Control animals were studied from the same age groups. Our results show NADPH-d-labeled cells within the periaqueductal gray and the deep gray layer of SC by P4, the earliest age examined. By P8-P9, cells in the IGL were well labeled by NADPH-d, while few in the superficial layers (SL) were labeled. SL cells were visible by P10 and were intensely labeled by P14. IGL cells transiently expressed NADPH-d in that the number of labeled cells increased from P8 to P35, then decreased in the adult. ChAT-labeled fibers first appeared in the IGL at P10, formed a characteristic two-tier pattern by P14, and established obvious patches by P21. Inhibition of NOS from birth produced no qualitative differences in the distribution or density of either ChAT-labeled fibers or NADPH-d-labeled cells and fibers at any of the ages examined. We therefore conclude that NO does not contribute to the refinement of cholinergic fiber patches in the rat SC, probably because the fiber system is not glutamatergic.
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PMID:Inhibition of nitric oxide synthase fails to disrupt the development of cholinergic fiber patches in the rat superior colliculus. 920 10

Nitric oxide (NO) has been shown to mediate refinement of glutamatergic axonal pathways during development. In this study, we investigated whether the development of a cholinergic pathway in the intermediate gray layer (IGL) of the mouse superior colliculus (SC) is also mediated by NO. The pathway was labeled using an antibody directed against choline acetyltransferase (ChAT) and its distribution examined in normal C57/BL6 mice and in knockout mice in which the genes for the neuronal isoform of nitric oxide synthase (NOS) or both the endothelial and neuronal isoforms of NOS had been disrupted. We also examined the development of expression of NOS using nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) staining. NADPHd labeled cells were found within the IGL by P8 and formed loose clusters of cells by P12-P15. ChAT and NADPHd labeled fibers were first observed at P12 and gradually established their characteristic two-tiered patchy pattern between P14 and P21. Comparison of the ChAT labeled fiber distribution in normal, single nNOS and double e,nNOS knockout mice revealed no differences between these three groups. We therefore conclude that nitric oxide does not mediate refinement of this cholinergic pathway.
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PMID:Failure to disrupt development of cholinergic fiber patches in the superior colliculus in nitric oxide synthase deficient mice. 1061 22

Since nitric oxide has a role in the refinement of the retinal projection to the superior colliculus (SC), we studied the onset of neuronal nitric oxide synthase (nNOS) expression in the mouse SC in order to compare its development with that of the refinement process. Sections from animals at ages P1, P5, P8, P11, P15, and P21 and adults were examined with nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry or immunocytochemistry using an antibody directed against nNOS. At all ages there was a wedge of labeled neurons in the dorsolateral periaqueductal gray extending into the deep layers of the SC. At P1 there was also a single superficial band of labeled neurons within the region that will become the intermediate gray layer (IGL). By P5, labeled neurons were also seen in what will become the superficial gray layer. There was a ventral to dorsal progression in nNOS expression with substantial changes in the numbers of labeled neurons in the different laminae between P5 and adulthood. The number of labeled neurons in the IGL peaked at P15, whereas in the superficial layers the numbers continued to increase through P21 and then declined in adults. At all ages these neurons represented a variety of morphological cell types. The onset of nNOS expression in the different laminae is earlier than has been reported in studies using NADPHd as a marker for nNOS. The temporal and spatial patterns of nNOS expression reported here match more closely the time course of pathway refinement in the SC, providing additional evidence for the involvement of nitric oxide in this process.
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PMID:Postnatal development of nitric oxide synthase expression in the mouse superior colliculus. 1105 65

Nitric oxide (NO) is a short-lived radical, which modulates synaptic plasticity, neuronal oscillations and cerebral blood flow. NOS-containing neurones can be detected anatomically by nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry or by NOS immunohistochemistry. Neuropeptide Y(NPY) is the most abundant peptide in the brain. NPY is connected with several vital functions, such as a feeding behaviour, sexual maturation, regulation of circadian rhythms, body temperature, blood pressure and neuroendocrine secretions. Neuropeptide Y also modulates anxiety-related disorders, limbic epileptic seizures as well as learning and memory processes. The study was performed on 45 Wistar rats of various ages (PO, P4, P7, P10, P14, P21, P30, P60, and P120; P--postnatal day). The free-floating sections were stained with standard immunohistochemistry methods. Thereafter the histological sections were studied using the confocal laser microscope equipped. For 3D reconstruction the image analysis program LaserSharp 2000v. 2.0 (Bio-Rad, UK) was used. We found that in the newborn rat both NOS- and NPY-immunoreactivity was weak. It had been increasing gradually until the 7th day of postnatal life, after that until P14 it was maintained on the similar level, and then the number of immunolabelled cells deceased. The developmental changes concerned cell morphology as well--until the 10th day of life the immunoreactive cells were immature, with round or oval bodies and had only a few fibres. From P14 the cells' morphology became similar to that in adult.
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PMID:Distribution of nitric oxide synthase and neuropeptide Y neurones during the development of the hippocampal formation in the rat. 1272 88

Nitric oxide (NO) is a diffusible neurotransmitter that has been implicated in key developmental events, including the refinement of retinogeniculate axons into ON/OFF sublayers in the ferret lateral geniculate nucleus (LGN), and in the formation of eye-specific laminae in other species. To understand the role of NO in the LGN, it is critical to fully characterize the pattern of brain nitric oxide synthase (bNOS) expression within the nucleus, including the phenotype of the neural elements that express it. We have examined the temporal and spatial pattern of bNOS expression in the ferret LGN during the first 6 weeks of postnatal development, and in the adult, by detecting bNOS with a monoclonal antibody as well as beta-nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry. We have found that bNOS is expressed in neurons in the A laminae of the LGN as early as postnatal day 7 (P7), a time coincident with eye-specific segregation of retinal axons. This expression continues through P35, with peak somatodendritic expression at P21. Fluorescent double labeling using antibodies to bNOS and glutamic acid decarboxylase indicate that bNOS is expressed in gamma-aminobutyric acid-ergic interneurons within the A laminae. Electron microscopic examination of bNOS-labeled cells showed synaptic contacts from terminals with two distinct morphologic profiles. Expression of bNOS within interneurons that receive contacts from multiple sources indicates that the synaptic circuitry associated with bNOS activation and the potential targets of NO may be more complex than originally thought and supports a potential new role for interneurons as cellular intermediaries in the refinement of pathways in the LGN. Our findings broaden the window of time that bNOS may be active within the developing LGN, suggesting an expanded role for NO during early postnatal development.
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PMID:Brain nitric oxide synthase expression in the developing ferret lateral geniculate nucleus: analysis of time course, localization, and synaptic contacts. 1279 37

Basic research and clinical chemoprevention trials support the protective role of selenium in cancer prevention but the mechanisms based on the molecular level remain to be fully defined. This mini-review focuses only on the elucidation of the molecular mechanisms of cancer prevention by selenium using the genomics approach; target organs discussed here are breast, prostate, colon and lung. The results described here support the utility of microarray technology in delineating the molecular mechanisms of cancer prevention by selenium. These results are based on studies employing human and rodent cell lines and tissues from animal models ranging from normal to frank cancer. The dose and the form of selenium are determining factors in cancer chemoprevention. The results of the microarray analysis reviewed here indicate that selenium, independent of its form and the target organ examined, alters several genes in a manner that can account for cancer prevention. Selenium can up regulate genes related to phase II detoxification enzymes, certain selenium-binding proteins and select apoptotic genes, while down regulating those related to phase I activating enzymes and cell proliferation. Independent of tissue type, selenium arrests cells in G1 phase of cell cycle, inhibits CYCLIN A, CYCLIN D1, CDC25A, CDK4, PCNA and E2F gene expressions while induces the expressions of P19, P21, P53, GST, SOD, NQO1, GADD153 and certain CASPASES. In addition to those described above, genes such as OPN, which is mainly involved in metastasis and recently reported to be down regulated by selenium, should be considered as potential molecular marker in clinical chemoprevention trials. Collectively, literature data indicate that some of these genes that were altered by selenium are also involved in the development of human cancers described in this review. It appears that androgen receptor status may influence the effect of selenium on gene expression profile in prostate cancer; whether estrogen receptor may influence the effect of selenium on gene expression in breast cancer requires further studies. Knowledge from gene array data in combination with proteomics approaches, using homogenous population of cell types with the aid of laser capture microdissection, may provide an individualized dimension of information on cancer risk and potential targets for its prevention. The molecular (genetic) biomarkers presented in this review will provide the foundation for future studies of the chemopreventive properties of structurally varied selenium compounds.
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PMID:Molecular chemoprevention by selenium: a genomic approach. 1609 79

The topographic ontogeny of nitric oxide synthase (NOS) within the paraventricular nucleus (PVN) of the rat hypothalamus was studied by nicotinamide adenine dinucleotide-diaphorase (NADPH-diaphorase) histochemistry. At Day 1 of postnatal life (P1), NOS-positive neurons were already present and achieved their maturity (in terms of perikarya number and dendritic arborization) about the time of weaning (P21). Across all ages studied (P1 to adulthood), intense NADPH-diaphorase staining was primarily confined within magnocellular cells of the PVN largely characterized by medium-sized (12-15 mum in diameter), ovoid bipolar neurons with prominent clear nuclei. To identify the neurosecretory cells of the adult PVN in which NOS was present, double-labeling studies were carried out via fluorescent immunocytochemistry. Magnocellular oxytocin (OT) and arginine vasopressin (AVP), as well as parvocellular corticotropin-releasing factor (CRF), were found to be colocalized with NOS. However, colocalization occurred significantly more frequently in OT-containing neurons, relative to AVP- or CRF-positive cells. Most of the colocalization occurring between NOS and OT was observed in the rostral constituent of the magnocellular subdivision of the PVN, as opposed to a more caudal defined PVN. To provide a distribution comparison of OT, AVP, and CRF to that of NOS in the adult PVN, in situ hybridization was carried out with (35)S-cRNA antisense probes for the aforementioned neuropeptides. The results obtained with this evaluation were correlated with NOS histochemistry in the same brain sections. As expected, specific labeling was observed for all three neuroactive substances over their topographically distinctive nuclei. Among these nuclei, labeling by the OT cRNA probe provided the closest topographical correlation of hybridized signal over NOS perikarya, thus reinforcing the tenet that a relatively small population of OT nerve cells are concurrently colocalized with the enzyme. Taken together, these results indicate that NOS is present in the PVN of the rat at all postnatal ages which we tested. They also indicate that among neurosecretory cells of the PVN, only OT prominently shared with NOS the same common nerve cell type. This suggests that NOS neurons may represent a distinct neuropil group among multiple neuroactive nuclei in the neuroendocrine hypothalamus. Finally, we demonstrate that NADPH-diaphorase histochemistry can be easily combined with immunocytochemical and in situ hybridization procedures to evaluate the colocalization and topographical distribution of NOS with other phenotypic neurons in the mammalian central nervous system.
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PMID:Ontogeny of the rat hypothalamic nitric oxide synthase and colocalization with neuropeptides. 1991 18

Epidermal keratinocytes are critical targets for UV-induced genotoxicity as their transformation by sunlight overexposure can lead to skin cancer such as basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). Therefore, assessment of photoprotection should involve early markers associated with DNA photodamage. Here, the same normal human keratinocytes either in monoculture (KC) or in full thickness reconstructed skin (RS) were compared with respect to their response to simulated solar UV (SSUV) exposure. Irradiation conditions (spectral power distribution and doses) were designed to mimic environmental zenithal UV from sunlight. At doses where survival was higher than 80%, comet assay showed more single strand breaks (SSB) and cyclobutane pyrimidine dimers (CPD) in keratinocytes in RS than in KC one hour post-exposure. The transcription factor p53 was activated in both models. While in KC p53 accumulation displayed a linear dose-dependency up to 24 h post-exposure, in RS it followed a bell-shaped profile and reverted to its basal rate. QRT-PCR demonstrated that among genes controlled by p53, P21 and MDM2 were clearly induced by SSUV in KC, whereas GADD45 expression was strongly and almost exclusively up-regulated in RS. Nrf2-dependent antioxidant genes (Ferritin light chain, NQO1) were only induced in RS, yet at low doses for NQO1. In vitro models such as KC or RS allowing the development of quantitative methodologies should be used as surrogates for in vivo tests assessing photogenotoxicity.
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PMID:In vitro tools for photobiological testing: molecular responses to simulated solar UV of keratinocytes growing as monolayers or as part of reconstructed skin. 2035 37


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