Annual Meeting of the Japanese Society of Toxicology
The 39th Annual Meeting of the Japanese Society of Toxicology
Session ID : P-27
Conference information

Poster Session
Arachidonic acid supplementation during gestational, lactational and post-weaning periods prevents retinal degeneration induced by N-methyl-N-nitrosourea in young Lewis rats
*Katsuhiko YOSHIZAWATomo SASAKIMaki KURONorihisa UEHARAHideho TAKADAAkiko HARAUMANaoki OHARAToru MORIGUCHIAiro TSUBURA
Author information
CONFERENCE PROCEEDINGS FREE ACCESS

Details
Abstract
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/kg MNU or vehicle and were fed the same diet as their mother for 7 days. Retinal apoptosis was analyzed by the TUNEL assay 24 hr after MNU treatment, and retinal morphology was examined 7 days post-MNU. Histologically, all rats that received MNU and were fed basal and 0.1% AA diets developed retinal degeneration characterized by the loss of photoreceptor cells (disappearance of the outer nuclear layer and photoreceptor layer) in the central retina. The 0.5% and 2.0% AA diets suppressed the retinal damage, and the 2.0% AA diet completely rescued rats from retinal damage. Morphometrically, in parallel with AA dose (0.5% and 2.0% AA), the photoreceptor ratio significantly increased and the retinal damage ratio decreased in the central retina, as compared to the corresponding ratios in basal diet–fed rats. In parallel to 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.
Content from these authors
© 2012 The Japanese Society of Toxicology
Previous article Next article
feedback
Top