scholarly journals GSH and Zinx Supplementation Attenuate Cadmium-Induced Cellular Stress and Stimulation of Choline Uptake in Cultured Neonatal Rat Choroid Plexus Epithelia

2021 ◽  
Vol 22 (16) ◽  
pp. 8857
Author(s):  
Samantha D. Francis Stuart ◽  
Alice R. Villalobos
Keyword(s):  
Choroid Plexus ◽  
Cellular Stress ◽  
Stress Protein ◽  
Buthionine Sulfoximine ◽  
Neonatal Rat ◽  
Choline Uptake ◽  
Glutamate Cysteine Ligase ◽  
Rate Limiting ◽  
Stimulation Of

Choroid plexus (CP) sequesters cadmium and other metals, protecting the brain from these neurotoxins. These metals can induce cellular stress and modulate homeostatic functions of CP, such as solute transport. We previously showed in primary cultured neonatal rat CP epithelial cells (CPECs) that cadmium induced cellular stress and stimulated choline uptake at the apical membrane, which interfaces with cerebrospinal fluid in situ. Here, in CPECs, we characterized the roles of glutathione (GSH) and Zinx supplementation in the adaptive stress response to cadmium. Cadmium increased GSH and decreased the reduced GSH-to-oxidized GSH (GSSG) ratio. Heat shock protein-70 (Hsp70), heme oxygenase (HO-1), and metallothionein (Mt-1) were induced along with the catalytic and modifier subunits of glutamate cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis. Inhibition of GCL by l-buthionine sulfoximine (BSO) enhanced stress protein induction and stimulation of choline uptake by cadmium. Zinx alone did not induce Hsp70, HO-1, or GCL subunits, or modulate choline uptake. Zinx supplementation during cadmium exposure attenuated stress protein induction and stimulation of choline uptake; this effect persisted despite inhibition of GSH synthesis. These data indicated up-regulation of GSH synthesis promotes adaptation to cadmium-induced cellular stress in CP, but Zinx may confer cytoprotection independent of GSH.

scholarly journals Stress-induced stimulation of choline transport in cultured choroid plexus epithelium exposed to low concentrations of cadmium

2014 ◽  
Vol 306 (5) ◽  
pp. R291-R303 ◽  
Author(s):  
Robin K. Young ◽  
Alice R. A. Villalobos
Keyword(s):  
Heavy Metals ◽  
Map Kinase ◽  
Choroid Plexus ◽  
Stress Proteins ◽  
Neonatal Rat ◽  
Choline Uptake ◽  
Choroid Plexus Epithelium ◽  
Choline Transport ◽  
Low Concentrations ◽  
Stimulation Of

The choroid plexus epithelium forms the blood-cerebrospinal fluid barrier and accumulates essential minerals and heavy metals. Choroid plexus is cited as being a “sink” for heavy metals and excess minerals, serving to minimize accumulation of these potentially toxic agents in the brain. An understanding of how low doses of contaminant metals might alter transport of other solutes in the choroid plexus is limited. Using primary cultures of epithelial cells isolated from neonatal rat choroid plexus, our objective was to characterize modulation of apical uptake of the model organic cation choline elicited by low concentrations of the contaminant metal cadmium (CdCl2). At 50–1,000 nM, cadmium did not directly decrease or increase 30-min apical uptake of 10 μM [3H]choline. However, extended exposure to 250–500 nM cadmium increased [3H]choline uptake by as much as 75% without marked cytotoxicity. In addition, cadmium induced heat shock protein 70 and heme oxygenase-1 protein expression and markedly induced metallothionein gene expression. The antioxidant N-acetylcysteine attenuated stimulation of choline uptake and induction of stress proteins. Conversely, an inhibitor of glutathione synthesis l-buthionine-sulfoximine (BSO) enhanced stimulation of choline uptake and induction of stress proteins. Cadmium also activated ERK1/2 MAP kinase. The MEK1 inhibitor PD98059 diminished ERK1/2 activation and attenuated stimulation of choline uptake. Furthermore, inhibition of ERK1/2 activation abated stimulation of choline uptake in cells exposed to cadmium with BSO. These data indicate that in the choroid plexus, exposure to low concentrations of cadmium may induce oxidative stress and consequently stimulate apical choline transport through activation of ERK1/2 MAP kinase.

Aging reduces responsiveness to BSO- and heat stress-induced perturbations of glutathione and antioxidant enzymes

2005 ◽  
Vol 289 (4) ◽  
pp. R1035-R1041 ◽  
Author(s):  
Joanna P. Morrison ◽  
Mitchell C. Coleman ◽  
Elizabeth S. Aunan ◽  
Susan A. Walsh ◽  
Douglas R. Spitz ◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Heat Stress ◽  
Redox Homeostasis ◽  
Buthionine Sulfoximine ◽  
Sod Activity ◽  
Glutamate Cysteine Ligase ◽  
Age Related ◽  
Rate Limiting ◽  
And Oxidative Stress

Aging alters cellular responses to both heat and oxidative stress. Thiol-mediated metabolism of reactive oxygen species (ROS) is believed to be important in aging. To begin to determine the role of thiols in aging and heat stress, we depleted liver glutathione (GSH) by administering l-buthionine sulfoximine (BSO) in young (6 mo) and old (24 mo) Fisher 344 rats before heat stress. Animals were given BSO (4 mmol/kg ip) or saline (1 ml ip) 2 h before heat stress and subsequently heated to a core temperature of 41°C over a 90-min period. Liver tissue was collected before and 0, 30, and 60 min after heat stress. BSO inhibited glutamate cysteine ligase (GCL, the rate-limiting enzyme in GSH synthesis) catalytic activity and resulted in a decline in liver GSH and GSSG that was more pronounced in young compared with old animals. Catalase activity did not change between groups until 60 min after heat stress in young BSO-treated rats. Young animals experienced a substantial and persistent reduction in Cu,Zn-SOD activity with BSO treatment. Mn-SOD activity increased with BSO but declined after heat stress. The differences in thiol depletion observed between young and old animals with BSO treatment may be indicative of age-related differences in GSH compartmentalization that could have an impact on maintenance of redox homeostasis and antioxidant balance immediately after a physiologically relevant stress. The significant changes in antioxidant enzyme activity after GSH depletion suggest that thiol status can influence the regulation of other antioxidant enzymes.

Distension of the uterus induces HspB1 expression in rat uterine smooth muscle

2011 ◽  
Vol 301 (5) ◽  
pp. R1418-R1426 ◽  
Author(s):  
B. G. White ◽  
D. J. MacPhee
Keyword(s):  
Protein Expression ◽  
Stress Protein ◽  
Late Pregnancy ◽  
Cytoplasmic Localization ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Myometrial Cells ◽  
Uterine Smooth Muscle ◽  
Stimulation Of

The uterine musculature, or myometrium, demonstrates tremendous plasticity during pregnancy under the influences of the endocrine environment and mechanical stresses. Expression of the small stress protein heat shock protein B1 (HspB1) has been reported to increase dramatically during late pregnancy, a period marked by myometrial hypertrophy caused by fetal growth-induced uterine distension. Thus, using unilaterally pregnant rat models and ovariectomized nonpregnant rats with uteri containing laminaria tents to induce uterine distension, we examined the effect of uterine distension on myometrial HspB1 expression. In unilaterally pregnant rats, HspB1 mRNA and Ser15-phosphorylated HspB1 (pSer15 HspB1) protein expression were significantly elevated in distended gravid uterine horns at days 19 and 23 (labor) of gestation compared with nongravid horns. Similarly, pSer15 HspB1 protein in situ was only readily detectable in the distended horns compared with the nongravid horns at days 19 and 23; however, pSer15 HspB1 was primarily detectable in situ at day 19 in membrane-associated regions, while it had primarily a cytoplasmic localization in myometrial cells at day 23. HspB1 mRNA and pSer15 HspB1 protein expression were also markedly increased in ovariectomized nonpregnant rat myometrium distended for 24 h with laminaria tents compared with empty horns. Therefore, uterine distension plays a major role in the stimulation of myometrial HspB1 expression, and increased expression of this small stress protein could be a mechanoadaptive response to the increasing uterine distension that occurs during pregnancy.

scholarly journals Removal of Cd(II) from Micro-Polluted Water by Magnetic Core-Shell Fe3O4@Prussian Blue

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2497
Author(s):  
Xinxin Long ◽  
Huanyu Chen ◽  
Tijun Huang ◽  
Yajing Zhang ◽  
Yifeng Lu ◽  
...  
Keyword(s):  
Prussian Blue ◽  
Co Adsorption ◽  
Magnetic Core ◽  
Diameter Distribution ◽  
Polluted Water ◽  
Core Shell ◽  
Freundlich Model ◽  
Rate Limiting Step ◽  
Rate Limiting

A novel core-shell magnetic Prussian blue-coated Fe3O4 composites (Fe3O4@PB) were designed and synthesized by in-situ replication and controlled etching of iron oxide (Fe3O4) to eliminate Cd (II) from micro-polluted water. The core-shell structure was confirmed by TEM, and the composites were characterized by XRD and FTIR. The pore diameter distribution from BET measurement revealed the micropore-dominated structure of Fe3O4@PB. The effects of adsorbents dosage, pH, and co-existing ions were investigated. Batch results revealed that the Cd (II) adsorption was very fast initially and reached equilibrium after 4 h. A pH of 6 was favorable for Cd (II) adsorption on Fe3O4@PB. The adsorption rate reached 98.78% at an initial Cd (II) concentration of 100 μg/L. The adsorption kinetics indicated that the pseudo-first-order and Elovich models could best describe the Cd (II) adsorption onto Fe3O4@PB, indicating that the sorption of Cd (II) ions on the binding sites of Fe3O4@PB was the main rate-limiting step of adsorption. The adsorption isotherm well fitted the Freundlich model with a maximum capacity of 9.25 mg·g−1 of Cd (II). The adsorption of Cd (II) on the Fe3O4@PB was affected by co-existing ions, including Cu (II), Ni (II), and Zn (II), due to the competitive effect of the co-adsorption of Cd (II) with other co-existing ions.

scholarly journals Uric Acid Is a Genuine Metabolite of Penicillium cyclopium and Stimulates the Expression of Alkaloid Biosynthesis in This Fungus

2002 ◽  
Vol 68 (4) ◽  
pp. 1524-1533 ◽  
Author(s):  
Florian Helbig ◽  
Jörg Steighardt ◽  
Werner Roos
Keyword(s):  
Uric Acid ◽  
Low Molecular Weight ◽  
Alkaloid Production ◽  
Alkaloid Biosynthesis ◽  
Penicillium Cyclopium ◽  
Measurable Activity ◽  
Reduced Rate ◽  
Rate Limiting

ABSTRACT On searching for endogenous, low-molecular-weight effectors of benzodiazepine alkaloid biosynthesis in Penicillium cyclopium uric acid was isolated from ethanolic or autoclaved mycelial extracts of this fungus. The isolation was based on a three-step high-pressure liquid chromatography procedure guided by a microplate bioassay, and uric acid was identified by mass spectrometry and the uricase reaction. Conidiospore suspensions that were treated with this compound during the early phase of outgrowth developed emerged cultures with an enhanced rate of alkaloid production. Uric acid treatment did not increase the in vitro measurable activity of the rate-limiting biosynthetic enzyme, cyclopeptine synthetase. However, these cultures displayed a reduced rate of uptake of the alkaloid precursor l-phenylalanine into the vacuoles of the hyphal cells as assayed in situ. It is suggested that the depressed capacity of vacuolar uptake caused by the contact of outgrowing spores with uric acid liberated from hyphal cells results in an enhanced availability of the precursor l-phenylalanine in the cytoplasm and thus accounts at least in part for the increase in alkaloid production.

scholarly journals Flow fields associated with in situ mineral leaching

1994 ◽  
Vol 36 (2) ◽  
pp. 133-151 ◽  
Author(s):  
Lawrence K. Forbes ◽  
Anthony M. Watts ◽  
Graeme A. Chandler
Keyword(s):  
Simple Model ◽  
Free Boundary ◽  
Numerical Method ◽  
Flow Rate ◽  
Recovery Rate ◽  
Flow Fields ◽  
Vertical Line ◽  
Rate Limiting ◽  
Mineral Leaching

AbstractA simple model for underground mineral leaching is considered, in which liquor is injected into the rock at one point and retrieved from the rock by being pumped out at another point. In its passage through the rock, the liquor dissolves some of the ore of interest, and this is therefore recovered in solution. When the injection and recovery points lie on a vertical line, the region of wetted rock forms an axi-symmetric plume, the surface of which is a free boundary. We present an accurate numerical method for the solution of the problem, and obtain estimates for the maximum possible recovery rate of the liquor, as a fraction of the injected flow rate. Limiting cases are discussed, and other geometries for fluid recovery are considered.

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