Diet-induced lipofuscin and ceroid formation in growing pigs.
Seven piglets, aged 2 weeks at the beginning of the experiment, were fed a diet lacking antioxidants (vitamin E and selenium) and enriched with thermally oxidated cod liver oil (the peroxide value of which was 310 meqv/kg). From one month before to 4 weeks after farrowing (weaning) the sow also received the experimental diet. One pig died at 9 days of age, due to degeneration of the parenchymal tissues. The oxidative stress produced was aggravated in four of the seven remaining pigs by giving them an injection of iron-dextran (300 mg) one day before the animals were killed for necropsy at the age of 2 months. The three other piglets were given an injection of a control saline solution. The nutritional myodegeneration produced ('white muscle disease') was characterized by a pale, yellowish colour and translucence of skeletal muscle, with degeneration, including swelling of the muscle fibres and slackening of the fibrillar pattern. The arrangement of nuclei in chains indicated repair. Ultrastructurally, skeletal muscle showed vacuolization of the sarcoplasmic reticulum, irregularities in the mitochondria and focal dissolution of myofibrils. The sarcoplasmic reticulum displayed condensation and lamellar formations. Hyaline degeneration of the heart muscle occurred both in iron-treated and control pigs, and in six animals a yellowish pigment resembling lipofuscin and ceroid was observed. Ultrastructurally, the ceroid deposits appeared as myelin-like figures. The livers were pale and brittle, four with centrilobular degeneration. By light microscopy, lipidosis was distinguished in four and ceroid accumulations in three pigs. Thiobarbituric-acid-reactive substances, creatine kinase activity and iron increased significantly in the serum as a result of the injection of iron-dextran.
Department of Pathological Anatomy, College of Veterinary Medicine, Helsinki, Finland.
B G
BG
de Gritz
T
T
Rahko
H
H
Korpela
D000821:Animal Feed / Q000009:adverse effects*; D000818:Animals; D002566:Ceroid / Q000096:biosynthesis*; D005296:Ferrous Compounds / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000502:physiology; D008064:Lipidoses / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000662:veterinary*; D008062:Lipofuscin / Q000096:biosynthesis*; D008099:Liver / Q000473:pathology; D009132:Muscles / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D010084:Oxidation-Reduction / Q000187:drug effects; D013552:Swine; D013553:Swine Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology
D002566:Ceroid; D005296:Ferrous Compounds; D008062:Lipofuscin