Testicular mitochondrial alterations in untreated streptozotocin-induced diabetic rats

被引:41
|
作者
Amaral, Sandra [1 ]
Mota, Paula C. [1 ]
Lacerda, Beatriz [1 ]
Alves, Marco [1 ]
Pereira, Maria de Lourdes [2 ]
Oliveira, Paulo J. [1 ]
Ramalho-Santos, Joao [1 ]
机构
[1] Univ Coimbra, Fac Sci & Technol, Dept Zool, Ctr Neurosci & Cell Biol, P-3004517 Coimbra, Portugal
[2] Univ Aveiro, Dept Biol CICECO, P-3810193 Aveiro, Portugal
关键词
Type; 1; diabetes; Rat; Streptozotocin-induced diabetes; Testis; Spermatogenesis; Reproduction; PERMEABILITY TRANSITION PORE; LIVER MITOCHONDRIA; OXIDATIVE STRESS; GOTO-KAKIZAKI; HEART-MITOCHONDRIA; VITAMIN-E; INSULIN; MELLITUS; BIOENERGETICS; HYPERGLYCEMIA;
D O I
10.1016/j.mito.2008.11.005
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Diabetes-induced complications are associated with mitochondrial dysfunction and increasing evidence suggests that diabetes has an adverse effect on male reproductive function. The STZ-induced diabetic rat was used as an animal model for the type I form of the disease with the aim of determining its effects in spermatogenesis and testicular mitochondrial function. Several aspects of mitochondrial function were measured, including respiratory and electric potential function, as well as mitochondrial calcium loading capacity. Additionally oxidative stress production, antioxidant levels and possible apoptotic alterations were also evaluated. We observed that diabetic animals present alterations in spermatogenesis in both the testis and epidydimus. However, and surprisingly, the overall results in mitochondrial parameters failed to reveal severe testicular mitochondrial dysfunction in diabetic animals, with the exception of a decrease in calcium load. Taken together, results suggest that in animal models that mimic untreated type 1 diabetes the severe effects of the condition on spermatogenesis are not directly mitochondrial-mediated. (C) 2008 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
引用
收藏
页码:41 / 50
页数:10
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