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From the Departments of * Anatomy II and
Pharmacology, Azabu University School of
Veterinary Medicine, Sagamihara, Japan.
| Correspondence to: Dr Masako Yamamoto, Department of Anatomy II, Azabu University School of Veterinary Medicine, 1-17-71 Fuchinobe, Sagamihara, Kanagawa 229-8501, Japan (e-mail: masako{at}azabu-u.ac.jp). |
mitochondrial RNAs (mRNAs) were unchanged, although
the StAR (steroidogenic acute regulatory protein) mRNA expression level was
increased at 6 weeks. On the other hand, when PCB169 was administered, plasma
testosterone levels were decreased at 3 and 6 weeks and were increased at 15
weeks. Plasma luteinizing hormone (LH) levels were decreased at 6 weeks, and
plasma follicle-stimulating hormone (FSH) levels were increased at 15 weeks.
The expression levels of 3ß-HSD and P45017 were
increased, and the mRNA level of 5-reductase 1 was decreased at 15
weeks. PCB169 treatment suppressed the conversion of round spermatids between
stages VII and VIII. These results indicate that in utero and lactational
exposure to PCB126 or PCB169 decreases plasma testosterone levels in
3-week-old rats, with no change in the expression levels of the mRNAs of
enzymes, and that PCB169 inhibits testicular steroid synthesis more strongly
than PCB126. PCB169 greatly altered the concentration of testosterone,
indicating a stronger inhibitory effect on spermatogenesis. Low testosterone
and LH levels in prenatally PCB169-exposed rats until 6 weeks after birth
presumably retard the functional differentiation of testicular Leydig cells;
however, the increased testosterone levels at 15 weeks suggest that Leydig
cells in PCB-exposed rats are virtually mature by the 15th week.
Key words: PCB, androgen, pituitary
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