title: Mitochondrial apoptotic pathways: a mechanism for low androgen-induced vascular endothelial injury in male rats.
abstract: The aim of the study was to investigate the role of mitochondrial apoptotic pathways in vascular endothelial injury in male rats with low androgen. 8 week-old adult male Sprague-Dawley (SD) rats were randomly divided into 3 groups (n=6/each group): control group, castrated group (low androgen), and replacement group (given androgen after castration). After 10 weeks, endothelial structure was observed by general light microscope and transmission electron microscope (TEM) respectively. Isolated mitochondria and mitochondrial membrane potential (MMP) were detected by fluorescence to access mitochondrial function. Chromatin degradation was measured by terminal deoxynucleotidyl transferase-mediated deoxyuridine-biotin nick end labeling (TUNEL) staining method. The mRNA and protein of bcl-2, cytochrome C (Cyt C), caspase-9, and caspase-3 were analyzed for apoptosis. Cell shrinkage and condensed chromatin, less mitochondria and a fall in MMP levels were observed in the castrated group, along with more apoptotic endothelial cells. Bcl-2 level was reduced and the expression of caspase-9, caspase-3 and Cyt C were elevated in the castrated group (p<0.05). But there was no significant difference between the replacement group and the control group (p>0.05). It was concluded that low androgen caused vascular endothelial damage. It may be, at least in part, related with the activating mitochondrial apoptotic pathways.
authors.affiliation: Institution and Department of Endocrinology and Metabolism, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China.
authors.forename: Y-X
authors.initials: YX
authors.lastname: Li
authors.forename: B
authors.initials: B
authors.lastname: Jiang
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.forename: F
authors.initials: F
authors.lastname: Xia
authors.forename: J
authors.initials: J
authors.lastname: Yu
authors.forename: L-z
authors.initials: LZ
authors.lastname: Yang
authors.forename: C
authors.initials: C
authors.lastname: Shi
authors.forename: Y-L
authors.initials: YL
authors.lastname: Lu
mesh_terms: D000728:Androgens / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001158:Arteries / Q000187:drug effects / Q000473:pathology; D001835:Body Weight / Q000187:drug effects; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D053453:Caspase 9 / Q000235:genetics / Q000378:metabolism; D045304:Cytochromes c / Q000378:metabolism; D042783:Endothelial Cells / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000473:pathology*; D005786:Gene Expression Regulation / Q000187:drug effects; D020287:In Situ Nick-End Labeling; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D013739:Testosterone / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology
chemical_list: D000728:Androgens; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D013739:Testosterone; D045304:Cytochromes c; D053148:Caspase 3; D053453:Caspase 9