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Exploitable results
4-NP, in relevant concentrations, suppresses gonadal development and sexual hormone production in three different fish species; the pubertal male African catfish, the maturing female rainbow trout and the maturing male tilapia, were exposed to relevant concentrations of a "model" environmental estrogen, 4-nonylphenol (4-NP). The present study identified several points along the brain-pituitary-gonad axis, the neuro-endocrine system that controls reproduction, which are affected by exposure to 4-NP.
Suppression of gonadal development is the most striking end-point effect of 4-NP exposure in these three species. It has to be expected that chronic exposure to 4-NP lead to a severe decrease, or even absence of viable germ cells. Male germ cell development (spermatogenesis) depends on the presence of male sex hormones (androgens). In both the African catfish and the tilapia, androgen secretion was severely suppressed by 4-NP exposure.
Based on the present results, the question of reversibility of the inhibition of testis growth and spermatogenesis should be addressed.
Although this result can be considered as a severe endocrine disruption, it is too early for a firm statement whether this will endanger fish populations and that there is by consequent reason for concern. Nevertheless, this result should be, considered in matters on animal health and welfare, biological monitoring and risk assessment.
for more details on project, click here: http://www.bio.uu.nl/~PEDSUTAB
Three different fish species, pubertal male African catfish, maturing female rainbow trout and maturing male tilapia, were exposed to relevant concentrations of a "model" environmental oestrogen, 4-nonylphenol (4-NP). The present study identified several points along the brain-pituitary- gonad axis, the neuro-endocrine system that controls reproduction, which are affected by exposure to 4-NP.
In the pituitary, two hormones that control gonadal functions are secreted: follicle stimulating hormone (FSH), mainly responsible for germ cell production, and luteinizing hormone (LH) that regulates sex hormone production. Exposure to 4-NP caused in trout and tilapia a decrease in FSH production (this hormone could not be measured in catfish). This effect is probably responsible for the disruption of cogenesis and spermatogenesis. Moreover, in catfish, LH gene expression and storage was stimulated, but its release was inhibited. LH plasma levels were not always affected in the other species.
FSH and LH secretion are under control of gonadotropin releasing hormone (GnRH) via specific GnRH receptors (GnRH-Rs) on the pituitary cells. Especially, the higher but still relevant 4-NP doses caused a down regulation of the GnRH-R gene expression in catfish, which may be responsible for a disruption of the functional connection between brain and pituitary.
For more information: (click here) http://www.bio.uu.nl/~PEDSUTAB
Already available in vitro methods developed to monitor the estrogenic activity of EEs only provide data reflecting estrogen receptor binding or mitogenic activity. Because of the pivotal role of GTHs within the BPG axis, it is essential to determine the effect of EEs on GnRH receptors and GTH synthesis and release. This can be achieved by experiments as outlined in the present research program. Although such an approach is necessary at the beginning, it is time-consuming and specialized expertise and suitable aquarium facilities are needed. Therefore, in the present program, it was attempted to develop an immortalized gonadotroph cell line, to be made available for future research on the cellular and molecular mechanisms of action of EEs (or other pollutants) in gonadotrophs. We did not succeed in the development of an immortalized gonadotroph cell line. The main obstacle was the terminally differentiated state of the gonadotroph cells even in juvenile fish. Trials to stimulate cells to re-enter cell cycling failed. Hence, the immortalisation strategy, introduction of an oncogene, remains ineffective.
We succeeded instead by adding IGF-1 to the culture medium, to extend the functional survival period of gonadotrophs in primary culture to 3 weeks.
This result can be used in similar research projects on the effects of potential endocrine disrupting agents on pituitary gonadotrophs.
For more details: (click here) http://www.bio.uu.nl/~PEDSUTAB
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