Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chemical alteration of the glucocorticoid, methylprednisolone, has led to the introduction of a new class of compounds called the 21-aminosteroids (21-ASs). The purpose of this study was to investigate the effect of the 21-AS, U74389G, on silica-induced acute lung injury. Male Fischer 344 rats were treated intraperitoneally with saline or U74389G in a total dose of 15 mg/kg divided into three injections of 5 mg/kg separated by 4 h. Following the first treatment, animals from the two groups were intratracheally instilled with silica (10 mg/100 g body wt in 0.5 ml of saline) or saline vehicle (0.5 ml). Twenty-four hours after the instillations, bronchoalveolar lavage (BAL) was performed. In the animals not receiving U74389G, marked increases in total protein, beta-glucuronidase, and lactate dehydrogenase (LDH) activities and number of neutrophils (PMNs) were demonstrated in the BAL fluid of the silica-treated animals compared to their controls. Silica also caused dramatic increases in the luminol-dependent chemiluminescence (CL) of lung tissue and BAL cells. The CL reaction was decreased by superoxide dismutase (SOD) and N-nitro-L-arginine methyl ester hydrochloride (L-NAME), a nitric oxide (NO) synthase inhibitor. In animals treated with U74389G, there was attenuation of the silica-induced increases in biochemical, cellular, and chemiluminescent indices of damage. This study demonstrates that U74389G significantly reduces acute lung injury caused by the intratracheal instillation of silica, and this drug may be of potential value for treatment of lung diseases in which damage caused by reactive oxygen species has been implicated.
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PMID:Attenuation of acute inflammatory effects of silica in rat lung by 21-aminosteroid, U74389G. 770 90

We determined the 5'-flanking sequences of two nuclear genes (SodCc1 and SodCc2) encoding cytosolic copper/zinc-superoxide dismutase in rice (Oryza sativa L.). Utilizing transient beta-glucuronidase (GUS) reporter assays, functional promoter-GUS analysis was performed in rice protoplasts exposed to the phytohormone abscisic acid (ABA) or the antioxidant sulfhydryl reagent, dithiothreitol (DTT). Transcriptional activities from both SodCc-GUS fusions were stimulated by DTT, which induces the promoter activity of the tobacco SodCc gene [Proc. Natl. Acad. Sci. USA 90 (1993) 3108-3112]. ABA had no effect on SodCcl-GUS expression but specifically induced the gene expression of the SodCc2-GUS fusion. The simultaneous application of ABA and gibberellin A3, however, abolished the enhancing effect of ABA. These results indicated that two rice SodCc promoters differentially respond to externally supplied ABA and that one of the regulatory factors for plant SodCc expression is ABA in addition to cellular redox-modulating antioxidants.
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PMID:Structure and differential response to abscisic acid of two promoters for the cytosolic copper/zinc-superoxide dismutase genes, SodCc1 and SodCc2, in rice protoplasts. 782 31

The present study demonstrates for the first time that iron ions can induce lipid peroxidation in intact macrophages without causing cell death. Macrophage lipid peroxidation increases cell-mediated oxidation of LDL, enhances the release of interleukin 1 and inhibits the release of apolipoprotein E from the macrophages. When cultured macrophages were exposed to ferrous ions (50 microM FeSO4) for 4 h at 37 degrees C, cellular lipid peroxidation (measured by analyses of malondialdehyde (MDA), conjugated dienes (CD), and lipid peroxides (PD)) increased 2-4-fold in comparison with non-treated cells. This process was iron-dose dependent, reached its maximum after 4 h of incubation, and was accompanied by 68% and 53% reductions in the content of the cellular linoleic (18:2), and arachidonic acid (20:4), respectively, and by 29% and 36% reductions of cellular vitamin E and vitamin A, respectively. Cell viability (measured by trypan blue exclusion, by [3H]thymidine incorporation into DNA, by analysis of the release of lactate dehydrogenase (LDH) or [3H]adenine), and cell morphology (studied by scanning electron microscopy) were not significantly affected by the iron-induced oxidative stress. Manitol and dimethylthiourea (DMTU), but not catalase or superoxide dismutase (SOD), significantly inhibited iron-induced cellular lipid peroxide formation, suggesting that hydroxyl radical, but not superoxides or hydrogen peroxides, mediated the iron-induced cellular lipid peroxidation. Incubation of LDL (0.2 mg of protein/ml) with oxidized macrophages resulted in LDL lipids peroxidation, as evidenced by an 8-fold increase in the LDL associated MDA in comparison with LDL that was incubated under similar conditions with non-oxidized macrophages. Furthermore, oxidation of LDL by oxidized macrophages in the presence of copper ions (10 microM CuSO4) was 2-fold higher in comparison with oxidation of LDL by non-oxidized macrophages. The release of apolipoprotein E from oxidized macrophages decreased by 50%, whereas macrophage release of beta-glucuronidase and of interleukin-1 beta increased by 83% and by a factor of 6, respectively. This study demonstrates for the first time that iron ions induce oxidation of the cellular polyunsaturated fatty acids in intact macrophages and that this cellular lipid peroxidation can subsequently induce LDL oxidation.
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PMID:Iron induces lipid peroxidation in cultured macrophages, increases their ability to oxidatively modify LDL, and affects their secretory properties. 784 Aug 15

Superoxide dismutases (SODs; superoxide: superoxide oxidoreductase, EC 1.15.1.1) play a key role in protection against oxygen radicals, and SOD gene expression is highly induced during environmental stress. To determine the conditions of SOD induction, the promoter of the cytosolic copper/zinc SOD (Cu/ZnSODcyt) gene was isolated in Nicotiana plumbaginifolia and fused to the beta-glucuronidase reporter gene. Oxidative stress is likely to alter the cellular redox in favor of the oxidized status. Surprisingly, the expression of the Cu/ZnSODcyt gene is induced by sulfhydryl antioxidants such as reduced glutathione, cysteine, and dithiothreitol, whereas the oxidized forms of glutathione and cysteine have no effect. It is therefore possible that reduced glutathione directly acts as an antioxidant and simultaneously activates the Cu/ZnSODcyt gene during oxidative stress.
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PMID:Redox-activated expression of the cytosolic copper/zinc superoxide dismutase gene in Nicotiana. 846 30

Exposure to silica, a cytotoxic and fibrogenic mineral dust, has been demonstrated to cause pulmonary inflammation and damage to the lung tissue. In contrast to the long-term consequences, little information exists on the sequence of inflammatory/damaging events occurring acutely after exposure to silica. The purpose of this study was to determine the minimum time after the administration of silica that the inflammatory/damage response is detectable and the temporal relationship of these processes. Male Fischer 344 rats were dosed intratracheally with silica (2.5 or 10 mg/100 g body weight) or saline vehicle. At 2 and 4 h after instillation, both cellular (total cell count and neutrophil count) and biochemical (total protein, albumin, and beta-glucuronidase and lactate dehydrogenase activities) parameters of inflammation and damage were evaluated in the bronchoalveolar lavage fluid. At 2 h, total protein levels were elevated at both silica doses, but all other parameters were unchanged; however, 4 h after silica exposure all parameters were elevated over those of the saline control. In a further attempt to characterize the inflammatory/damage processes, luminol-dependent chemiluminescence (LDCL) was performed on aliquots of chopped lung. At 2 h after silica instillation, phorbol myristate acetate-stimulated lung tissue from silica-treated rats had no increase in light production when compared to controls, whereas after 4 h there were significant increases in LDCL activity in both dose groups when compared to controls. The addition of superoxide dismutase (SOD) decreased LDCL activity of the 2.5 mg/100 g group by 59% (2 h) and 66% (4 h), and of the 10 mg/100 g group by 49% (2 h) and 73% (4 h). Alternatively, the addition of N-omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, decreased the 2.5 mg/100 g group by 52% (2 h) and 60% (4 h). The 10 mg/100 g group was decreased by 67% (2 h), but only exhibited a 12% reduction at 4 h. SOD and L-NAME also inhibited the background LDCL in saline-treated rats. These reductions in LDCL activity indicate that reactive oxygen and nitrogen species play a role in the acute phase pulmonary response from silica. The results of this study indicate that the initial stages of damage begin to appear by 2 h, but damage and inflammation are definitive by 4 h after administration of silica in rats.
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PMID:Characteristics of the acute-phase pulmonary response to silica in rats. 856 14

The effect of curcumin on the biochemical changes induced by isoproterenol (ISO) administration in rats was examined. ISO (300 mg Kg-1 administered subcutaneously twice at an interval of 24 h) caused a decrease in body weight and an increase in heart weight, water content as well as in the levels of serum marker enzymes viz creatine kinase (CK), lactate dehydrogenase (LDH) and LDH1 isozyme. It also produced electrocardiographic changes such as increased heart rate, reduced R amplitude and ST elevation. Curcumin at a concentration of 200 mg.Kg-1, when administered orally, showed a decrease in serum enzyme levels and the electrocardiographic changes got restored towards normalcy. Myocardial infarction was accompanied by the disintegration of membrane polyunsaturated fatty acids expressed by increase of thiobarbituric acid reactive substance (TBARS), a measure of lipid peroxides and by the impairment of natural scavenging, characterized by the decrease in the levels of superoxide dismutase, catalase, glutathione peroxidase, ceruloplasmin, alpha tocopherol, reduced glutathione (GSH) and ascorbic acid. The oral pretreatment with curcumin two days before and during ISO administration decreased the effect of lipid peroxidation. It was shown to have a membrane stabilizing action by inhibiting the release of beta-glucuronidase from nuclei, mitochondria, lysosome and microsome. Curcumin pre- and co-treatment decreased the severity of pathological changes and thus, could have a protective effect against the damage caused by myocardial infarction (MI).
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PMID:Protective role of curcumin against isoproterenol induced myocardial infarction in rats. 885 58

Our knowledge of superoxide dismutase (SODs) in tobacco has increased greatly during the past few years. Genes encoding the four identified SOD isoforms of tobacco have been isolated and characterized. Analysis of promoter-beta-glucuronidase fusions has provided information on the cellular expression of SODs in tobacco and has constituted the basis for studying SOD regulation. Constitutive overproduction of SOD has been shown to confer increased tolerance to stress and has started to reveal subtle biochemical differences between SOD isoforms. Thus, thanks to its convenience for molecular and physiological studies, tobacco has come forth in recent years as an excellent model system for studying the regulation and function of SOD in dicotyledonous plants.
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PMID:The regulation and function of tobacco superoxide dismutases. 921 90

Xanthomonas campestris pv. campestris (Xcc) is a vascular pathogen of cruciferous plants that normally gains entry to plants via hydathodes. In order to study the basis of the preference for this protal of entry we have developed an Arabidopsis thaliana model with attached or detached leaves partially immersed in a bacterial suspension. Entry of bacteria into leaves, assessed by resistance to surface sterilization, could be detected after 1 h. Dissection of leaves and histochemical staining for beta-glucuronidase produced by the bacteria indicated that they were located in hydathodes. In contrast, similar experiments with the leaf-spotting pathogen X. campestris pv. armoraciae gave patterns of localized staining dispersed over the leaf area, indicative of entry through stomata. A survey of 41 A. thaliana accessions showed that they fell into three classes distinguishable by total numbers of Xcc that entered under standard conditions and by preference for hydathode colonization. Previously isolated Xcc mutants affected in pathogenicity were tested for hydathode colonization: an hrp mutant behaved indistinguishably from the wild type, and rpf regulatory mutants gave 10-fold reduced colonization, whereas with rfaX mutants with altered lipopolysaccharide, few if any viable bacteria were recoverable from hydathodes. This fact, together with the rapid induction of superoxide dismutase in the bacteria located in hydathodes, suggests that an early defense reaction is mounted in the hydathode.
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PMID:Entry of Xanthomonas campestris pv. campestris into hydathodes of Arabidopsis thaliana leaves: a system for studying early infection events in bacterial pathogenesis. 961 52

We investigated pulmonary clearance of yttrium (Y) and acute lung injury following intratracheal instillation (i.t.) of yttrium chloride (YCl3) in saline- or YCl3-pretreated rats (30 days before the second challenge). About 67% of the initial dose of Y remained in the lung even 31 days after the i.t. treatment. The pretreatment with YCl3 significantly reduced i.t.-YCl3-induced increases in biochemical inflammatory indicators in bronchoalveolar lavage fluid (BALF), such as lactate dehydrogenase, beta-glucuronidase, and alkaline phosphatase activities and protein concentration, while the pretreatment increased the number of polymorphonuclear leukocyte (PMN) in BALF. These results suggest that the augmentation of PMN infiltration does not play an important role, if any, in i.t. YCl3-induced increases in biochemical indicators in BALF. The reduction of the increases in those biochemical inflammatory indicators may be due, at least in part, to the increase of manganese-superoxide dismutase (Mn-SOD) activity in the lung tissue, because the lung Mn-SOD activity in the YCl3-pretreated group was two times higher than that of the saline-pretreated group.
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PMID:Effects of intratracheal pretreatment with yttrium chloride (YCl3) on inflammatory responses of the rat lung following intratracheal instillation of YCl3. 980 Oct 29

Portal hypertensive gastropathy is associated with a broad spectrum of gastric mucosal damage inspite of decreased gastric acid secretion, suggestive of compromised endogenous protective mechanisms. To determine the mechanisms of damage in portal hypertensive gastropathy we measured lipid peroxidation, glutathione, antioxidant and lysosomal enzymes in gastric mucosal homogenates from male Wistar rats with elevated intrasplenic pulp pressure, eighteen days after common bile duct ligation. Thiobarbituric acid-reactive substances and lysosomal enzymes (beta-glucuronidase and acid phosphatase) were increased in the common bile duct ligated group as compared to the sham-operated group. The levels of antioxidant defense enzymes, superoxide dismutase, glutathione peroxidase, catalase and glutathione were decreased as compared to the sham-operated controls. Pre-operative vitamin E administration decreased mucosal lipid peroxidation increased the levels of antioxidant defense enzymes and lowered the lysosomal enzymes. The plasma vitamin E levels in this group were lower when compared to animals receiving it post-operatively. In conclusion, free radical and lysosomal enzyme mediated damage may play a role in portal hypertensive gastropathy.
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PMID:Gastropathy and defense mechanisms in common bile duct ligated portal hypertensive rats. 1072 35


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