The present work examined the changes in testicular activities in relation to testicular oxidative stress in
cyclophosphamide as well as human chorionic gonadotrophin (hCG) co-treated
cyclophosphamide treated Wistar strain rats. Testicular activities were evaluated by the quantification of spermatogenesis and by the measurement of steroidogenic key
enzyme activities along with plasma levels of
testosterone. Testicular oxidative stress in relation to
cyclophosphamide treatment was monitored by the study of products of
free radicals like conjugated dienes and
malondialdehyde (MDA) as well as the activity of testicular
antioxidant enzymes like
peroxidase and
catalase.
Cyclophosphamide treatment at the dose of 5 mg/kg
body weight/day for 28 days resulted a significant diminution in the activities of testicular delta 5,
3 beta-hydroxysteroid dehydrogenase (delta 5, 3 beta-HSD), 17 beta-
hydroxysteroid dehydrogenase (17 beta-HSD) activities, plasma level of
testosterone along with significant reduction in the number of germ cells at stage-VII of spermatogenesis. Levels of testicular MDA and conjugated dienes both were elevated whereas testicular
peroxidase and
catalase activities both were inhibited significantly in
cyclophosphamide treated rats in comparison to control. After hCG co-administration at the dose of 5 I.U./kg
body weight/day for 28 days in
cyclophosphamide treated rats resulted a significant protection in the activities of testicular
peroxidase and
catalase along with significant decrease in the levels of MDA and conjugated dienes to the control level. Moreover, the testicular steroidogenic key
enzyme activities and spermatogenesis along with plasma levels of
testosterone were restored to the control level. Therefore, it may be concluded that there is a correlation between testicular steroidogenic activities as well as spermatogenesis and testicular oxidative stress in
cyclophosphamide treated rats. Moreover, as restoration of plasma
testosterone to the control level is noted in hCG co-treated
cyclophosphamide treated rat, therefore, the results suggest that
testosterone may be the key regulator for this correlation.