 di(2-ethylhexyl ) phthalate ( dehp ) produced seminiferous tubular atrophy and reductions in seminal vesicle and prostate weight in 4-week - old , but not in 15-week - old rats . 
 di - n - pentyl phthalate ( dpp ) did produce atrophy in the older rats but this developed more slowly than in young animals . 
 coadministration of testosterone or gonadotrophins did not protect against phthalate - induced testicular toxicity but did partly reverse the depression of seminal vesicle and prostate weight . 
 secretion of seminiferous tubule fluid and androgen binding protein by the sertoli cells was markedly suppressed within 1 hr of a dose of dpp or mono-2-ethylhexyl phthalate ( mehp ) in immature rats . 
 this occurred less rapidly in mature rats . 
 [ 14c]mono - n - pentyl phthalate and [ 14c]mehp penetrated the blood testis barrier only to a very limited extent . 
 these findings and the early morphological changes in the sertoli cells produced by dpp suggest that phthalate esters may act initially to cause sertoli cell injury , the subsequent loss of germ cells occurring as a consequence of this . 
 some features of the testicular lesion could be reproduced in primary cocultures of rat sertoli and germ cells . 
 structure activity studies with a range of phthalate monoesters showed good agreement between the induction of germ cell detachment in culture and testicular toxicity in vivo . 
 three metabolites of mehp ( metabolites v , vi , and ix ) were much less toxic in culture than mehp itself , suggesting that the latter may be the active testicular toxin from dehp.imagesfigure 1.figure 2 . 
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