Holmes R S, Andrews S, Jones J T
J Exp Zool. 1979 Aug;209(2):255-9. doi: 10.1002/jez.1402090207.
Lactate dehydrogenase (LDH) C, activity was observed in testis extracts from normal mice but was progressively reduced in mice carrying the male-sterile translocations T31H, T32H, T37H, T38H, T40H and T42H, with no detectable activity being observed in the last two mice. None of the vesicular gland extracts from these male-steriles showed LDH-C4 activity, unlike normal mice. The differential LDH-C4 activity in male-sterile testes is interpreted as reflecting the varying stages of the spermatogenic defect during meiosis. In general, early meiotic defects exhibited no LDH-C4 activity whereas late stage (usually after metaphase-1 stage) defect animals exhibited some activity. The results also provide evidence for contaminating sperm being the source of normal vesicular gland LDH-C4 activity.
在正常小鼠的睾丸提取物中观察到乳酸脱氢酶(LDH)C的活性,但在携带雄性不育易位T31H、T32H、T37H、T38H、T40H和T42H的小鼠中,该活性逐渐降低,在最后两只小鼠中未检测到活性。与正常小鼠不同,这些雄性不育小鼠的精囊提取物均未显示LDH-C4活性。雄性不育睾丸中LDH-C4活性的差异被解释为反映减数分裂过程中生精缺陷的不同阶段。一般来说,早期减数分裂缺陷没有LDH-C4活性,而晚期(通常在中期-1期之后)缺陷动物表现出一些活性。结果还为污染精子是正常精囊LDH-C4活性的来源提供了证据。