Mead acid supplementation does not rescue rats from cataract and retinal degeneration induced by N-methyl-N-nitrosourea.
Mead acid supplementation does not rescue rats from cataract and retinal degeneration induced by N-methyl-N-nitrosourea.
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DOI：
10.1293/tox.2014-0036
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发表时间：
2015-01
影响因子：
1.2
通讯作者：
Tsubura A
中科院分区：
文献类型：
--
作者：
Emoto Y;Yoshizawa K;Hamazaki K;Kinoshita Y;Yuki M;Yuri T;Kawashima H;Tsubura A
脂肪酸及其衍生物在对眼部疾病的反应中发挥作用。我们目前的研究探讨了膳食中补充蜂蜜酒酸（MA，5，8，11-二十碳三烯酸）对N-甲基-N-亚硝基脲（MNU）诱导的Sprague-Dawley大鼠白内障和视网膜变性的影响。实验1旨在抑制白内障形成，母鼠在哺乳期饲喂2.4%MA或基础（<0.01%MA）饮食。在出生后第7天，雄性幼仔接受50 mg/kg MNU或溶剂的单次腹膜内（ip）注射。在MNU注射后7天和14天检查透镜混浊和形态。实验2旨在抑制视网膜变性，并与雌性断奶后大鼠进行。在本实验中，母鼠在哺乳期饲喂2.4% MA或基础日粮。此后，在断奶后期间，雌性幼仔连续饲喂相同的饲料。在出生后第21天（断奶时），幼仔接受50 mg/kg MNU单次ip注射。在MNU注射后7天检查视网膜形态。在实验3中，6周龄雌性大鼠在注射MNU前一周开始喂食2.4%MA或基础饮食，然后连续喂食相同的饮食直至处死。给7周龄的大鼠单次ip注射40 mg/kg MNU，然后在注射MNU后1周对视网膜进行形态学检查。在实验1中，在所有的MNU治疗组中发现成熟的白内障，有或没有MA补充。在实验2和3中，分别在有或没有MA补充的情况下，暴露于MNU的所有大鼠的外周和中央外视网膜均发生萎缩。无论是否补充MA，大鼠白内障和视网膜萎缩的严重程度相似。膳食米德酸，这是作为一种替代品，在人体必需脂肪酸缺乏症，不修改MNU诱导的白内障和视网膜变性的大鼠模型。
Fatty acids and their derivatives play a role in the response to ocular disease. Our current study investigated the effects of dietary mead acid (MA, 5,8,11-eicosatrienoic acid) supplementation on N-methyl-N-nitrosourea (MNU)-induced cataract and retinal degeneration in Sprague-Dawley rats. Experiment 1 was designed to inhibit cataract formation, with the dams fed a 2.4% MA or basal (<0.01% MA) diet during lactational periods. On postnatal day 7, male pups received a single intraperitoneal (ip) injection of 50 mg/kg MNU or vehicle. Lens opacity and morphology were examined 7 and 14 days after the MNU injection. Experiment 2 was designed to inhibit retinal degeneration and was performed with female postweaning rats. In this experiment, dams were fed the 2.4% MA or basal diet during the lactational periods. Thereafter, the female pups were continuously fed the same diets during their postweaning periods. On postnatal day 21 (at weaning), pups received a single ip injection of 50 mg/kg MNU. Retinal morphology was examined 7 days after the MNU injection. In experiment 3, six-week-old female rats were fed the 2.4% MA or basal diet starting at one week before the MNU injection and were then continuously fed the same diets until sacrifice. Rats at 7 weeks of age were given a single ip injection of 40 mg/kg MNU, and the retina was then examined morphologically one week after the MNU injection. In experiment 1, mature cataract was found in all of the MNU-treated groups, with or without MA supplementation. In experiments 2 and 3, atrophy of both the peripheral and central outer retina occurred in all rats exposed to MNU, with or without MA supplementation, respectively. The severities of the cataracts and retinal atrophy in the rats were similar regardless of MA supplementation. Dietary mead acid, which is used as a substitute in essential fatty acid deficiency in the body, does not modify MNU-induced cataract and retinal degeneration in rat models.