Effect of dietary fish oil on acute light-induced photoreceptor damage in the rat retina.
OBJECTIVE
Previous studies have shown that ingestion of fish oil (FO) containing a high proportion of n-3 polyunsaturated fatty acids increases the susceptibility of cellular membranes to oxidative damage in various tissues. In the retina, lipid peroxidation is thought to be a major mechanism contributing to light-induced lesions. Therefore, we investigated the effect of FO on acute light-induced photoreceptor damage.


METHODS
For 2 months, weanling rats were fed diets containing either soybean oil (SOY) or FO as main lipid component.


RESULTS
Rats fed FO had significantly higher levels of eicosapentaenoic acid (EPA, 20:5n-3) and higher ratios of EPA to arachidonic acid (AA, 20:4n-6) in retinal phospholipids and diacylglycerols than rats fed SOY. The levels of docosahexaenoic acid (DHA, 22:6n-3) were similar in both dietary groups. The susceptibility to lipid peroxidation was enhanced in the isolated retina of FO-fed rats as shown by higher levels of thiobarbituric acid reactive substances after incubation of retinal membranes with Fe2+/ascorbate. The retinal content of alpha-tocopherol was similar in SOY- and FO-fed animals. Light damage consisting of acute rod outer segment (ROS) disruptions was induced by exposing dark-adapted animals to 600 to 700 lux (230 to 260 microW/cm2) of white fluorescent light for 30 minutes. Damage was quantitated using a computerized multifunctional image analysis of retinal thin sections. Although structural alterations of the ROS were present in both groups, FO-fed rats showed less damage at the base of the ROS. This occurred in spite of higher rhodopsin levels in FO-fed rats. There was no effect of diet on retinal morphology in dark-adapted rats.


CONCLUSIONS
These results indicate that FO does not enhance the susceptibility to acute ROS disk disruptions in the rat retina. Our study further suggests that FO exerts a partial protective effect that may be related to changes in the formation of lipid mediators derived from EPA and AA in retinal phospholipids.
Remé
C E
CE
University Eye Clinic, Zürich, Switzerland.
Malnoë
A
A
Jung
H H
HH
Wei
Q
Q
Munz
K
K
D000208:Acute Disease; D000818:Animals; D004032:Diet; D005227:Fatty Acids / Q000378:metabolism; D005395:Fish Oils / Q000008:administration & dosage*; D008027:Light / Q000009:adverse effects*; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D010743:Phospholipids / Q000378:metabolism; D010786:Photoreceptor Cells / Q000473:pathology* / Q000528:radiation effects; D011833:Radiation Injuries, Experimental / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects*; D012243:Rhodopsin / Q000378:metabolism; D013024:Soybean Oil / Q000008:administration & dosage; D014810:Vitamin E / Q000378:metabolism
D005227:Fatty Acids; D005395:Fish Oils; D008054:Lipid Peroxides; D010743:Phospholipids; D014810:Vitamin E; D013024:Soybean Oil; D012243:Rhodopsin