Apoptosis in the erectile tissues of diabetic and healthy rats

被引:38
作者
Alici, B
Gümüstas, MK
Özkara, H
Akkus, E
Demirel, G
Yencilek, F
Hattat, H
机构
[1] Istanbul Univ, Cerrahpasa Med Fac, Sexual Dysfunct Ctr, Dept Urol, Istanbul, Turkey
[2] Istanbul Univ, Cerrahpasa Med Fac, Sexual Dysfunct Ctr, Dept Biochem, Istanbul, Turkey
[3] Pakize Tarzi Labs, Istanbul, Turkey
关键词
apoptosis; erectile dysfunction; diabetes; flow cytometry;
D O I
10.1046/j.1464-410x.2000.00420.x
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Objective To compare the frequency of apoptosis in the erectile tissue of chronic diabetic and healthy rats. Materials and methods Fourteen chronic diabetic and 10 healthy Sprague-Dawley rats were killed, their penises harvested and stored at -70 degrees C until staining and now cytometric analysis for apoptosis. A cell suspension was obtained from the penile tissue by scraping the inside of the cavernosum with a scalpel and filtering through a mesh. Samples of the cell suspension (0.5 x 10(6) cells) were stained with Annexin V (an indicator of apoptosis) and propidium iodide (PI, which stains dead cells), incubated for 15 min at room temperature and analysed by now cytometry. The DNA content was also analysed in each sample. Results In normal erectile tissue, a mean of 6.2% of cells were stained with Annexin V, while only 2.7% were stained with PI; DNA content analyses showed 7.5% were hypodiploid cells. In diabetic rats 19.5% of cells were stained with Annexin V and 5.2% with PI; 22.9% of cells were hypodiploid. Conclusion The ratio of apoptotic cells in the erectile tissues of diabetic rats was significantly greater than in normal rats. The high rate of apoptosis in diabetic rats may play a role in the pathophysiology of erectile dysfunction.
引用
收藏
页码:326 / 329
页数:4
相关论文
共 21 条
[1]
APPARENT HYDROXYL RADICAL PRODUCTION BY PEROXYNITRITE - IMPLICATIONS FOR ENDOTHELIAL INJURY FROM NITRIC-OXIDE AND SUPEROXIDE [J].
BECKMAN, JS ;
BECKMAN, TW ;
CHEN, J ;
MARSHALL, PA ;
FREEMAN, BA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (04) :1620-1624
[2]
Briehl MM, 1996, CELL DEATH DIFFER, V3, P63
[3]
Increase in TUNEL positive cells in aorta from diabetic rats [J].
Chu, Y ;
Faraci, FM ;
Ooboshi, H ;
Heistad, DD .
ENDOTHELIUM-NEW YORK, 1997, 5 (04) :241-250
[4]
A POTENTIAL ROLE FOR APOPTOSIS IN NEURODEGENERATION AND ALZHEIMERS-DISEASE [J].
COTMAN, CW ;
ANDERSON, AJ .
MOLECULAR NEUROBIOLOGY, 1995, 10 (01) :19-45
[5]
DRESSIER LG, 1993, HDB FLOW CYTOMETRY M, P106
[6]
FADOK VA, 1992, J IMMUNOL, V148, P2207
[7]
BCL-2 FUNCTIONS IN AN ANTIOXIDANT PATHWAY TO PREVENT APOPTOSIS [J].
HOCKENBERY, DM ;
OLTVAI, ZN ;
YIN, XM ;
MILLIMAN, CL ;
KORSMEYER, SJ .
CELL, 1993, 75 (02) :241-251
[8]
BCL-2 INHIBITION OF NEURAL DEATH - DECREASED GENERATION OF REACTIVE OXYGEN SPECIES [J].
KANE, DJ ;
SARAFIAN, TA ;
ANTON, R ;
HAHN, H ;
GRALLA, EB ;
VALENTINE, JS ;
ORD, T ;
BREDESEN, DE .
SCIENCE, 1993, 262 (5137) :1274-1277
[9]
SHRINKAGE NECROSIS - DISTINCT MODE OF CELLULAR DEATH [J].
KERR, JFR .
JOURNAL OF PATHOLOGY, 1971, 105 (01) :13-+
[10]
APOPTOSIS - BASIC BIOLOGICAL PHENOMENON WITH WIDE-RANGING IMPLICATIONS IN TISSUE KINETICS [J].
KERR, JFR ;
WYLLIE, AH ;
CURRIE, AR .
BRITISH JOURNAL OF CANCER, 1972, 26 (04) :239-+