Characterization of a female-specific hepatic mitochondrial cytochrome P-450 whose steady-state level is modulated by testosterone

Biochemistry ◽  
1991 ◽  
Vol 30 (34) ◽  
pp. 8323-8330 ◽  
Author(s):  
Sankar Addya ◽  
Yong Mu Zheng ◽  
Rass M. Shayiq ◽  
Jianying Fan ◽  
Narayan G. Avadhani
Keyword(s):  
Steady State ◽  
State Level ◽  
Steady State Level ◽  
Mitochondrial Cytochrome ◽  
Female Specific ◽  
Cytochrome P 450

scholarly journals Characterization of the Bradyrhizobium japonicum ftsH Gene and Its Product

1999 ◽  
Vol 181 (23) ◽  
pp. 7394-7397 ◽  
Author(s):  
Franz Narberhaus ◽  
Carmen Urech ◽  
Hauke Hennecke
Keyword(s):  
Escherichia Coli ◽  
Steady State ◽  
Western Blot ◽  
Bradyrhizobium Japonicum ◽  
State Level ◽  
Growth Conditions ◽  
Cellular Function ◽  
Steady State Level

ABSTRACT The Bradyrhizobium japonicum ftsH gene was cloned by using a set of widely applicable degenerated oligonucleotides. Western blot experiments indicated that the FtsH protein was produced under standard growth conditions and that it was not heat inducible. Attempts to delete the ftsH gene in B. japonicum failed, suggesting a pivotal cellular function of this gene. The expression ofB. japonicum ftsH in an ftsH-negativeEscherichia coli strain significantly enhanced the fitness of this mutant and reduced the steady-state level of ς32.

scholarly journals Characterization of the calcium-sequestering process associated with human platelet intracellular membranes isolated by free-flow electrophoresis

1984 ◽  
Vol 222 (2) ◽  
pp. 413-417 ◽  
Author(s):  
S Menashi ◽  
K S Authi ◽  
F Carey ◽  
N Crawford
Keyword(s):  
Steady State ◽  
Human Platelet ◽  
State Level ◽  
Free Flow ◽  
Ionophore A23187 ◽  
Steady State Level ◽  
Uptake Process ◽  
Steady State Levels ◽  
Gradient Fractionation

By using density-gradient fractionation and high-voltage free-flow electrophoresis, human platelet membranes were separated into highly purified subfractions of surface (SM) and intracellular (IM) origin. Associated exclusively with the IM fraction is an ATP-dependent Ca2+ uptake that, in the absence of oxalate, reaches steady-state levels in 5-10 min. When Ca2+-EGTA buffers were used to control the external Ca2+ concentrations (range 0.1-50 microM) there was an increase in the intravesicle steady-state level of Ca2+ up to 10 microM external Ca2+ concentration. Above this level the intravesicle space becomes saturated at a concentration between 10 and 20 nmol of Ca2+ X (mg of protein)-1. The ionophore A23187 promotes a rapid and almost total release of the sequestered Ca2+ (greater than 90%, t1/2 1-2 min). The presence of oxalate in the external medium greatly enhances the Ca2+ accumulation to levels as high as 200 nmol X (mg of protein)-1, but the uptake process is more variable and rarely reaches steady-state level even after 2 h incubation. Moreover, accumulation in the presence of oxalate effects ionophore release with less than 80% depletion in 45-60 min. These findings, taken together with the known presence in the platelet of a wide variety of functional and metabolic processes triggered by this cation, suggest that the platelet IM has a key role in controlling cytosolic Ca2+ concentrations.

Possible Interaction of Ranitidine with Phenytoin

1988 ◽  
Vol 22 (12) ◽  
pp. 979-980 ◽  
Author(s):  
Diane Bramhall ◽  
Marc Levine
Keyword(s):  
Steady State ◽  
Animal Studies ◽  
Inhibitory Action ◽  
Clinical Investigation ◽  
State Level ◽  
Steady State Level ◽  
Factors Affecting ◽  
Steady State Serum ◽  
Cytochrome P 450 ◽  
Hepatic Cytochrome

Clinical and animal studies have shown that cimetidine and ranitidine can inhibit hepatic cytochrome P-450-mediated metabolism of a variety of other drugs. This occurs to a lesser extent with ranitidine than with cimetidine at doses commonly used to treat gastric acid-related disorders. We recently observed a 66-year-old man whose steady-state serum phenytoin concentration increased 40 percent during one month after the addition to his regimen of ranitidine 150 mg bid. Because the ranitidine had been prescribed postsurgically for prophylaxis, it was discontinued and the patient's serum phenytoin concentration declined to the previous steady-state level with no change in dose or other drug therapy. This case indicates that the serum phenytoin concentration should be monitored for the first month after the addition of ranitidine to the regimens of patients on chronic phenytoin therapy. As well, further clinical investigation of factors affecting the interindividual inhibitory action of ranitidine is warranted.

Tacrolimus initial steady state level in post-transplant cyclophosphamide-based GvHD prophylaxis regimens

2021 ◽  
Author(s):  
Janny M. Yao ◽  
Dongyun Yang ◽  
Mary C. Clark ◽  
Salman Otoukesh ◽  
Thai Cao ◽  
...  
Keyword(s):  
Steady State ◽  
State Level ◽  
Steady State Level ◽  
Post Transplant ◽  
Gvhd Prophylaxis

Ascorbate and glutathione homeostasis in vascular smooth muscle cells: cooperation with endothelial cells

1998 ◽  
Vol 275 (4) ◽  
pp. C1031-C1039 ◽  
Author(s):  
Ilia Voskoboinik ◽  
Karin Söderholm ◽  
Ian A. Cotgreave
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Steady State ◽  
Smooth Muscle Cells ◽  
Umbilical Vein ◽  
State Level ◽  
Muscle Cells ◽  
Free Access ◽  
Steady State Level ◽  
Human Umbilical Vein

Human umbilical vein smooth muscle cells (HUVSMCs) utilize extracellular cystine, glutathione (GSH), and N-acetylcysteine (NAC) to synthesize cellular GSH. Extracellular cystine was effective from 5 μM, whereas GSH and NAC were required at 100 μM for comparable effects. The efficacy of extracellular GSH was dependent on de novo GSH synthesis, indicating a dependence on cellular γ-glutamyltransferase (glutamyl transpeptidase). Coculture of syngenetic HUVSMCs and corresponding human umbilical vein endothelial cells (HUVECs) on porous supports restricted cystine- or GSH-stimulated synthesis of HUVSMC GSH when supplied on the “luminal” endothelial side. Thus HUVSMC GSH rapidly attained a steady-state level below that achieved in the absence of interposed HUVECs. HUVSMCs also readily utilize both reduced ascorbate (AA) and oxidized dehydroascorbate (DHAA) over the range 50–500 μM. Phloretin effectively blocked both AA- and DHAA-stimulated assimilation of intracellular AA, indicating a role for a glucose transporter in their transport. Uptake of extracellular AA was also sensitive to extracellular, but not intracellular, thiol depletion. When AA was applied to the endothelial side of the coculture model, assimilation of intracellular AA in HUVSMCs was restricted to a steady-state level below that achieved by free access.

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