3β-hydroxysteroid dehydrogenase (3β-HSD) is a steroidogenic enzyme that catalyzes the conversion of 3β-hydroxysteroids to 3-ketosteroids. Two different subtypes of human 3β-HSD, HSD3B1 and HSD3B2, have been cloned, with HSD3B2 primarily expressed in the testes. HSD3B2 exhibits 3β-HSD2 activity and is a dual-substrate enzyme that binds with co-factors NAD + and 3β-steroids. Many endocrine disruptors, including industrial compounds (phthalates, bisphenols, perfluoroalkyl substances, and benzophenones), pesticides and fungicides (organochlorine pesticides and organotins), food additives (butylated hydroxyanisole, resveratrol, gossypol, flavonoids and isoflavonoids, curcuminoids, and chalcones), and drugs (etomidate, mifepristone, and ketoconazole) inhibit testicular 3β-HSD, potentially interfering with androgen synthesis. In this review, we summarized the unique testicular subtypes of 3β-HSD, their genes, chemistry, subcellularity, location, and the endocrine disruptors that directly inhibit testicular 3β-HSD and their modes of inhibition, to provide reference for clinical research on androgen regulation methods and the development of androgen-targeted drugs.

3β-hydroxysteroid dehydrogenase (3β-HSD) is a steroidogenic enzyme that catalyzes the conversion of 3β-hydroxysteroids to 3-ketosteroids. Two different subtypes of human 3β-HSD, HSD3B1 and HSD3B2, have been cloned, with HSD3B2 primarily expressed in the testes. HSD3B2 exhibits 3β-HSD2 activity and is a dual-substrate enzyme that binds with co-factors NAD + and 3β-steroids. Many endocrine disruptors, including industrial compounds (phthalates, bisphenols, perfluoroalkyl substances, and benzophenones), pesticides and fungicides (organochlorine pesticides and organotins), food additives (butylated hydroxyanisole, resveratrol, gossypol, flavonoids and isoflavonoids, curcuminoids, and chalcones), and drugs (etomidate, mifepristone, and ketoconazole) inhibit testicular 3β-HSD, potentially interfering with androgen synthesis. In this review, we summarized the unique testicular subtypes of 3β-HSD, their genes, chemistry, subcellularity, location, and the endocrine disruptors that directly inhibit testicular 3β-HSD and their modes of inhibition, to provide reference for clinical research on androgen regulation methods and the development of androgen-targeted drugs.

Objective To assess sperm chromatin structure assay (SCSA) and sperm chromatin dispersion test (SCD) for DNA fragmentation evaluation in human infertility, and the correlation between these two methods. Methods We used SCSA and SCD assays to detect DNA fragmentation in sperm from 134 infertile men. The correlation of SCSA and SCD assays was analyzed. The sperm DNA fragmentation index (DFI) was divided into 3 groups (≤15%DFI, >15~≤30%DFI and>30%DFI), and the difference between SCSA and SCD assays was assessed. Results The SCSA assay was strongly correlated with the SCD assay for sperm DNA fragmentation (r=0.915, P<0.001). There was no significant difference between>15~ ≤30%DFI and>30%DFI groups. However, SCD showed higher levels of DNA fragmentation than that measured by SCSA for≤15%DFI group (13.50 4.82 vs 9.79 2.60, P<0.001). Conclusion There is a strong positive correlation between SCSA and SCD assays in detection of DNA fragmentation. SCD assay showed higher levels of DNA fragmentation than that measured by SCSA for≤15%DFI group.