Jacob Maria H V M, Janner Daiane da R, Belló-Klein Adriane, Llesuy Susana F, Ribeiro Maria F M
Laboratório de Interação Neuro-Humoral, Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rio Grande do Sul, Brazil.
J Steroid Biochem Mol Biol. 2008 Nov;112(1-3):138-44. doi: 10.1016/j.jsbmb.2008.09.008. Epub 2008 Sep 20.
Dehydroepiandrosterone (DHEA) is an endogenous steroid synthesized mainly in the adrenal cortex. It is known that DHEA is a precursor of sex steroids and that part of its effects depends on its conversion to estrogens and androgens. Sex steroids exert profound and controversial effects on cardiovascular function. Exogenous DHEA can exert a dual effect, antioxidant or prooxidant, depending on the dose and on the tissue specificity [1,2] (F. Celebi, I. Yilmaz, H. Aksoy, M. Gümüs, S. Taysi, D. Oren, Dehydroepiandrosterone prevents oxidative injury in obstructive jaundice in rats, J. Int. Med. Res. 32 (4) (2004) 400-405; S.K. Kim, R.F. Novak, The role of intracellular signaling in insulin-mediated regulation of drug metabolizing enzyme gene and protein expression, Pharmacol. Ther. 113 (1) (2007) 88-120). Akt signaling pathway is one of the anti-proliferative mechanisms of DHEA (Y. Jiang, T. Miyazaki, A. Honda, T. Hirayama, S. Yoshida, N. Tanaka, Y. Matsuzaki, Apoptosis and inhibition of the phosphatidylinositol 3-kinase/Akt signaling pathway in the anti-proliferative actions of dehydroepiandrosterone, J. Gastroenterol. 40 (5) (2005) 490-497). Heart homogenates were prepared to quantify lipid peroxidation (LPO), concentration of superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), 4-hydroxy-2-nonenal (HNE) and p-Akt/Akt ratio, and the activities of those antioxidant enzymes. When administrated to male Wistar rats in short-term (6 or 24h) intraperitoneally, DHEA produced significant differences in some parameters of oxidative stress in rat hearts among the distinct doses (1, 10, and 50mg/kg) used. The results here presented, regarding 6 and 24h oxidative stress status, have shown that DHEA injections promoted a prooxidant answer in healthy Wistar rat hearts.
脱氢表雄酮（DHEA）是一种主要在肾上腺皮质合成的内源性甾体激素。已知DHEA是性甾体激素的前体，其部分作用取决于其向雌激素和雄激素的转化。性甾体激素对心血管功能有深远且存在争议的影响。外源性DHEA可产生双重作用，即抗氧化或促氧化，这取决于剂量和组织特异性[1,2]（F. Celebi、I. Yilmaz、H. Aksoy、M. Gümüs、S. Taysi、D. Oren，脱氢表雄酮预防大鼠梗阻性黄疸中的氧化损伤，《国际医学研究杂志》32 (4) (2004) 400 - 405；S.K. Kim、R.F. Novak，细胞内信号传导在胰岛素介导的药物代谢酶基因和蛋白表达调控中的作用，《药理学与治疗学》113 (1) (2007) 88 - 120）。Akt信号通路是DHEA的抗增殖机制之一（Y. Jiang、T. Miyazaki、A. Honda、T. Hirayama、S. Yoshida、N. Tanaka、Y. Matsuzaki，脱氢表雄酮抗增殖作用中的细胞凋亡及磷脂酰肌醇3激酶/Akt信号通路抑制，《胃肠病学杂志》40 (5) (2005) 490 - 497）。制备心脏匀浆以定量脂质过氧化（LPO）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽 - S - 转移酶（GST）、4 - 羟基 - 2 - 壬烯醛（HNE）的浓度以及p - Akt/Akt比值，以及这些抗氧化酶的活性。当以短期（6或24小时）腹腔注射方式给予雄性Wistar大鼠时，DHEA在所使用的不同剂量（1、10和50mg/kg）下，使大鼠心脏氧化应激的某些参数产生了显著差异。此处呈现的关于6小时和24小时氧化应激状态的结果表明，DHEA注射在健康Wistar大鼠心脏中引发了促氧化反应。
