Over expression of thioredoxin-1 in transgenic mice attenuates germ cell apoptosis induced by experimental cryptorchidism.

PURPOSE: Experimental cryptorchidism induces apoptosis in testicular germ cells by generating reactive oxygen species. We investigated the effects of a redox regulating molecule, thioredoxin-1 (TRX1), on testicular damage caused by experimental cryptorchidism.

MATERIALS AND

METHODS

Unilateral cryptorchidism was surgically induced in TRX1 transgenic (TRX1-Tg) or WT adult C57BL6 mice. The contralateral scrotal testis served as a control.

RESULTS

Experimental cryptorchidism decreased testicular weight in WT mice from 4 days after surgery. The decrease in testicular weight was significantly attenuated in TRX1-Tg mice compared with WT mice 7 to 14 days after surgery (p <0.01). However, the difference between the 2 groups was not significant 28 days after surgery. Histological analysis and TUNEL assays demonstrated that apoptosis occurred in germ cells of the cryptorchid testis in each group but the appearance of apoptotic germ cells was delayed by 3 days in TRX1-Tg mice.

CONCLUSIONS

TRX1 over expression suppressed apoptosis in testicular germ cells induced by experimental cryptorchidism, indicating that TRX1 intensification may be a useful therapeutic strategy for male infertility associated with heat stress.