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Title: Effects of lanthanides on ornithine decarboxylase induction, cell volume changes and calcium inflow in reuber H-35 rat hepatoma cells
Authors: Kwok, Platini Peng Fei
Department: Dept. of Biology and Chemistry
Degree: Master of Philosophy
Issue Date: 1997
Publisher: City University of Hong Kong
Subjects: Ornithine decarboxylase
Notes: Bibliography: leaves 136-155.
CityU Call Number: QP613.O75 K9 1997
Thesis (M.Phil.)--City University of Hong Kong, 1997
xii, 155 leaves : ill. ; 30 cm.
Type: Thesis
Abstract: To understand the interrelationship of ornithine decarboxylase (ODC) induction, cell volume changes and calcium inflow, the effects of the lanthanides (Ln3+) such as lanthanum (La3+), gadolinium (Gd3+), europium(Eu3+) and ytterbium (Yb3+) were studied. In a normal buffered glucose/salt medium, Ln3+ did not induce ODC. Low concentrations (20-200 µM) of Gd3+, Eu3+ and Yb3+ enhanced ASN-induced ODC activity but high concentrations (> 500 µM) of the ions did the opposite. La3+ inhibited enzyme induction at high concentrations (1000 µM). In Ca2+-free medium, only Gd3+ could stimulate ASN-induced ODC. In a hypotonic medium, ODC induction was increased by low concentrations (10-200 µM) of anyone of the four Ln3+ but was inhibited by high concentrations (> 500 µM) of these ions. In a ca2'-free medium, Gd3+, Eu3- and Yb3+ enhanced hypotonicity-induced ODC activity. Cell volume changes induced by ASN or hypotonic treatment was not drastically affected by 5 µM Ln3+, either in the presence or absence of extracellular Ca2+. However, in the presence of 2 mM extracellular Ca2+, addition of 25 µM Ln3+ increased the ASN-caused cell swelling and the hypotonicity-caused initial cell swelling and RVD. In the absence of extracellular Ca2+, 25 µM Ln3+ partially stalled the ASN-caused cell swelling and the hypotonicity-caused initial cell swelling and RVD to control levels. It was found that Gd3+ had stimulatory effect on the initial rate of 45 Ca2+ uptake. Gd3+ was most effective at 20 µM in ASN-treated and at 50 µM in hypotonicity-treated cells. Gd3+ was also found to be able to increase Ca2+ accumulation but ASN or hypotonic treatment alone could not. The stimulation of Ca2+ uptake by Gd3+ was also concentration dependent with the maximum at 20 µM Gd3+. Hypotonic treatment and the action of Gd3+ was synergistic on the accumulation of cellular Ca2+. Gd3+ -sensitive stretch activated calcium inflow system(s) may be present in H-35 cells which could be activated by ASN or hypotonic treatment. Micro-molar of Ln3+ was enough to elevate initial basal 45Ca2+ uptake with a maximal stimulation at 50 µM Gd3- and 20 µM La3+. As Ln3+ affected only the initial basal rate of 45Ca2+ uptake but had no effects on steady rate of 45Ca2+ uptake, it suggested that they activated the Ln3+-activated calcium inflow system(s) which then quickly returned to normal. The stimulation of initial basal 45Ca2+ uptake by Ln3+ was not related to their ionic sizes. The destruction of Ca2+ gradient between ER and cytoplasm by thapsigargin, an effective inhibitor of Ca2+ active transport from cytoplasm to ER, did not have any effect on the La3+ and Gd3+ up-regulated initial rate of 45Ca2+ uptake. Vasopressin, a hormone that stimulates Ca2+ inflow through receptor activated calcium inflow system(s) (RACSs), raised only the steady rate of 45Ca2- uptake while Gd3+ and La3+ raised only the initial rate of 45Ca2+ uptake. G3+ and La3+ acted independently of vasopressin and vice versa. Presumably, Ln3+-activated inflow system(s) is different from RACSs and other calcium inflow system(s) or channel(s).
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