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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)
Under nitrogen-limiting conditions, legumes interact with symbiotic rhizobia to produce nitrogen-fixing root nodules. We have previously shown that glutathione and homoglutathione [(h)
GSH
] deficiencies impaired Medicago truncatula symbiosis efficiency, showing the importance of the low M(r) thiols during the nodulation process in the model legume M. truncatula. In this study, the plant transcriptomic response to Sinorhizobium meliloti infection under (h)
GSH
depletion was investigated using cDNA-amplified fragment length polymorphism analysis. Among 6,149 expression tags monitored, 181 genes displayed significant differential expression between inoculated control and inoculated (h)
GSH
depleted roots. Quantitative reverse transcription polymerase chain reaction analysis confirmed the changes in mRNA levels. This transcriptomic analysis shows a down-regulation of genes involved in meristem formation and a modulation of the expression of stress-related genes in (h)
GSH
-depleted plants. Promoter-
beta-glucuronidase
histochemical analysis showed that the putative MtPIP2 aquaporin might be up-regulated during nodule meristem formation and that this up-regulation is inhibited under (h)
GSH
depletion. (h)
GSH
depletion enhances the expression of salicylic acid (SA)-regulated genes after S. meliloti infection and the expression of SA-regulated genes after exogenous SA treatment. Modification of water transport and SA signaling pathway observed under (h)
GSH
deficiency contribute to explain how (h)
GSH
depletion alters the proper development of the symbiotic interaction.
...
PMID:(Homo)glutathione depletion modulates host gene expression during the symbiotic interaction between Medicago truncatula and Sinorhizobium meliloti. 1958 96
Inflammatory reactions that result from microbial infections, both localized and systemic, are reported to cause transient or permanent male infertility. The cellular mechanisms underlying the inhibitory effect of microbial infection on spermatogenesis is not fully understood. However, there is evidence that spermatogenesis is affected by bacterial lipopolysaccharides (LPS) that induce acute inflammatory responses. The aim here was to use LPS treatments to investigate the potential oxidative stress and toxicity in primary cultures of adult rat Sertoli cells. The Sertoli cells were established and incubated with different concentrations of LPS (5, 10 or 20 microg/ml) for 6, 12 and 24h. Lipid peroxidation (LPO) and hydrogen peroxide (H(2)O(2)) production, along with superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR), reduced glutathione (
GSH
), lactate, lactic acid dehydrogenase (LDH), gamma-glutamyl transpeptidase (gamma-GT) and
beta-glucuronidase
were measured in these cells. LPO as well as H(2)O(2) production were significantly increased while antioxidant enzyme activities and
GSH
concentration were significantly depressed. Effects were dose and time-dependent at all incubation periods with 10 and 20 microg/ml LPS. Moreover, markers of Sertoli cell function such as lactate production, LDH, gamma-GT and
beta-glucuronidase
activities were decreased in a time and dose-dependent manner. Incubation of Sertoli cells with 5 microg/ml LPS for 12 and 24h significantly increased oxidative status but significantly decreased the antioxidant enzyme activities,
GSH
concentration and Sertoli cell markers. In contrast, the oxidative and antioxidant status and markers of Sertoli cell function did not show any significant change in treated Sertoli cells with 5 microg/ml LPS for 6h. Therefore, it may be concluded that LPS induces oxidative stress in Sertoli cells and adversely affects Sertoli cell functions.
...
PMID:Bacterial lipopolysaccharide-induced oxidative stress in adult rat Sertoli cells in vitro. 2421 63
The present study was designed to investigate the cardioprotective potential of lycopene (LYC) on isoproterenol (ISO)-induced oxidative stress and heart lysosomal damage in rats. Male Sprague Dawley rats were pretreated with LYC (4mg/kg, p.o.) once daily for 21 days. After the treatment period, ISO (85mg/kg) was injected subcutaneously, once daily, to rats for 2 days. Hemodynamic parameters, cardiac marker enzymes, antioxidant, and oxidative stress parameters in serum and heart tissues were measured. ISO treated rats showed significant changes in heart rates, heart weights and serum lipid profiles. The activity of aspartate aminotranferase (AST), lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB) and cardiac troponin T (cTnT) were increased significantly (p<0.01) in the serum of ISO rats. The levels of lipid peroxides (thiobarbituric acid reactive substances, TBARS), protein carbonyl content (PCC) and neutrophil infiltration marker; myeloperoxidase (MPO) were significantly (p<0.01) increased. In addition, the activities of lysosomal enzymes (
beta-glucuronidase
, beta-N-acetylglucosaminidase, and cathepsin-d) in the serum and heart of ISO rats were increased significantly. Furthermore, a marked decrease in the levels of serum and cardiac reduced glutathione (
GSH
), vitamin C and cardiac enzymatic antioxidants; superoxide dismutase (SOD), glutathione peroxidase (
GSH
-Px) and catalase (CAT) were observed. In vitro study confirmed the strong antioxidant effect of LYC on total antioxidant activity. In conclusion, the present study demonstrated that LYC supplementation to ISO rats significantly ameliorated lysosomal membrane damage as well as the alterations in cardiac enzymes, lipid profile and oxidative stress markers. These findings revealed the cardioprotective effects of LYC against ISO-induced oxidative stress and cardiotoxicity in rats. These observed effects are mediated via antioxidant power and free radical scavenging activity of LYC.
...
PMID:Lycopene attenuates oxidative stress and heart lysosomal damage in isoproterenol induced cardiotoxicity in rats: A biochemical study. 2264 Jul 23
At high altitude (HA) hypobaric hypoxic environment manifested several pathophysiological consequences of which gastrointestinal (GI) disorder are very common phenomena. To explore the most possible clue behind this disorder intestinal flora, the major player of the GI functions, were subjected following simulated hypobaric hypoxic treatment in model animal. For this, male albino rats were exposed to 55 kPa (approximately 4872.9 m) air pressure consecutively for 30 days for 8 h/day and its small intestinal microflora, their secreted digestive enzymes and stress induced marker protein were investigated of the luminal epithelia. It was observed that population density of total aerobes significantly decreased, but the quantity of total anaerobes and Escherichia coli increased significantly after 30 days of hypoxic stress. The population density of strict anaerobes like Bifidobacterium sp., Bacteroides sp. and Lactobacillus sp. and obligate anaerobes like Clostridium perfringens and Peptostreptococcus sp. were expanded along with their positive growth direction index (GDI). In relation to the huge multiplication of anaerobes the amount of gas formation as well as content of IgA and IgG increased in duration dependent manner. The activity of some luminal enzymes from microbial origin like a-amylase, gluco-amylase, proteinase, alkaline phosphatase and
beta-glucuronidase
were also elevated in hypoxic condition. Besides, hypoxia induced in formation of malondialdehyde along with significant attenuation of catalase, glutathione peroxidase, superoxide dismutase activity and lowered
GSH
/GSSG pool in the intestinal epithelia. Histological study revealed disruption of intestinal epithelial barrier with higher infiltration of lymphocytes in lamina propia and atrophic structure. It can be concluded that hypoxia at HA modified GI microbial imprint and subsequently causes epithelial barrier dysfunction which may relate to the small intestinal dysfunction at HA.
...
PMID:Modulation of small intestinal homeostasis along with its microflora during acclimatization at simulated hypobaric hypoxia. 2543 5
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