Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A brief report is given on the possible role of oxygen-derived free radicals and cholecystokinin in the pathogenesis of experimentally induced acute pancreatitis. Furthermore, use of scavengers (superoxide dismutase, catalase), CCK-receptor antagonists and somatostatin are discussed in the therapy of acute pancreatitis induced in animal models. It is suggested that both the term of direct pancreatic cytoprotection of the above-mentioned agents and the validity of the animal models used for induction of acute pancreatitis have to be reconsidered.
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PMID:Pancreatic cytoprotection: new approaches. 134 8

Somatostatin and octreotide share with vasoactive intestinal peptide the property of having an inhibitory effect on leukocyte functions. While there are studies reporting the inhibitory effect of the latter on respiratory burst in human monocytes, no such reports are available about similar inhibitory effects of the former. The aim of the present study was to investigate such effects of somatostatin and octreotide on human monocytes. Release of superoxide anion from monocytes was measured by superoxide dismutase-inhibitable reduction of cytochrome c in vitro. Somatostatin 1-14, somatostatin 1-28 and octreotide inhibited release of superoxide anion from stimulated monocytes. Formylpeptide-stimulated reduction of cytochrome c was inhibited by 1 mumol/l of octreotide and somatostatin 1-14 by about 50% and 35%, respectively. The effect was dose-dependent with half-maximal effective peptide concentrations at about 10 nmol/l. Somatostatin 1-28, which is the major form found in circulating plasma, also antagonized formylpeptide-stimulated respiratory burst activity; when directly compared to the effect of 1 mumol/l of somatostatin 1-14, somatostatin 1-28 was significantly more active (P less than 0.05). Our observations suggest that somatostatin-related peptides have a regulatory role in oxygen radical metabolism and a mediator role in the neuro-immune axis.
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PMID:Suppression of superoxide release from human monocytes by somatostatin-related peptides. 136 Jun 87

We used rabbit antisera against manganese (Mn)-superoxide dismutase for immunohistochemical studies of localization in the rat neostriatum. Immunostaining was intense in large-sized neurons and several medium-sized neurons, but it was moderate to weak in other cells. Double immunostaining with monoclonal antibody to choline acetyltransferase or somatostatin demonstrated large-sized, Mn-SOD immunoreactive neurons to be cholinergic, and some medium-sized neurons which were intensely immunoreactive for Mn-SOD to contain somatostatinergic.
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PMID:Localization of Mn-superoxide dismutase (Mn-SOD) in cholinergic and somatostatin-containing neurons in the rat neostriatum. 168 20

Molecular probes were used as markers in the backcross (Czech II X BALB/cPt) X Czech II to determine the positions of six genes on mouse chromosome 16 (MMU 16). The order of the genes mapped is (centromere), protamine-1 (Prm-1), immunoglobulin lambda 1 light chain (Igl-1), preprosomatostatin (Smst), an endogenous mouse mammary tumor virus locus (Mtv-6), and two more distal sequences, superoxide dismutase, cytoplasmic form (Sod-1), and the proto-oncogene sequence Ets-2. The largest recombination frequency between any two adjacent markers is 24 cM, and thus the position of any marker on MMU 16 that is polymorphic between these two strains can be readily determined in this backcross. A region of MMU 16 which corresponds to the Down syndrome region of human chromosome 21 is located near the distal end of the chromosome.
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PMID:Genetic mapping of Prm-1, Igl-1, Smst, Mtv-6, Sod-1, and Ets-2 and localization of the Down syndrome region on mouse chromosome 16. 288 55

The distribution of somatostatin in both the human and rat brain suggests that it is involved in numerous functions, including endocrine regulation, cognition and memory, autonomic regulation and motor activity. We have examined the regulation of somatostatin mRNA in the striatum, a brain region involved in motor and cognitive behaviour. Somatostatin and its mRNA are expressed in this region in interneurons which are resistant to ischaemia, excitotoxicity and Huntington's disease, possibly because they express high levels of superoxide dismutase. Striatal somatostatin mRNA is increased by stimulation of NMDA (N-methyl-D-aspartate) receptors. Ischaemia-induced cortical lesions also increase somatostatin gene expression in the striatum. In contrast, the levels of striatal somatostatin mRNA decrease after treatment with haloperidol, an antipsychotic agent that produces extrapyramidal symptoms, but not clozapine, which does not. Further evidence for a role for striatal somatostatin in extrapyramidal symptoms includes the observation that somatostatin mRNA levels decrease in the striatum after lesions are made in the dopaminergic pathway, a feature of Parkinson's disease. The largest change in somatostatin gene expression after dopaminergic lesions is the increase in somatostatin mRNA level sin neurons of the internal pallidum and lateral hypothalamus projecting to the lateral habenula. The results suggest that changes in brain somatostatin gene expression occur in pathological conditions and may be related to their symptoms.
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PMID:Anatomical localization and regulation of somatostatin gene expression in the basal ganglia and its clinical implications. 758 52

Ten patients with SDAT received the ECP therapy. The examination of Hasegawa's Dementia Scale (HDS), single photor emission computed tomography (SPECT) brain imaging, and some biochemical parameters in blood and CSF were selected to evaluate the effect of ECP for SDAT. After ECP treatment, the average HDS score of the patients increased, the value of P was close to 0.05; and the cortical cerebellar ratios of SPECT brain scan, the superoxide dismutase (SOD) activity and the concentrations of somatostatin-like immunoreactivity (SLI), dynorphin AL-13 (Dyn Al-13) in blood and/or CSF were significantly elevated. The results indicated that ECP could not only improve cerebral blood flow, but also make a notable impact on biological active substances in blood and CSF. It is suggested that ECP is beneficial to SDAT patients.
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PMID:Study of the external counterpulsation (ECP) therapy for senile dementia of the Alzheimer's type (SDAT). 783 2

In the present study, it was observed that somatostatin could significantly protect rat gastric mucosa from injury induced by cold-restraint stress and inhibit the stress induced increase of malonaldehyde (MDA) content. In the gastric mucosa of stress rats, the xanthine oxidase (XO) activity were increased and the glutathione peroxidase (GSH-Px) activity were decreased respectively, while the superoxide dismutase (SOD) activity showed no change. After pretreatment with somatostatin, the decrease of GSH-Px activity was significantly reversed, whereas XO and SOD activities were not significantly affected. The above results show that the protective effect of somatostatin against the stress-induced injury of gastric mucosa may be related to an enhancement of the ability of gastric mucosa to scavenge oxygen-derived free radicals.
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PMID:[Protective effect of somatostatin against stress injury of gastric mucosa may be related to the scavenge of free radicals]. 797 28

To investigate whether differences in vulnerability to free radicals might underlie differences among striatal neurons in their vulnerability to neurodegenerative processes such as occur in ischemia and Huntington's disease, we have analyzed the localization of superoxide free radical scavengers in different striatal neuron types in normal rhesus monkey. Single- and double-label immunohistochemical experiments were carried out using antibodies against the enzymes copper, zinc superoxide dismutase (SOD1), or manganese superoxide dismutase (SOD2), and against markers of various striatal cell types. Our results indicate that the striatal cholinergic and parvalbumin interneurons are enriched in SOD1 and/or SOD2, whereas striatal projection neurons and neuropeptide Y/somatostatin (NPY+/SS+) interneurons express only low levels of both SOD1 and SOD2. We also found that projection neurons of the matrix compartment express significantly higher levels of SOD than those in the striosome compartment. Since projection neurons have been reported to be more vulnerable than interneurons and striosome neurons more vulnerable than matrix neurons to neurodegenerative processes, our results are consistent with the notion that superoxide free radicals are at least partly involved in producing the differential neuron loss observed in the striatum following global brain ischemia or in Huntington's disease.
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PMID:Differential abundance of superoxide dismutase in interneurons versus projection neurons and in matrix versus striosome neurons in monkey striatum. 872 Aug 60

1. Oxygen free radicals have been suggested to be a contributory factor in complications of diabetes mellitus. There are many reports indicating the changes in parameters of oxidative stress in diabetes mellitus. In this study we aimed to identify whether oxidative stress occurs in the liver and pancreas in the initial stages of development of diabetes. 2. We therefore investigated the lipid peroxide level (thiobarbituric acid-reactive substances, TBARS) and activities of antioxidant enzymes [superoxide dismutase (SOD), catalase and glutathione peroxidase] in liver and pancreas of control and streptozotocin-induced diabetic rats at various stages of development of diabetes. 3. Male Sprague-Dawley rats were divided into two groups: group I, control (n = 42) and group II, diabetic (n = 42). Each group was further subdivided into seven groups consisting of six rats each. Rats in these subgroups were studied at weekly intervals (0 to 6 weeks). Plasma glucose levels, TBARS levels and activities of antioxidant enzymes were measured in liver and pancreas at various time intervals. 4. There was a significant (P < 0.05) and progressive increase in TBARS levels of liver and pancreas in the diabetic group. Total SOD and Cu-Zn-SOD activity increased (P < 0.05) with progression of diabetes while Mn-SOD activity showed no significant change in either tissue. Catalase and glutathione peroxidase activities increased significantly (P < 0.05) in liver and pancreas. 5. Immunohistochemical study of pancreatic islet revealed a decrease in the expression of insulin with progression of diabetes. However, glucagon and somatostatin showed an increase in immunoreactivity and a difference in their distribution pattern. 6. The findings of the present study suggest that oxidative stress starts at early onset of diabetes mellitus and increases progressively. In conclusion, the structural damage to these tissues or complications of diabetes mellitus may be due to oxidative stress.
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PMID:Increased oxidative stress in rat liver and pancreas during progression of streptozotocin-induced diabetes. 985 60

An understanding of the metabolic fate of radiometal-labeled peptides is important due to their application in the areas of diagnostic imaging and targeted radiotherapy. Radioisotopes of copper ((64)Cu, T(1/2) = 12.7 h; (67)Cu, T(1/2) = 62 h) have been labeled to monoclonal antibodies (mAbs) and peptides and have applications in the areas of PET imaging and targeted radiotherapy of cancer. Copper-64-TETA-D-Phe(1)-octreotide ([(64)Cu]TETA-OC) has been shown to bind to the somatostatin receptor, both in vitro and in vivo, and this agent inhibited the growth of somatostatin-receptor positive tumors in rats. Copper-64-TETA-OC, however, showed a retention of activity in the blood, liver, and bone marrow, suggesting possible dissociation of (64)Cu from TETA-OC in vivo. The purpose of this study was to determine if (64)Cu dissociates from [(64)Cu]TETA-OC and binds to the protein, superoxide dismutase (SOD) in rat liver. The liver metabolism of [(64)Cu]TETA-OC was examined in normal rats using a gel-electrophoresis assay specific for SOD and size-exclusion chromatography. The major metabolite in rat liver at 20 h postinjection had a molecular weight of 32 kDa as shown by size-exclusion chromatography. A gel electrophoresis assay specific for the detection of SOD [nitro-blue tetrazolium (NBT)] showed that a (64)Cu-labeled protein isolated from rat liver homogenates comigrated with SOD. Evaluating the metabolic fate of copper radiopharmaceuticals demonstrated that Cu(II) dissociates from macrocyclic chelators such as TETA and binds to proteins in high concentrations, namely SOD in rat liver.
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PMID:In vivo transchelation of copper-64 from TETA-octreotide to superoxide dismutase in rat liver. 1089 74


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