A transplantable rat Leydig cell tumour.

Erichsen, Aage; Clausen, O. P. F.; Torjesen, P.; Dahl, Eystein; Wetteland, P; Hansson, V.

doi:10.1530/acta.0.1190291

Acta Endocrinologica

1988

DOI: 10.1530/acta.0.1190291

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A transplantable rat Leydig cell tumour.

Aage Erichsen

O. P. F. Clausen

P. Torjesen³

et al.

Abstract: Growth rate and morphology were studied in a transplantable rat Leydig cell tumour (H-540) grown in intact, castrated and hypophysectomized rats. The plasma levels of pituitary hormones and testosterone were measured in the same rats. The results can be

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Cited by 3 publications

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References 10 publications

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“…In a previous study we observed stimulatory effects of a variety of hormones and drugs on the adenylate cyclase (AC) activity in membrane particles from a transplantable rat Leydig cell tumour (Erichsen et al 1984a). The strongest activator ap¬ peared to be prostaglandin E, (PGE,), which acti¬ vated the AC system 3-to 5-fold (Erichsen et al 1984a(Erichsen et al , 1986.…”

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A transplantable rat Leydig cell tumour. Properties of the prostaglandin E receptor

Erichsen

Hansson²

1989

Acta Endocrinologica

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In the present paper we have examined the properties of the prostaglandin E (PGE) receptor in a transplantable rat Leydig cell tumour (H-540). It appears that PGE 1 and PGE2 share a common receptor in membrane particles from this Leydig cell tumour. From saturation analysis and modified Hofstee plots, the specific binding sites for PGE1 can be divided into a high (25%) and low affinity state (75%) with apparent equilibrium constants of dissociation (Kd) of 2.4 \m=.\10\m=-\7 mol/1 and 4.4 \ m=. \10\ m=-\ 6 mol/l, respectively. Association rate kinetics at different temperatures employing 5 10\ m=-\ 9 mol/l [3H]PGE1 showed that specific binding was time-and temperature-dependent. At 37\s=deg\C an apparent steady state was achieved after approximately 4 h incubation. The binding of [3H]PGE1 was very tight and no dissociation was observed at 20\s=deg\Cduring the first 20 h. The free PGE1 receptor appears to be very unstable. Binding was reduced rapidly by storage at 0\ s=deg\ C,by freezing and thawing of membrane particles, and by incubation of concentrated membrane particles. Specificity curves showed that PGA1 and PGA2 displaced [3H]PGE1 from receptor to a somewhat lesser degree than PGE2 and PGE1, whereas PGs of the B, D, I and F series had little or no effect. The fact that inhibition of [3H]PGE1 binding by cold PGE1 occurred in the same concentration range as PGE1 activation of adenylate cyclase, indicates that the specific binding of PGE observed here represents functional receptors coupled to the adenylate cyclase.

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mentioning

confidence: 98%

“…The strongest activator ap¬ peared to be prostaglandin E, (PGE,), which acti¬ vated the AC system 3-to 5-fold (Erichsen et al 1984a(Erichsen et al , 1986. In a recent paper we demonstrated specific [3 ] [ binding in Percoli purified Leydig tumour cells and PGE,-stimulated testos¬ terone production in vitro (Erichsen et al 1988).…”

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confidence: 99%

A transplantable rat Leydig cell tumour. Properties of the prostaglandin E receptor

Erichsen

Hansson²

1989

Acta Endocrinologica

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Expression of cytochrome P-45017α, 3β-hydroxysteroid dehydrogenase/Δ5 → 4-isomerase, and steroid 5α-reductase in rat H540 Leydig tumor cells

Mack

Lorence

Andersson

et al. 1990

Molecular and Cellular Endocrinology

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Nongenomic effect of testosterone on chloride secretion in cultured rat efferent duct epithelia

Leung

Cheng-Chew

Wong

2001

American Journal of Physiology-Cell Physiology

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Short-circuit current (I(sc)) technique was used to investigate the role of testosterone in the regulation of chloride secretion in cultured rat efferent duct epithelia. Among the steroids tested, only testosterone, and to a lesser extent, 5alpha-dihydrotestosterone (5alpha-DHT), reduced the basal and forskolin-induced I(sc) in cultured rat efferent duct epithelia when added to the apical bathing solution. Indomethacin, a 3alpha-hydroxysteroid dehydrogenase, did not affect the inhibitory effect of 5alpha-DHT. The effect of testosterone occurred within 10-20 s upon application and was dose dependent with apparent IC(50) value of 1 microM. The effect was abolished by removal of Cl(-) but not HCO from the normal Krebs-Henseleit solution, suggesting that testosterone mainly inhibited Cl(-) secretion. The efferent duct was found to be most sensitive to testosterone, while the caput and the cauda epididymidis were only mildly sensitive. Cyproterone acetate, a steroidal antiandrogen, or flutamide, a nonsteroidal antiandrogen, did not block the effect of testosterone on the forskolin-induced I(sc), nor did protein synthesis inhibitors, cycloheximide, or actinomycin D. However, pertussis toxin, a G(i) protein inhibitor, attenuated the inhibition of forskolin-induced I(sc) by testosterone. Testosterone caused a dose-dependent inhibition of forskolin-induced rise in cAMP in efferent duct cells. It is suggested that the rapid effect of testosterone was mediated through a membrane receptor that is negatively coupled to adenylate cyclase via G(i) protein. The role of nongenomic action of testosterone in the regulation of electrolyte and fluid transport in the efferent duct is discussed.

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A transplantable rat Leydig cell tumour.

Abstract: Growth rate and morphology were studied in a transplantable rat Leydig cell tumour (H-540) grown in intact, castrated and hypophysectomized rats. The plasma levels of pituitary hormones and testosterone were measured in the same rats. The results can be

Cited by 3 publications

References 10 publications

A transplantable rat Leydig cell tumour. Properties of the prostaglandin E receptor

A transplantable rat Leydig cell tumour. Properties of the prostaglandin E receptor

Expression of cytochrome P-45017α, 3β-hydroxysteroid dehydrogenase/Δ5 → 4-isomerase, and steroid 5α-reductase in rat H540 Leydig tumor cells

Nongenomic effect of testosterone on chloride secretion in cultured rat efferent duct epithelia

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