Agents that increase phosphatidic acid inhibit the LH-induced testosterone production

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Standard

Agents that increase phosphatidic acid inhibit the LH-induced testosterone production. / Lauritzen, L.; Nielsen, L.-L.A.; Vinggaard, Anne Marie; Hansen, Harald S.

I: Molecular and Cellular Endocrinology, Bind 104, Nr. 2, 01.09.1994, s. 229-235.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Lauritzen, L, Nielsen, L-LA, Vinggaard, AM & Hansen, HS 1994, 'Agents that increase phosphatidic acid inhibit the LH-induced testosterone production', Molecular and Cellular Endocrinology, bind 104, nr. 2, s. 229-235.

APA

Lauritzen, L., Nielsen, L-LA., Vinggaard, A. M., & Hansen, H. S. (1994). Agents that increase phosphatidic acid inhibit the LH-induced testosterone production. Molecular and Cellular Endocrinology, 104(2), 229-235.

Vancouver

Lauritzen L, Nielsen L-LA, Vinggaard AM, Hansen HS. Agents that increase phosphatidic acid inhibit the LH-induced testosterone production. Molecular and Cellular Endocrinology. 1994 sep 1;104(2):229-235.

Author

Lauritzen, L. ; Nielsen, L.-L.A. ; Vinggaard, Anne Marie ; Hansen, Harald S. / Agents that increase phosphatidic acid inhibit the LH-induced testosterone production. I: Molecular and Cellular Endocrinology. 1994 ; Bind 104, Nr. 2. s. 229-235.

Bibtex

@article{c1a2dbc054aa4e0bad22b6f376e5cbc1,
title = "Agents that increase phosphatidic acid inhibit the LH-induced testosterone production",
abstract = "The results of the present study point to phosphatidic acid (PtdOH) as a possible intracellular messenger, which might be involved in local modulation of testicular testosterone production in vivo. Propranolol (27-266 µM) induced an increased level of [H]PtdOH in isolated rat Leydig cells, prelabeled with [H]myristate, and at the same time a strong dose-dependent inhibition of the acute testosterone production stimulated by luteinizing hormone (LH). The inhibition was not bypassed by the addition of dibutyryl-cAMP but was overcome, when 22(R)-hydroxycholesterol was added as a direct substrate for cytochrome P-450 side chain cleavage enzyme. Thus, the inhibition appears to be exerted at a point distal to cAMP-generation but before the first enzyme in the testosterone synthetic pathway. Treatment with other agents (4{\ss}-phorbol 12-myristate 13-acetate (PMA), A23187, and sphingosine) giving rise to increases in the PtdOH-level resulted in the inhibition of the LH-induced testosterone formation as well, thus indicating a connection between the two effects. Furthermore, we were able to demonstrate a highly significant correlation between the PtdOH-increase and the inhibition of the LH-stimulated testosterone production. This may suggest a causal relationship between these two parameters.",
author = "L. Lauritzen and L.-L.A. Nielsen and Vinggaard, {Anne Marie} and Hansen, {Harald S.}",
year = "1994",
month = "9",
day = "1",
language = "English",
volume = "104",
pages = "229--235",
journal = "Molecular and Cellular Endocrinology",
issn = "0303-7207",
publisher = "Elsevier Ireland Ltd",
number = "2",

}

RIS

TY - JOUR

T1 - Agents that increase phosphatidic acid inhibit the LH-induced testosterone production

AU - Lauritzen, L.

AU - Nielsen, L.-L.A.

AU - Vinggaard, Anne Marie

AU - Hansen, Harald S.

PY - 1994/9/1

Y1 - 1994/9/1

N2 - The results of the present study point to phosphatidic acid (PtdOH) as a possible intracellular messenger, which might be involved in local modulation of testicular testosterone production in vivo. Propranolol (27-266 µM) induced an increased level of [H]PtdOH in isolated rat Leydig cells, prelabeled with [H]myristate, and at the same time a strong dose-dependent inhibition of the acute testosterone production stimulated by luteinizing hormone (LH). The inhibition was not bypassed by the addition of dibutyryl-cAMP but was overcome, when 22(R)-hydroxycholesterol was added as a direct substrate for cytochrome P-450 side chain cleavage enzyme. Thus, the inhibition appears to be exerted at a point distal to cAMP-generation but before the first enzyme in the testosterone synthetic pathway. Treatment with other agents (4ß-phorbol 12-myristate 13-acetate (PMA), A23187, and sphingosine) giving rise to increases in the PtdOH-level resulted in the inhibition of the LH-induced testosterone formation as well, thus indicating a connection between the two effects. Furthermore, we were able to demonstrate a highly significant correlation between the PtdOH-increase and the inhibition of the LH-stimulated testosterone production. This may suggest a causal relationship between these two parameters.

AB - The results of the present study point to phosphatidic acid (PtdOH) as a possible intracellular messenger, which might be involved in local modulation of testicular testosterone production in vivo. Propranolol (27-266 µM) induced an increased level of [H]PtdOH in isolated rat Leydig cells, prelabeled with [H]myristate, and at the same time a strong dose-dependent inhibition of the acute testosterone production stimulated by luteinizing hormone (LH). The inhibition was not bypassed by the addition of dibutyryl-cAMP but was overcome, when 22(R)-hydroxycholesterol was added as a direct substrate for cytochrome P-450 side chain cleavage enzyme. Thus, the inhibition appears to be exerted at a point distal to cAMP-generation but before the first enzyme in the testosterone synthetic pathway. Treatment with other agents (4ß-phorbol 12-myristate 13-acetate (PMA), A23187, and sphingosine) giving rise to increases in the PtdOH-level resulted in the inhibition of the LH-induced testosterone formation as well, thus indicating a connection between the two effects. Furthermore, we were able to demonstrate a highly significant correlation between the PtdOH-increase and the inhibition of the LH-stimulated testosterone production. This may suggest a causal relationship between these two parameters.

UR - http://www.scopus.com/inward/record.url?scp=0028144761&partnerID=8YFLogxK

M3 - Journal article

AN - SCOPUS:0028144761

VL - 104

SP - 229

EP - 235

JO - Molecular and Cellular Endocrinology

JF - Molecular and Cellular Endocrinology

SN - 0303-7207

IS - 2

ER -

ID: 45561843