Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.3.1 (Mg2+-ATPase)
 1,484 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A major mechanism of azole resistance in Candida albicans is overexpression of the genes encoding the ATP binding cassette transporters Cdr1p and Cdr2p due to gain-of-function mutations in Tac1p, a transcription factor of the zinc cluster family. To identify the Tac1p regulon, we analyzed four matched sets of clinical isolates representing the development of CDR1- and CDR2-mediated azole resistance by using gene expression profiling. We identified 31 genes that were consistently up-regulated with CDR1 and CDR2, including TAC1 itself, and 12 consistently down-regulated genes. When a resistant strain deleted for TAC1 was examined similarly, expression of almost all of these genes returned to levels similar to those in the matched azole-susceptible isolate. Using genome-wide location (ChIP-chip) analysis (a procedure combining chromatin immunoprecipitation with hybridization to DNA intergenic microarrays), we found 37 genes whose promoters were bound by Tac1p in vivo, including CDR1 and CDR2. Sequence analysis identified nine new genes whose promoters contain the previously reported Tac1p drug-responsive element (CGGN(4)CGG), including TAC1. In total, there were eight genes whose expression was modulated in the four azole-resistant clinical isolates in a TAC1-dependent manner and whose promoters were bound by Tac1p, qualifying them as direct Tac1p targets: CDR1, CDR2, GPX1 (putative glutathione peroxidase), LCB4 (putative sphingosine kinase), RTA3 (putative phospholipid flippase), and orf19.1887 (putative lipase), as well as IFU5 and orf19.4898 of unknown function. Our results show that Tac1p binds under nonactivating conditions to the promoters of its targets, including to its own promoter. They also suggest roles for Tac1p in regulating lipid metabolism (mobilization and trafficking) and oxidative stress response in C. albicans.
 ...
PMID:Genome-wide expression and location analyses of the Candida albicans Tac1p regulon. 1790 26

Arsenic is a known global groundwater contaminant. The organochlorine insecticide endosulfan has gained significance as an environmental pollutant due to its widespread use in the control of many food- and non-food-crop-damaging insects. The adverse effects produced by arsenic or endosulfan alone in humans and animals are well documented, but very little is known about the consequences of their coexposure. We evaluated whether their simultaneous exposure can induce oxidative stress and affect antioxidative systems and certain membrane-bound enzymes in erythrocytes of broiler chickens. Day-old chicks were exposed to 3.7 ppm of arsenic via drinking water or 30 ppm of endosulfan-mixed feed or similarly coexposed to these in the same dose levels for 60 days. At term, the impact of their coexposure was assessed by evaluating lipid peroxidation (LPO), activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST), different ATPases and acetylcholinesterase (AChE) in erythrocytes, serum glucose, and levels of glutathione (GSH) and glycosylated hemoglobin (GHb) in blood. LPO was increased with all of the treatments. Catalase was decreased with endosulfan and the coexposure, but not with arsenic, whereas GSH was decreased with arsenic and endosulfan, but not with the coexposure. All of the treatments increased SOD and GPx activities. GST activity was increased only in the coexposed birds. None of the treatments affected the activities of total ATPase and Mg2+-ATPase. Na+-K+-ATPase activity was decreased in the endosulfan-treated and the coexposed birds. All three exposures increased erythrocyte AChE activity. Endosulfan increased the serum glucose level and arsenic and endosulfan increased GHb levels, but these were not altered in the coexposed birds. Erythrocyte protein content was insignificantly decreased with these treatments. Overall, the effects of coexposure were not appreciably different from either of the agents, except on AChE, GSH, and glucose. The results do not reflect any specific type of interaction between these agents in chicken erythrocytes, but they do indicate that the coexposure induces a low level of oxidative stress, which is comparable to that induced by arsenic or endosulfan.
 ...
PMID:Effects of subchronic coexposure to arsenic and endosulfan on the erythrocytes of broiler chickens: a biochemical study. 1844 43

By decreasing water salinity gradually, the Pampus argenteus juveniles were cultured at water salinity 25, 20, 15 and 10, for 24 h, 48 h, 96 h and 120 h, respectively, with the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione-S-transferase (GST), and glutathione reductase (GR) in liver and the activities of Na+/K+- and Ga2+/Mg2+ -ATPase in gill and kidney determined. With the lowering of water salinity and the elongation of treated time, the liver SOD and GST activities had a trend of decreasing after an initial increase (P < 0.05), while the CAT activity was lower than the control except that it had a slight increase at salinity 20 cultured for 24 h and at salinity 15 cultured for 48 h (P < 0.05). The liver GPX activity had an increasing trend (P < 0.05), while the GR activity at salinity 15 cultured for 24 h increased first and then fell down to a relatively low level (P < 0.05). The Na+/K+ - and Ga2+/Mg2+-ATPase activities in the gill and kidney also decreased after an initial increase (P < 0.05), only the increase of ATPase activity at the thresholds of water salinity and treated time differed between the two organs. The results indicated that the decrease of water salinity could effectively stimulate and enhance the antioxidant enzyme activities in juvenile P. argenteus liver and the ATPase activities in its gill and kidney, and thereby, could effectively eliminate the excessive reactive oxygen species (ROS), sustain the intracellular homeostasis, and minimize the body damage. However, characterized by certain specificity and time sequentiality, the activation of test enzymes could also be inhibited when the salinity varied beyond the tolerance range of the body.
 ...
PMID:[Effects of low salinity stress on the antioxidant enzyme activities in juvenile Pampus argenteus liver and the APTase activities in its gill and kidney]. 2177 33

Brief episodes of myocardial ischemia-reperfusion (IR) employed during reperfusion after a prolonged ischemic insult may attenuate the total ischemia-reperfusion injury. This phenomenon has been termed ischemic postconditioning. In the present study, we studied the possible effect of ischemic postconditioning on an ischemic reperfusion (IR)-induced myocardium oxidative injury in rat model. Results showed that ischemic postconditioning could improve arrhythmia cordis, reduce myocardium infarction and serum creatin kinase (CK), lactate dehydrogenase (LDH) and aspartate transaminase (AST) activities in IR rats. In addition, ischemic postconditioning could still decrease myocardium malondialdehyde (MDA) level, and increased myocardium Na+-K+-ATPase, Ca2+-Mg2+-ATPase, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) activities. It can be concluded that ischemic postconditioning possesses strong protective effects against ischemia reperfusion-induced myocardium oxidative injury in IR rats.
 ...
PMID:Protective effect of ischemic postconditioning against ischemia reperfusion-induced myocardium oxidative injury in IR rats. 2245 31

American ginseng (Panax quinquefolium L.) was reported to have extensive biological activities and pharmaceutical properties. In most of the studies, the anti-fatigue effects of American ginseng are attributed to ginsenoside, and in only a few studies, they have been attributed to oligopeptides. Therefore, the aim of this study was to observe the anti-fatigue effects of small-molecule oligopeptides isolated from Panax quinquefolium L. (QOPs) in mice. At first, mice chosen for the study were randomly divided into four experimental groups; each group of mice was further divided into five subgroups: vehicle control group, whey protein group (450 mg per kg BW), and three groups of QOPs at different doses (225 mg per kg BW, 450 mg per kg BW, and 900 mg per kg BW). Test substances were given by gavage once a day for 30 days. QOPs can significantly prolong the forced swimming time, decrease the serum urea nitrogen (SUN) and blood lactate (BLA) levels, and increase the lactate dehydrogenase (LDH) activity and hepatic glycogen content. QOPs also markedly enhanced the superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity and attenuated the malondialdehyde (MDA) levels. Notably, QOPs enhanced the activity of succinate dehydrogenase (SDH), Na+-K+-ATPase, and Ca2+-Mg2+-ATPase and increased the mRNA expression of nuclear respiratory factor 1 (NRF-1) and mitochondrial transcription factor A (TFAM) and the mitochondrial DNA (mtDNA) content in skeletal muscles. These results indicate that treatment with QOPs induces anti-fatigue effects, which may be due to the inhibition of oxidative stress and the improvement of mitochondrial function in skeletal muscles. QOPs can be used as a novel natural agent for relieving physical fatigue.
 ...
PMID:Anti-fatigue effects of small-molecule oligopeptides isolated from Panax quinquefolium L. in mice. 3002 91

This study was conducted to evaluate the toxic effects of cadmium (Cd) on the kidney function and bone development in laying hens. A total of 480 Hy-line laying hens aged 38 weeks were randomly allocated into five treatments, each of which included six replicates of 16 birds. The concentrations of Cd in the diets of the five groups were 0.47, 7.58, 15.56, 30.55, and 60.67 mg/kg. Results showed that serum calcium (Ca) levels decreased significantly in the 60.67 mg Cd/kg diet group (p < 0.05). The activities of serum alkaline phosphatase (ALP) and bone ALP (BALP) decreased significantly in the 15.56, 30.55 and 60.67 mg Cd/kg diet groups (p < 0.05). The levels of parathyroid hormone (PTH) increased significantly in the 30.55 and 60.67 mg Cd/kg diet groups, and the estradiol (E2), 1,25-(OH)2-D3 and calcitonin (CT) decreased significantly with the increase of dietary Cd supplementation (p < 0.05). Histological results presented enlargements of renal tubules and tubular fibrosis in the kidney and decreased trabecular bone in the tibia. Tartrate-resistant acidic phosphatase (TRAP) staining results of tibia showed that osteoclast was significantly increased at the relatively high dose of dietary Cd (p < 0.05). In addition, the renal function indicators of blood urea nitrogen (BUN), urea acid (UA), and creatinine were significantly increased in Cd supplemented groups compared with the control group (p < 0.05). Low dose Cd exposure induced antioxidant defenses accompanying the increase in activities of catalase (CAT), glutathione peroxidase (GSH-Px), and the levels of glutathione (GSH) in renal tissue. At the same time, with the increased Cd levels, the activities of CAT, GSH-Px decreased significantly, and the level of malondialdehyde (MDA) increased significantly (p < 0.05). The activities of Na+/K+-ATPase and Ca2+/Mg2+-ATPase decreased significantly in the relatively high levels of dietary Cd (p < 0.05). These results suggest that Cd can damage renal function and induce disorders in bone metabolism of laying hens.
 ...
PMID:Dietary Cadmium Chloride Supplementation Impairs Renal Function and Bone Metabolism of Laying Hens. 3175 7