Moreno María Cecilia, Campanelli Julieta, Sande Pablo, Sánez Daniel A, Keller Sarmiento María Inés, Rosenstein Ruth E
Laboratorio de Neuroquímica Retiniana y Oftalmología Experimental, Departmento de Bioquímica Humana, Universidad de Buenos Aires, CONICET, Buenos Aires, Argentina.
Free Radic Biol Med. 2004 Sep 15;37(6):803-12. doi: 10.1016/j.freeradbiomed.2004.06.001.
Glaucoma is an optic neuropathy in which retinal ganglion cells die probably through an apoptotic process. Apoptosis is known to involve free radicals in several systems including the retina. In this context, the aim of the present work was to analyze retinal oxidative damage in rats with glaucoma induced by the chronic injection of hyaluronic acid in the eye anterior chamber. The results showed a significant decrease in total retinal superoxide dismutase and catalase activities after 6 and 3 weeks of treatment with hyaluronic acid, respectively. Also, although GPX activity increased after 10 weeks of ocular hypertension, GSH levels significantly decreased at 6 weeks of treatment with hyaluronic acid. Moreover, retinal lipid peroxidation significantly increased in a time-of-hypertension-dependent manner. On the other hand, a significant decrease in both diurnal and nocturnal retinal melatonin content was detected at 3, 6, or 10 weeks of treatment with hyaluronic acid. The present results suggest that retinal oxidative stress may be involved in glaucomatous cell death. Thus, manipulation of intracellular redox status using antioxidants may be a new therapeutic tool to prevent glaucomatous neurodegeneration.
青光眼是一种视神经病变,其中视网膜神经节细胞可能通过凋亡过程死亡。已知凋亡在包括视网膜在内的多个系统中涉及自由基。在此背景下,本研究的目的是分析通过在前房慢性注射透明质酸诱导青光眼的大鼠的视网膜氧化损伤。结果显示,分别在透明质酸治疗6周和3周后,视网膜超氧化物歧化酶和过氧化氢酶的总活性显著降低。此外,虽然在高眼压10周后谷胱甘肽过氧化物酶活性增加,但在透明质酸治疗6周时谷胱甘肽水平显著降低。此外,视网膜脂质过氧化以高血压时间依赖性方式显著增加。另一方面,在透明质酸治疗3周、6周或10周时,检测到昼夜视网膜褪黑素含量均显著降低。目前的结果表明,视网膜氧化应激可能与青光眼性细胞死亡有关。因此,使用抗氧化剂操纵细胞内氧化还原状态可能是预防青光眼性神经变性的一种新的治疗工具。