Selenium Increases Testicular Steroidogenesis and Growth Factors Expression in Streptozotocin-induced Diabetic Rats

Document Type : Original Article

Authors

1 Medical Physiology Department, Faculty of Medicine, Sohag University, Egypt.

2 Medical Biochemistry Department, Faculty of Medicine, Sohag University, Egypt.

3 Zoology Department, Faculty of Science; South Valley University, Qena, 83523,Egypt.

Abstract

Selenium (Se) is an essential trace element and found to have important roles in maintaining normal growth and reproduction. The effect of Se on testicular steroidogenesis and testicular expression of vascular endothelial growth factor (VEGF) and nerve growth factor-beta (NGF-β) was studied in streptozotocin (STZ)- induced diabetic rats. The study included 45 male albino rats randomly divided into 3 groups; control (group I, n=15), diabetic (group II, n=15) and diabetic supplemented with Se (group III, n=15). The investigation revealed that, diabetic group (group II) had a significant decrease in Se level and testicular steroidogenesis evidenced by the decrease in testosterone and in the activity of two important enzymes synthesizing testosterone 3-beta-hydroxysteroid dehydrogenase (3β-HSDH) and 17-beta-hydroxysteroid dehydrogenase (17β- HSDH) compared to control group (P < 0.05). In addition, there was a significant decrease in testicular tissue levels of VEGF and NGF-β in diabetic rats compared to control rats (P < 0.05). While, diabetic group supplemented with Se (group III) exhibited a significant increase in Se level, the activity of 3 β-HSDH, 17 β-HSDH and testosterone concentration compared to group II. Also, group III exhibited a significant increase in the testicular tissue levels of VEGF and NGF-β compared to group II. In addition, Se supplementation improved testicular weight, the seminiferous tubules atrophy, the germinal epithelial cells lining tubules, Sertoli cells and interstitial cell of Leydig. In conclusion, Se supplementation increases testicular steroidogenesis and the expression of VEGF and NGF-β in STZ-induced diabetic rats.

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