Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal.
Neurochem Int. 2010 Feb;56(3):431-6. doi: 10.1016/j.neuint.2009.11.017. Epub 2009 Dec 3.
Methamphetamine (MA) is a psychostimulant that target the sensory systems, with the neurosensory retina having been shown to be affected. In the brain, MA-related toxicity can be linked to oxidative stress; the same relationship has yet to be established for the retina. The aim of this study, therefore, was to evaluate the effects of repeated exposure to MA on oxidative stress parameters in the rat retina. Oxidative stress parameters in the blood plasma were also assessed. Male Wistar rats were given 5mg/kg MA every 2h for a period of 6h (i.e., 4 injections) daily between postnatal day (PND) 91 and 100. Evolution of body weight was registered. Rats were sacrificed at PND 110. Blood plasma was collected and immediately frozen for storage at -70 degrees C. The eyes were enucleated, and the retina and choroids rapidly dissected on ice under dim light also to be stored at -70 degrees C. Lipid peroxidation activity was measured by the thiobarbituric acid (TBA) test. Total antioxidant status, superoxide dismutase (SOD) activity, catalase (Cat) activity, and nitrogen oxides contents were also determined. Lipid peroxidation was significantly higher in the retina and blood plasma of the MA-treated rats. Total antioxidant levels were significantly lower in both retina and blood plasma of the MA-treated rats. The activity of SOD was significantly increased in the retina and blood plasma of MA-treated rats. Catalase activity did not differ between groups in either the retina or the blood plasma. Nitric oxide production was significantly higher in both the retina and blood plasma in the MA-treated animals. The overall findings show that the oxidative stress defence mechanisms in the retina are compromised by MA toxicity. The results are similar to those found in the brain, and, moreover, showed some correlation with the blood plasma.
甲基苯丙胺（MA）是一种作用于感觉系统的精神兴奋剂，现已证实其对神经感觉视网膜有影响。在大脑中，MA 相关的毒性与氧化应激有关；而这种关系尚未在视网膜中建立。因此，本研究的目的是评估反复接触 MA 对大鼠视网膜氧化应激参数的影响。同时还评估了血浆中的氧化应激参数。雄性 Wistar 大鼠从出生后第 91 天至 100 天期间，每天每 2 小时接受 5mg/kg MA（即 4 次注射）。记录体重变化。大鼠在出生后第 110 天被处死。收集血浆并立即冷冻保存在-70°C。眼球被摘除，视网膜和脉络膜在冰上快速解剖，同样保存在-70°C。通过硫代巴比妥酸（TBA）试验测量脂质过氧化活性。还测定了总抗氧化状态、超氧化物歧化酶（SOD）活性、过氧化氢酶（Cat）活性和氮氧化物含量。MA 处理组大鼠的视网膜和血浆中的脂质过氧化明显升高。MA 处理组大鼠的视网膜和血浆中的总抗氧化水平明显降低。MA 处理组大鼠视网膜和血浆中的 SOD 活性明显增加。视网膜和血浆中的过氧化氢酶活性在各组之间没有差异。MA 处理组大鼠的视网膜和血浆中的一氧化氮生成明显升高。总体研究结果表明，MA 毒性会损害视网膜的氧化应激防御机制。结果与大脑中的结果相似，并且与血浆中的结果存在一些相关性。
