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.
Effect of arsenic on ovarian steroidogenesis at the dose available in drinking water at wide areas of West Bengal is reported here. Weights of ovary, uterus and vagina along with biochemical activities of ovarian delta 5-3 beta-hydroxysteroid dehydrogenase (delta 5-3 beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) and plasma levels of LH, FSH and estrogen were measured in mature rats of the Wistar strain at diestrous phase following subchronic treatment with sodium arsenite at a dose of 0.4 ppm/rat/day for 16 days (4 estrous cycles) and 28 days (7 estrous cycles). A significant reduction in plasma levels of LH, FSH and estrogen along with significant diminution in the activities of ovarian delta 5-3 beta-HSD and 17 beta-HSD were observed following sodium arsenite treatment for 28 days. This duration of treatment also resulted in a marked degree in diminution in the weights of ovary, uterus and vagina, but 16 days of treatment did not exhibit any significant effect on these above parameters. Arsenic-treated rats exhibited a prolonged diestrous phase in the estrous cycle in contrast to control rats having 4 days of a regular estrous cycle. Deposition of arsenic in ovary, uterus, vagina and plasma was also monitored in arsenic-treated rats. The results of our experiment suggest that duration of arsenic treatment is the critical factor for its adverse effect on ovarian activities at the dose within the range noted in drinking water at several areas of West Bengal in India.
Arsenic, a major water pollutant in India, produces toxic effects on female reproductive system in rodent models at the dose available in drinking water in arsenic-intoxicated zones. This study examines the coadministration of L-ascorbate (vitamin C) on ovarian steroidogenesis, plasma levels of gonadotrophins, brain monoamines, and ovarian as well as uterine peroxidase activities in sodium arsenite-treated rats. After sodium arsenite treatment, relative ovarian and uterine weights, ovarian Delta5-3beta-HSD and 17beta-HSD activities, plasma levels of gonadotrophins, norepinephrine levels in midbrain and diencephalon, and the activities of peroxidase in ovary and uterus were decreased significantly. On the other hand, serotonin levels in midbrain and diencephalon were increased significantly 28 days after sodium arsenite treatment at the dose of 0.4 ppm/100 g body weight/rat/day. All these parameters were protected significantly and in most cases were unchanged from control level when L-ascorbate at 25 mg/100 g body weight/rat/day was coadministered orally with sodium arsenite. This cotreatment of L-ascorbate with sodium arsenite also restored the estrous cycle in a regular manner. We concluded that L-ascorbate plays a pivotal role in maintaining normal ovarian activities and brain monoamines in arsenic-treated rats.
Effects of ascorbic acid supplementation on the activity of acid phosphatase (ACP), alkaline phosphatase (ALP), glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) on liver, kidney and serum in cyclophosphamide-treated female virgin rats were investigated. Oral administration of cyclophosphamide at the dose of 5 mg/kg body weight/day for 12 days resulted in a significant elevation in ACP and ALP activities in liver, kidney and serum. Ascorbic acid supplementation at the dose of 25 mg/kg body weight/day showed a significant protection in the activity of ACP in liver, kidney and serum, but only in ALP activity in kidney. ALP activities in liver and serum were not restored to control level by ascorbic acid supplementation. Activities of GOT and GPT were elevated significantly in liver, kidney and serum after cyclophosphamide treatment, and were protected and restored to control level by ascorbic acid supplementation.
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