Inhibition of iodide accumulation by perchlorate and thiocyanate in a model of the thyroid iodide transport system

1983 ◽  
Vol 104 (4) ◽  
pp. 456-461 ◽  
Author(s):  
Koshi Saito ◽  
Kunihiro Yamamoto ◽  
Takaji Takai ◽  
Sho Yoshida
Keyword(s):  
Plasma Membrane ◽  
Transport System ◽  
Competitive Inhibitor ◽  
Biological Model ◽  
Phospholipid Vesicles ◽  
Iodide Transport ◽  
Plot Analysis ◽  
Soybean Phospholipids ◽  
Slight Depression ◽  
Burk Plot

Abstract. The manner of inhibition of thyroid I− accumulation by perchlorate (ClO4−) and thiocyanate (SCN−) was studied using a newly developed biological model of the I− transport system. ClO4− inhibited I− accumulation in phospholipid vesicles made from thyroid plasma membrane and soybean phospholipids by decreasing Na+-dependent I− influx. The anion did not at all induce I− leakage from the vesicles. On the basis of Lineweaver-Burk plot analysis, it did not change Vmax for I− concentration. These results suggest that ClO4− is a competitive inhibitor of thyroid I− transport. In contrast, SCN− did increase I− leakage from the phospholipid vesicles to diminish I− accumulation. This anion might cause only slight depression of Na+-dependent I− entry, if any. The results do not support the idea that SCN− may be a competitive inhibitor, in spite of the fact that the anion did not change Vmax for I− transport on the basis of Lineweaver-Burk plot analysis.

scholarly journals ETHIDIUM BROMIDE INHIBITION OF NAA-INDUCED ROOTING IN MUNG BEAN CUTTINGS

HortScience ◽  
1992 ◽  
Vol 27 (6) ◽  
pp. 670f-671
Author(s):  
Francis H. Witham ◽  
Charles W. Heuser ◽  
Jun Chen
Keyword(s):  
Ethidium Bromide ◽  
Mung Bean ◽  
Kinetic Studies ◽  
Competitive Inhibitor ◽  
Progressive Increase ◽  
Transcriptional Level ◽  
Plot Analysis ◽  
Similar Kinetic ◽  
Influence Gene Expression ◽  
Burk Plot

Ethidium bromide (EB), at 10-5 to 10-4 M, progressively inhibits NAA-induced rooting of mung bean cuttings. Cycloheximide (CH), 6-methylpurine (6-MP) and kinetin (KIN) also inhibited rooting at the same concentrations, although CH and 6-MP were more effective. At 70 and up to 130 hours of incubation, after cuttings received a 1-ml pulse of NAA (10-4 M), they exhibited a progressive increase in the number of observed adventitious roots. The addition of one of the inhibitors, 6-MP, EB or KIN to cuttings, pulsed 48 hours earlier with NAA, showed an initial slight inhibition with increased inhibition over time. CH, however, inhibited rooting immediately after addition. From these and other similar kinetic studies, it appears that 6-MP, EB and KIN operate at the transcriptional level and that CH inhibits translation. Lineweaver-Burk plot analysis of NAA-induced rooting inhibition showed that EB may act as a competitive inhibitor of NAA. Since EB is a known intercalating agent and competitively inhibits NAA-induced rooting, NAA may influence gene expression by ultimately binding to DNA. Studies with space-filling and computer-generated models show that both NAA and EB can bind to certain dinucleotides by an intercalation mechanism.

Iodide transport of thyroid plasma membranes

1981 ◽  
Vol 98 (2) ◽  
pp. 227-233 ◽  
Author(s):  
Y. Endo ◽  
H. Nakagawa ◽  
E. Aikawa ◽  
S. Ohtaki
Keyword(s):  
Plasma Membrane ◽  
Kinetic Study ◽  
Transport System ◽  
Plasma Membranes ◽  
External Medium ◽  
Membrane Vesicles ◽  
Monovalent Cations ◽  
Transport Activity ◽  
Iodide Concentration ◽  
Iodide Transport

Abstract. Plasma membranes consisting of closed vesicles were isolated from hog thyroid homogenate. The membrane vesicles showed uphill transport of iodide from an external medium containing monovalent cations, of which K+ induced iodide transport more potently than Na+. The activity of the iodide transport expressed as T/M[I−] was as little as 3 to 11 in the presence of K+, but was invariably present. The ratio reached a maximum within about 10 min and then decreased fairly rapidly to unity. The addition of SCN− or ClO−4 to the external medium inhibited iodide transport. The transport activity was found to be maximum at pH 7.0 to 7.5 in the external medium. A kinetic study showed that the transport rate was saturated with respect to the iodide concentration. These observations suggested the presence of a carrier-mediated iodide transport system which was coupled with K+ flux across the plasma membrane.

Mechanism of cystine reaccumulation by cystinotic fibroblasts in vitro

1990 ◽  
Vol 10 (2) ◽  
pp. 225-229 ◽  
Author(s):  
Susan Forster ◽  
Lynne Scarlett ◽  
John B. Lloyd
Keyword(s):  
Plasma Membrane ◽  
Culture Medium ◽  
Human Fibroblasts ◽  
Competitive Inhibitor ◽  
Free Medium ◽  
Lysosome Membrane ◽  
Putative Mechanism

It is well established that when cystine-depleted cystinotic cells are cultured in cystine-containing medium, they reaccumulate cystine within their lysosomes more rapidly than when cultured in cystine-free medium. This has been a puzzling result, since the lysosome membrane of cystinotic cells is impermeable to cystine. To probe the mechanism of cystine reaccumulation, we have measured reaccumulation in the presence of colchicine, an inhibitor of pinocytosis, or of glutamate, a competitive inhibitor of cystine transport into human fibroblasts. Colchicine had no effect, thus eliminating pinocytosis as a putative mechanism for cystine translocation from the culture medium to the lysosomes. Glutamate, however, strongly inhibited cystine reaccumulation. It is concluded that the true mechanism is as follows. 1. Exogenous cystine crosses the plasma membrane on the cystine-glutamate porter. 2. Cystine is reduced in the cytoplasm by GSH. 3. The cysteine that is generated enters the lysosome, where it becomes cystine by participating in the reduction of cystine residues during intralysosomal proteolysis, or by autoxidation.

Sex differences in hepatic fatty acid uptake reflect a greater affinity of the transport system in females

1992 ◽  
Vol 263 (3) ◽  
pp. G380-G385 ◽  
Author(s):  
D. Sorrentino ◽  
S. L. Zhou ◽  
E. Kokkotou ◽  
P. D. Berk
Keyword(s):  
Plasma Membrane ◽  
Fatty Acid ◽  
Transport System ◽  
Fatty Acid Uptake ◽  
Surface Expression ◽  
Female Rats ◽  
Acid Uptake ◽  
Fatty Acid Binding ◽  
Male And Female Rats

In this study, we examined the hypothesis that the reported sex difference in hepatic free fatty acid (FFA) uptake involves the putative FFA transport system, the plasma membrane fatty acid binding protein (FABPpm). In hepatocytes isolated from both male and female rats, initial [3H]oleate uptake velocity reflected transmembrane influx and not subsequent metabolism and was a saturable function of the unbound oleate concentration. Although Vmax values were similar (61 +/- 2 vs. 65 +/- 5 pmol.min-1.5 x 10(4) cells-1 for females and males, respectively), the apparent Km was significantly smaller in females (40 +/- 4 vs. 90 +/- 11 nM; P less than 0.05), reflecting faster influx velocities in female cells over a range of unbound oleate concentrations. The oleate efflux rate constant was also greater in females (0.280 +/- 0.014 vs. 0.198 +/- 0.020 min-1; P less than 0.05) despite their greater hepatic content of cytosolic FABP. Finally, despite the greater rates of transmembrane FFA flux in female hepatocytes, the surface expression of FABPpm was virtually identical in the two sexes (2.5 +/- 0.5 vs. 2.4 +/- 0.4 microgram/10(6) cells). Collectively, these data indicate that at FFA-to-albumin ratios occurring in vivo the plasma membrane of female hepatocytes transports oleate bidirectionally at a greater rate than that of male hepatocytes. A sex-related difference in the functional affinity of FABPpm for FFA appears the most likely explanation for the greater oleate uptake in females.

A natural protective mechanism against hyperglycaemia in vascular endothelial and smooth-muscle cells: role of glucose and 12-hydroxyeicosatetraenoic acid

2002 ◽  
Vol 362 (2) ◽  
pp. 413-422 ◽  
Author(s):  
Evgenia ALPERT ◽  
Arie GRUZMAN ◽  
Hanan TOTARY ◽  
Nurit KAISER ◽  
Reuven REICH ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Plasma Membrane ◽  
Smooth Muscle Cells ◽  
Transport System ◽  
Muscle Cells ◽  
Vascular Endothelial ◽  
Vascular Cells ◽  
Hexose Transport ◽  
Glut 1 ◽  
Glucose Levels

Bovine aortic endothelial and smooth-muscle cells down-regulate the rate of glucose transport in the face of hyperglycaemia, thus providing protection against deleterious effects of increased intracellular glucose levels. When exposed to high glucose concentrations these cells reduced the mRNA and protein content of their typical glucose transporter, GLUT-1, as well as its plasma-membrane abundance. Inhibition of the lipoxygenase (LO) pathway, and particularly 12-LO, reversed this glucose-induced down-regulatory process and restored the rate of hexose transport to the level seen in vascular cells exposed to normal glucose levels. This reversal was accompanied by increased levels of GLUT-1 mRNA and protein, as well as of its plasma-membrane content. Exposure of the vascular cells to elevated glucose concentrations increased by 2–3-fold the levels of cell-associated and secreted 12-hydroxyeicosatetraenoic acid (12-HETE), the product of 12-LO. Inhibition of 15- and 5-LO, cyclo-oxygenases 1 and 2, and eicosanoid-producing cytochrome P450 did not modify the hexose-transport system in vascular cells. These results suggest a role for HETEs in the autoregulation of hexose transport in vascular cells. 8-Iso prostaglandin F2α, a non-enzymic oxidation product of arachidonic acid, had no effect on the hexose-transport system in vascular cells exposed to hyperglycaemic conditions. Taken together, these findings show that hyperglycaemia increases the production rate of 12-HETE, which in turn mediates the down-regulation of GLUT-1 expression and the glucose-transport system in vascular endothelial and smooth-muscle cells.

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