Morphological responses of the rabbit testis to ischemic/reperfusion injury due to torsion.
OBJECTIVE
To investigate the morphological effects of free radical injury on spermatogenic cells in both testes of the rabbit experimental model of testicular torsion.


METHODS
The left testes of 8 peripubertal NZW rabbits (3-6 months) were subjected to 0, 15, 30, 60, 90, 120, and 180 min of ischemia by applying a clamp to the spermatic cord, followed by reperfusion. Another set of 8 rabbits was subjected to 60 min of ischemia and administered antioxidants (acetylsalicylic acid, ascorbic acid, allopurinol, quercetin, superoxide dismutase) before reperfusion. Both testes of 4 animals per group were harvested at 24 h and the remaining 4 at 3 months. Johnsen scores for spermatogenic activity and other changes were assessed histologically and these were compared with testicular malondialdehyde (MDA), a measure of free radical damage, assayed on testicular homogenates using the thiobarbiturate method.


RESULTS
In the 24-hour reperfusion group, apoptotic bodies and giant cells were more prominent in the seminiferous tubules of the left testes compared to the right, and were maximal after 90 min. In the 3-month reperfusion group, giant cells were absent, and apoptotic bodies were reduced in both testes. Testicular MDA showed an increase only in the left testes in the 24-hour reperfusion group, while the 3-month group showed increased MDA levels in both testes, but more on the left. The Johnsen score fell only to 8.0 in the left testes in the 24-hour reperfusion group, but dropped to 2.3 in the 3-month reperfusion group. Only in the 3-month reperfusion group, did antioxidant-treated animals show a fall in Johnsen scores in the left testes, regardless of the type of antioxidant.


CONCLUSIONS
These findings confirm a role for reactive oxygen species (ROS) in damage to spermatogenic cells in both the ipsilateral and contralateral testes following torsion, with longer term effects in the torted testis. Currently available antioxidants do not provide any significant long-term protection against morphological damage to the testis by ROS generated in testicular torsion.
Anim
J T
JT
Department of Pathology, Faculty of Medicine, Kuwait University, Safat, Kuwait. anim@hsc.edu.kw
Kehinde
E O
EO
Prasad
Asa
A
Varghese
R
R
D000818:Animals; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D004195:Disease Models, Animal; D005500:Follow-Up Studies; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008854:Microscopy, Electron; D011817:Rabbits; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D012720:Severity of Illness Index; D013086:Spermatic Cord Torsion / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D013737:Testis / Q000098:blood supply / Q000378:metabolism / Q000648:ultrastructure*
D015415:Biomarkers; D017382:Reactive Oxygen Species; D008315:Malondialdehyde