Túnez Isaac, Feijóo Montserrat, Collado Juan A, Medina Francisco J, Peña José, Muñoz María del C, Jimena Ignacio, Franco Francisco, Rueda Ignacio, Muntané Jordi, Montilla Pedro
Departamento de Bioquimica y Biologia Molecular, Facultad de Medicina, Universidad de Cordoba, Avda. Menendez Pidal s/n, 14004 Cordoba, Spain.
Life Sci. 2007 Mar 6;80(13):1221-7. doi: 10.1016/j.lfs.2006.12.013. Epub 2007 Jan 9.
This paper evaluates the effects of testosterone (0.5 mg/kg subcutaneously (s.c.) for 8 days) on oxidative stress and cell damage induced by 3-nitropropionic acid (20 mg/kg intraperitoneally (i.p.) for 4 days) in ovariectomized rats. Gonadectomy triggered oxidative damage and cell loss, evaluated by the detection of caspase-3, whereas 3-nitropropionic acid increased the levels of oxidative stress induced by ovariectomy and prompted cell damage characterized by enhanced levels of lactate dehydrogenase. These changes were blocked by testosterone administration. Our results support the following conclusions: i) ovariectomy triggers oxidative and cell damage via caspase-3 in the striatum; ii) 3-nitropropionic acid exacerbates oxidative stress induced by ovariectomy and leads to cell damage characterized by increased levels of lactate dehydrogenase; iii) testosterone administration decreases oxidative stress and cell damage. Additionally, these data support the hypothesis that testosterone might play an important role in the onset and development of neurodegenerative diseases.
本文评估了睾酮（皮下注射0.5毫克/千克，共8天）对去卵巢大鼠由3-硝基丙酸（腹腔注射20毫克/千克，共4天）诱导的氧化应激和细胞损伤的影响。通过检测半胱天冬酶-3评估，性腺切除引发了氧化损伤和细胞丢失，而3-硝基丙酸增加了去卵巢诱导的氧化应激水平，并促使以乳酸脱氢酶水平升高为特征的细胞损伤。睾酮给药可阻断这些变化。我们的结果支持以下结论：i）去卵巢通过纹状体中的半胱天冬酶-3引发氧化和细胞损伤；ii）3-硝基丙酸加剧去卵巢诱导的氧化应激并导致以乳酸脱氢酶水平升高为特征的细胞损伤；iii）睾酮给药可降低氧化应激和细胞损伤。此外，这些数据支持睾酮可能在神经退行性疾病的发生和发展中起重要作用的假说。
