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Effects of methyltestosterone, letrozole, triphenyltin and fenarimol on histology of reproductive organs of the copepod Acartia tonsa

Authors :
Burkard Watermann
Leah Wollenberger
Katarina Gnass
Thierry Dagnac
K. Ole Kusk
Vasilios A. Sakkas
Triantafyllos A. Albanis
Publication Year :
2013
Publisher :
Elsevier, 2013.

Abstract

The marine calanoid copepod Acartia tonsa was exposed to methyltestosterone (MET, 1.6-126 μg L(-1)), letrozole (LET, 10-1000 μg L(-1)), triphenyltin chloride (TPT, 0.0014-0.0088 μg L(-1) TPT-Sn) and fenarimol (FEN, 2.8-105 μg L(-1)) for 21 d covering a full life-cycle. All four compounds investigated are known to act as androgens in vertebrates. The digestive tract, musculature, nervous system, reproductive organs, gonad and accessory sexual glands were examined by light microscopy after routine staining and immune-labelling for detection of apoptosis and determination of proliferation activities. MET induced an inhibition of oogenesis, oocyte maturation and yolk formation, respectively, which was most pronounced at the lowest concentrations tested. In LET exposed males, spermatogenesis was enhanced with very prominent gamete stages; in some stages apoptosis occurred. The spermatophore was hypertrophied and displayed deformations. In females, LET induced a disorder of oogenesis and disturbances in yolk synthesis. TPT stimulated the male reproductive system at 0.0014 and 0.0035 μg TPT-SnL(-1), whereas inhibiting effects were observed in the female gonad at 0.0088 μg TPT-SnL(-1). In FEN exposed females proliferation of gametes was reduced and yolk formation showed irregular features at 2.8-105 μgL(-1). In FEN exposed males an elevated proliferation activity was observed. No pathological alterations in other organ systems, e.g. the digestive tract including the hindgut acting as respiratory organ, the nervous system, or the musculature were seen. This indicates that the effects on gonads might be caused rather by disturbance of endocrine signalling or interference with hormone metabolism than by general toxicity.

Details

Language :
English
Database :
OpenAIRE
Accession number :
edsair.doi.dedup.....b29207c61b7fd56ae83f321c24be2364