کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1066907 948852 2015 15 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Zebrafish retinal defects induced by ethanol exposure are rescued by retinoic acid and folic acid supplement
ترجمه فارسی عنوان
نقص شبکیه گورخرماهی ناشی از قرار گرفتن در معرض اتانول توسط رتینوئیک اسید و مکمل اسید فولیک برطرف می شود
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
چکیده انگلیسی


• A zebrafish FASD model showed retinal defects similar to those seen in FASD patients.
• Ethanol exposure severely disrupted retinal morphogenesis.
• RA and FA co-supplement reversed ethanol-induced retinal differentiation defects.
• RA post-supplementation but not FA reversed retinal cell differentiation defects.

Fetal Alcohol Spectrum Disorder (FASD) is caused by prenatal alcohol exposure, producing craniofacial, sensory, motor, and cognitive defects. FASD is highly prevalent in low socioeconomic populations, which are frequently accompanied by malnutrition. FASD-associated ocular pathologies include microphthalmia, optic nerve hypoplasia, and cataracts. The present study characterizes specific retinal tissue defects, identifies ethanol-sensitive stages during retinal development, and dissects the effect of nutrient supplements, such as retinoic acid (RA) and folic acid (FA) on ethanol-induced retinal defects. Exposure to pathophysiological concentrations of ethanol (during midblastula transition through somitogenesis; 2–24 h post fertilization [hpf]) altered critical transcription factor expression involved in retinal cell differentiation, and produced severe retinal ganglion cell, photoreceptor, and Müller glial differentiation defects. Ethanol exposure did not alter retinal cell differentiation induction, but increased retinal cell death and proliferation. RA and FA nutrient co-supplementation rescued retinal photoreceptor and ganglion cell differentiation defects. Ethanol exposure during retinal morphogenesis stages (16–24 hpf) produced retinal defects like those seen with ethanol exposure between 2 and 24 hpf. Significantly, during an ethanol-sensitive time window (16–24 hpf), RA co-supplementation moderately rescued these defects, whereas FA co-supplementation showed significant rescue of optic nerve and photoreceptor differentiation defects. Interestingly, RA, but not FA, supplementation after ethanol exposure could reverse ethanol-induced optic nerve and photoreceptor differentiation defects. Our results indicate that various ethanol-sensitive events underlie FASD-associated retinal defects. Nutrient supplements like retinoids and folate were effective in alleviating ethanol-induced retinal defects.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Alcohol - Volume 49, Issue 2, March 2015, Pages 149–163
نویسندگان
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