Influence of rat seminiferous tubules on Leydig cell testosterone production in vitro

Parvinen, Martti; Nikula, Hannu; Huhtaniemi, Ilpo

doi:10.1016/0303-7207(84)90103-5

Cited by 106 publications

(35 citation statements)

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“…The more likely explanation is that opposing mechanisms do exist, as with most biological regulatory systems, and which of the effects is obtained in uitro may be determined by the particular culture systems employed. It would certainly seem logical if the androgendependent stage VII tubules positively regulated testosterone production whilst the nonandrogen-dependent stages exerted a negative counter-balancing effect (see also p. 789) The available evidence is consistent with this interpretation (Parvinen et al, 1984;Syed et a[., 1985;Vihko & Huhtaniemi, 1989) (see Fig. 4).…”

Section: Potential P a R A C R I N E Mechanisms F O R R E G U L A T Isupporting

confidence: 75%

“…As it is well established that the volume of SER correlates positively with the capacity of Leydig cells to secrete testosterone (Ewing & Zirkin, 1983), this finding is still consistent with stage VII tubules regulating the levels of testosterone in their immediate environment. A study involving the co-culture of Leydig cells with isolated segments of seminiferous tubules at specific stages of the spermatogenic cycle also suggested that stage VII tubules positively regulate testosterone production (Parvinen et al, 1984), whilst later stages may exert a negative effect (Syed el al., 1985;Vihko & Huhtaniemi, 1989).…”

Section: T H E I N T R a T E S T I C U L A R Role(s) O F T E S T O S mentioning

confidence: 99%

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Intratesticular Control Of Steroidogenesis

Sharpe

1990

Clinical Endocrinology

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Men are men because of testosterone, and the effects of this hormone are evident in virtually every organ or tissue in a normal adult man. Because testosterone is a classical endocrine hormone with effects throughout the body, many endocrinologists will have failed to realize that, in terms of its effects on fertility, the primary role of testosterone is not endocrine but paracrine, as it is the local action of testosterone on spermatogenesis which determines fertility. When looked at from this perspective it is logical to question the traditional endocrine teaching which states that testosterone secretion is controlled solely by pituitary luteinizing hormone (LH). Certainly, the levels of testosterone and LH in peripheral blood show a close relationship, but it is not the level of testosterone in peripheral blood which determines fertility. If the primary role of testosterone is within the testis, then it is not unreasonable to expect that local mechanisms may exist to regulate the intratesticular levels of this steroid. The object of this review is to examinecritically the evidence for such mechanisms, their possible nature and their physiological and clinical significance (if any).Before reviewing the data on intratesticular control of steroidogenesis it is essential to place it in perspective. To do this, three principal questions need to be answered: ( I ) Why might intratesticular mechanisms for local control of testosterone production be required? (2) What is the role (or roles) of testosterone within the testis? A proper understanding of how testosterone controls spermatogenesis is essential if the local regulation of testosterone production is to be evaluated from a physiological perspective. ( 3 ) What are the constraints or problems relating to studies on the intratesticular control of steroidogenesis? It is essential to understand the potential limitations of studies on this subject so that a reasoned interpretation of the results can be made. Most relevant data is derived from studies in uitro, and the relationship of such data to the situation in uivo is often difficult to establish. W H Y M I G H T INTRATESTICULAR M E C H A N I S M S F O R T H E C O N T R O L OF TESTOSTERONE P R O D U C T I O N BE REQUIRED?It can be argued that paracrine control of testicular testosterone production is irrelevant, because (a) the serum levels of LH and testosterone clearly change together (i.e. they control each other) and (b) the removal of LH in animals by hypophysectomy or immunoneutralization lowers intratesticular testosterone levels so drastically that 787

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Section: Potential P a R A C R I N E Mechanisms F O R R E G U L A T Isupporting

confidence: 75%

Section: T H E I N T R a T E S T I C U L A R Role(s) O F T E S T O S mentioning

confidence: 99%

Intratesticular Control Of Steroidogenesis

Sharpe

1990

Clinical Endocrinology

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“…Whilst it is possible that this stimulatory activity may originate from the Sertoli cell, the relationship between this activity in interstitial fluid and those reported by Parvinen et al (1984), Janecki et al (1985), Syed et al (1985,1986) and Verhoeven & Cailleau (!985, 1986) is unknown. Nevertheless, disruption of spermatogenesis and alteration of Sertoli cell function result in an increase in the concentration of stimulatory activity in testicular interstitial fluid.…”

Section: Discussionmentioning

confidence: 71%

Effect of cryptorchidism on steroidogenic and mitogenic activities in rat testicular interstitial fluid

Risbridger

Drummond²,

Kerr³

et al. 1987

Reproduction

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Summary. There was a significant (P < 0\m=.\05) and consistent increase in the potency of steroidogenic stimulatory activity (testosterone production by purified Leydig cells in vitro) in testicular interstitial fluid of the cryptorchid compared to the scrotal testis from 1 to 4 weeks after the induction of unilateral cryptorchidism. In contrast, the level of mitogenic activity ([3H]thymidine incorporation into 3T3 cells) was not significantly different between interstitial fluid from cryptorchid and scrotal testes for up to 4 weeks after surgery. These results indicate that the steroidogenic activity and the mitogenic activity are due to different, as yet unidentified, factors in testicular interstitial fluid.

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“…For the experiments, 50 pieces of each pool of stage were dissected. The tubule preparations do not contain significant amounts of interstitial Leydig cells as judged from their inability to respond to stimulation by the luteinizing hormone [14]. The tissue pieces were washed and incubated in 1 ml Eagle's minimal essential medium lacking methionine and supplied with antibiotics, at 32'C in humidified 5% CO2 atmosphere.…”

Section: Resultsmentioning

confidence: 99%

Local synthesis of plasminogen by the seminiferous tubules of the testis

Saksela

Vihko

1986

FEBS Letters

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Plasminogen activation occurs through conversion of plasminogen to plasmin by plasminogen activators. In adult mammals, liver has been the only known site for plasminogen synthesis. Seminiferous tubules secrete plasminogen activator, but are behind a barrier that excludes the entrance of many macromolecules to this tissue. Therefore, it became of interest to study the existence of plasminogen in this system. After metabolic labeling, a 90 kDa lysine-binding polypeptide was found. This protein could be immunoblotted by anti-plasminogen antibody, and was shown to possess urokinase-dependent proteolytic activity. The findings suggest that plasminogen is synthesized by seminiferous tubules. We propose that local plasminogen synthesis may occur in tissues which are separated by specific anatomical barriers. Plasminogen synthesis (Seminiferous tubule, Testis)

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Influence of rat seminiferous tubules on Leydig cell testosterone production in vitro

Cited by 106 publications

References 14 publications

Intratesticular Control Of Steroidogenesis

Intratesticular Control Of Steroidogenesis

Effect of cryptorchidism on steroidogenic and mitogenic activities in rat testicular interstitial fluid

Local synthesis of plasminogen by the seminiferous tubules of the testis

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