title: Arachidonic acid supplementation during gestational, lactational and post-weaning periods prevents retinal degeneration induced in a rodent model.
abstract: Fatty acids and their derivatives play a role in the response to retinal injury. The effects of dietary arachidonic acid (AA) supplementation on N-methyl-N-nitrosourea (MNU)-induced retinal degeneration was investigated in young Lewis rats during the gestational, lactational and post-weaning periods. Dams were fed 0·1, 0·5 or 2·0% AA diets or a basal (< 0·01% AA) diet. On postnatal day 21 (at weaning), male pups received a single intraperitoneal injection of 50 mg MNU/kg or vehicle, and were fed the same diet as their mother for 7 d. Retinal apoptosis was analysed by the terminal deoxynucleotidyl transferase-mediated dUTP digoxigenin nick-end labelling (TUNEL) assay 24 h after the MNU treatment, and retinal morphology was examined 7 d post-MNU. Histologically, all rats that received MNU and were fed the basal and 0·1% AA diets developed retinal degeneration characterised by the loss of photoreceptor cells (disappearance of the outer nuclear layer and the photoreceptor layer) in the central retina. The 0·5 and 2·0% AA diets rescued rats from retinal damage. Morphometrically, in parallel with the AA dose (0·5 and 2·0% AA), the photoreceptor ratio significantly increased and the retinal damage ratio decreased in the central retina, compared with the corresponding ratios in basal diet-fed rats. In parallel with the increase in serum and retinal AA levels and the AA:DHA ratio, the apoptotic index in the central retina was dose-dependently decreased in rats fed the 0·5 and 2·0% AA diets. In conclusion, an AA-rich diet during the gestation, lactation and post-weaning periods rescued young Lewis rats from MNU-induced retinal degeneration via the inhibition of photoreceptor apoptosis. Therefore, an AA-enriched diet in the prenatal and postnatal periods may be an important strategy to suppress the degree of photoreceptor injury in humans.
authors.affiliation: Department of Pathology II, Kansai Medical University, 10-15 Fumizono, Moriguchi, Osaka 570-8506, Japan. yoshizak@takii.kmu.ac.jp
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Yoshizawa
authors.forename: Tomo
authors.initials: T
authors.lastname: Sasaki
authors.forename: Maki
authors.initials: M
authors.lastname: Kuro
authors.forename: Norihisa
authors.initials: N
authors.lastname: Uehara
authors.forename: Hideho
authors.initials: H
authors.lastname: Takada
authors.forename: Akiko
authors.initials: A
authors.lastname: Harauma
authors.forename: Naoki
authors.initials: N
authors.lastname: Ohara
authors.forename: Toru
authors.initials: T
authors.lastname: Moriguchi
authors.forename: Airo
authors.initials: A
authors.lastname: Tsubura
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D016718:Arachidonic Acid / Q000032:analysis / Q000097:blood / Q000494:pharmacology*; D019587:Dietary Supplements; D004195:Disease Models, Animal; D005260:Female; D020287:In Situ Nick-End Labeling; D007774:Lactation; D008770:Methylnitrosourea; D020419:Photoreceptor Cells, Vertebrate / Q000166:cytology / Q000187:drug effects*; D011247:Pregnancy; D051381:Rats; D011917:Rats, Inbred Lew; D012160:Retina / Q000473:pathology / Q000503:physiopathology; D012162:Retinal Degeneration / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*
chemical_list: D016718:Arachidonic Acid; D008770:Methylnitrosourea