Maternal diabetes increases apoptosis in mice oocytes, not 2-cell embryos.
Apoptosis may be closely involved in diabetes-induced embryonic malformations. We aimed to investigate the occurrence of apoptosis at an early stage of development, in oocytes and 2-cell embryos of streptozotocin-induced diabetic mice and nondiabetic mice. Diabetic mouse ovarian sections stained with hematoxylin and eosin showed reduced number of growing follicles and delayed oocyte development. Annexin V-positive oocytes were higher in number in diabetic mice than in nondiabetic mice. Quantitative RT-PCR and immunofluorescence analysis revealed the expression of Bax and caspase-3 significantly higher in diabetic than nondiabetic oocytes. In contrast, 2-cell embryos of diabetic and nondiabetic mice showed no annexin V-positive staining. Bax expression was elevated in diabetic 2-cell embryos, but caspase-3 expression did not significantly differ between diabetic and nondiabetic 2-cell embryos. Electron microscopy revealed increased number of swollen mitochondria in diabetic 2-cell embryos. These results suggested that maternal diabetes might increase oocyte apoptosis by a Bax-caspase-3 pathway to play a role in embryonic malformations by delayed oocyte development. Development of 2-cell embryos might be adversely affected by maternal diabetes, but not through Bax-regulated caspase-3 apoptotic pathway.
Lin
Shaoda
S
Department of Endocrinology, The First Affiliated Hospital of Shantou University Medical College, 515041 Shantou, China. linshaoda@126.com
Lin
Kun
K
Li
Weiping
W
Zhou
Xiaolin
X
Huang
Tianhua
T
D000818:Animals; D017209:Apoptosis; D002970:Cleavage Stage, Ovum / Q000473:pathology* / Q000502:physiology / Q000648:ultrastructure; D003921:Diabetes Mellitus, Experimental / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D005260:Female; D051379:Mice; D009865:Oocytes / Q000473:pathology*; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000235:genetics / Q000378:metabolism / Q000473:pathology*