Vanadium induced ultrastructural changes and apoptosis in male germ cells

被引:37
作者
Aragón, MA
Ayala, ME
Fortoul, TI
Bizarro, R
Altamirano-Lozano, M
机构
[1] UAT, CINVESTAV, Ctr Invest Reprod Anim, Tlaxcala, Mexico
[2] Univ Nacl Autonoma Mexico, Fac Estudios Super Zaragoza, Unidad Invest Biol Reprod, Mexico City, DF, Mexico
[3] Univ Nacl Autonoma Mexico, Dept Biol Celular & Tisular, Fac Med, Mexico City, DF, Mexico
[4] Univ Nacl Autonoma Mexico, Fac Estudios Super Zaragoza, Unidad Invest Genet & Toxicol Ambiental, Mexico City 15000, DF, Mexico
关键词
male reproductive toxicology; vanadium; testes; spermatogenesis stages; seminiferous epithelium ultrastructure; germ cell death; testosterone; progesterone;
D O I
10.1016/j.reprotox.2004.11.016
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Vanadium is a transition metal that is emitted to the atmosphere during combustion of fossil fuels. In the environment, vanadium occurs in the (V) oxidized form. but in the body it is found exclusively in the (IV) oxidized form. Vanadium tetraoxide is an inorganic chemical species in the (IV) oxidized form that has been shown to induce toxic effects in vitro and in vivo. The reproductive toxicity of vanadium in males was studied through monitoring germ cell apoptosis during spermatogenesis. We analyzed ultrastructural damage, and testosterone and progesterone concentrations following vanadium tetraoxide administered to male mice for 60 days. Spermatogenesis stages I-III and X-XII frequently showed apoptotic germ cells in control and treated animals; vanadium tetraoxide treatment induced an increase in the number of Germ cell apoptosis in stages I-III and XII at 9.4 and 18.8 mg/kg, respectively. Although spermatogenesis is regulated by testosterone, in our study this hormone level was not modified by vanadium administration; thus, germ cell death was not related with testosterone concentration. At the ultrastructural level. we observed inclusion structures that varied as to location and content in the Sertoli and germ cells. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:127 / 134
页数:8
相关论文
共 39 条
[1]  
Allan, 1987, CELL DEATH SPERMATOG
[2]  
AltamiranoLozano M, 1996, TERATOGEN CARCIN MUT, V16, P7, DOI 10.1002/(SICI)1520-6866(1996)16:1<7::AID-TCM2>3.0.CO
[3]  
2-M
[4]   Sperm and testicular modifications induced by subchronic treatments with vanadium (IV) in CD-1 mice [J].
Aragón, AM ;
Altamirano-Lozano, M .
REPRODUCTIVE TOXICOLOGY, 2001, 15 (02) :145-151
[5]  
BARAN JE, 1998, VANADIUM ENV, V2, P317
[6]   APOPTOSIS IN TESTIS GERM-CELLS - DEVELOPMENTAL-CHANGES IN GONADOTROPIN DEPENDENCE AND LOCALIZATION TO SELECTIVE TUBULE STAGES [J].
BILLIG, H ;
FURUTA, I ;
RIVIER, C ;
TAPANAINEN, J ;
PARVINEN, M ;
HSUEH, AJW .
ENDOCRINOLOGY, 1995, 136 (01) :5-12
[7]   IMMUNOHISTOCHEMICAL LOCALIZATION OF ANDROGEN RECEPTORS IN THE RAT TESTIS - EVIDENCE FOR STAGE-DEPENDENT EXPRESSION AND REGULATION BY ANDROGENS [J].
BREMNER, WJ ;
MILLAR, MR ;
SHARPE, RM ;
SAUNDERS, PTK .
ENDOCRINOLOGY, 1994, 135 (03) :1227-1234
[8]  
BRINKWORTH MH, 1995, J REPROD FERTIL, V105, P25, DOI 10.1530/jrf.0.1050025
[9]   Induction of apoptosis in the germ cells of adult male rats after exposure to cyclophosphamide [J].
Cai, L ;
Hales, BF ;
Robaire, B .
BIOLOGY OF REPRODUCTION, 1997, 56 (06) :1490-1497
[10]   Spermicidal activity of metallocene complexes containing vanadium(IV) in humans [J].
D'Cruz, OJ ;
Ghosh, P ;
Uckun, FM .
BIOLOGY OF REPRODUCTION, 1998, 58 (06) :1515-1526