Linoleic Acid as Causative Agent of Encephalomalacia in Chickens Fed Oxidized Fats.

Machlin, L. J.; Gordon, Rebecca

doi:10.3181/00379727-103-25626

Cited by 56 publications

(7 citation statements)

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“…The addition of 7, 5 and 4 % cottonseed oil and 7 % distilled free fatty acids from soybean oil to the basic diet was sufficient to produce N E repeatedly under controlled experimental conditions. This is in accord with the established concept that the inclusion of high levels of linoleic acid in a vitamin E deficient diet will induce N E (CENTURY and HORWIIT, 1959;MACHLIN and GORDON, 1960;CHEVILLE, 1966). In addition, it was observed from Trials A and C that an increase in the dietary content of cottonseed oil accelerated the clinical appearance of NE.…”

Section: Discussionsupporting

confidence: 85%

Morphological Studies on Nutritional Encephalomalacia in Chicks, with Special Reference to Mineralized Deposits in the Cerebellum

Hassan

Jönsson

Hakkarainen

1985

Zentralblatt für Veterinärmedizin Reihe A

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Summary Nutritional encephalomalacia (NE) was produced experimentally in chicks by diets low in vitamin E and enriched with polyunsaturated fatty acids. The diets were further supplemented with graded levels of DL‐α‐tocopheryl acetate. Neurological signs of NE started to develop at 2 weeks age in the groups receiving no or low dietary DL‐α‐tocopherylacetate supplementation. Pathognomonic alterations of NE and abundant mineralized deposits were observed in the cerebellum of chicks killed prior to or after developing clinical symptoms of NE. The present study indicated that the brain damage was of ischaemic character caused by swelling of the vascular endothelium and microthrombi. Brain damage and mineral deposits existed without signs of ataxia and the mineralization process may even have an acute character. The molecular layer was the main site for mineralization, while the granular layer, followed by the Purkinje cell layer, were less susceptible. Only minor deposits were observed in the white matter and blood vessels. Mineralization was localized to macrophages and astrocytes. Histochemical examination always revealed a stronger reaction for calcium than for iron. Zusammenfassung Morphologische Untersuchungen zur ernährungsbedingten Enzephalomalazie bei Küken unter besonderer Berücksichtigung von mineralisierten Ablagerungen im Kleinhirn Bei Küken wurde eine ernährungsbedingte Enzephalomalazie (NE) experimentell ausgelöst durch eine Diät, die arm war an Vitamin E und angereichert mit mehrfach ungesättigten Fettsäuren. Diese Diät wurde mit unterschiedlichen Mengen von DL‐α‐Tocopherolacetat supplementiert. Neurologische Anzeichen einer NE begannen sich ab einem Alter von 2 Wochen zu entwickeln in denjenigen Gruppen, die keine oder nur eine geringe Supplementation mit DL‐α‐Tocopherolacetat erhielten. Pathognomonische Veränderungen einer NE und reichliche mineralisierte Ablagerungen wurden im Cerebellum von Küken beobachtet, die vor oder nach der Manifestation klinischer Symptome einer NE getötet wurden. Die vorliegenden Untersuchungen weisen darauf hin, daß die Hirnschädigung ischämischer Art war, hervorgerufen durch die Anschwellung des Gefäßendothels und durch Mikrothromben. Hirnschädigung und mineralisierte Ablagerungen kamen ohne Anzeichen einer Ataxie vor und die Mineralisierungsvorgänge können sogar akuter Art sein. Die Molekularschicht war am häufigsten betroffen hinsichtlich der Mineralisierung, während die Körnerschicht, gefolgt von der Purkinje Zellschicht, weniger empfänglich waren. Nur minime Ablagerungen wurden in der weißen Substanz und in Blutgefäßen beobachtet. Die Mineralisierung war in Makrophagen und Astrozyten lokalisiert. Die histochemische Untersuchung ergab jeweils eine stärkere Reaktion für Kalzium als für Eisen. Résumé Recherches morphologiques sur l'encéphalomalazie des poussins dues à l'alimentation avec une attention particulière sur les dépôts minéralisés dans le cervelet Une encéphalomalazie liée à l'alimentation a été expérimentalement déclenchée chez des poussins par un régime pauvr...

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Section: Discussionsupporting

confidence: 85%

Morphological Studies on Nutritional Encephalomalacia in Chicks, with Special Reference to Mineralized Deposits in the Cerebellum

Hassan

Jönsson

Hakkarainen

1985

Zentralblatt für Veterinärmedizin Reihe A

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“…(11) Rahman et al (1960); (12) ; (13) Nesheim and Scott (1958); (14) Dam (1944); (15) Bieri etal. (1959); (21) Machlin and Gordon, (1960a); (22) Singsen et al (1955); (23) Bunnell et al (1955); (24) Ames and Swanson, (1958); (25) ; (26) Bieri et al (1960); (27) Kokatnur et al (1960); (28) Dam et al (1952); (29) Machlin and Shalkop (1956); (30) Nesheim et al (1958); (31) Dam and S^ndergaard (1957); (32) Scott and Calvert (1960); (33) Nesheim et al (1960). toms in the young chicken. (1959); (21) Machlin and Gordon, (1960a); (22) Singsen et al (1955); (23) Bunnell et al (1955); (24) Ames and Swanson, (1958); (25) ; (26) Bieri et al (1960); (27) Kokatnur et al (1960); (28) Dam et al (1952); (29) Machlin and Shalkop (1956); (30) Nesheim et al (1958); (31) Dam and S^ndergaard (1957); (32) Scott and Calvert (1960); (33) Nesheim et al (1960). toms in the young chicken.…”

Section: Discussionmentioning

confidence: 99%

“…INTRODUCTION I N THE young chicken a dietary deficiency of vitamin E will result in either encephalomalacia, exudative diathesis, muscular degeneration or some combination of these symptoms. Recently several major observations have clarified the factors involved, namely that; selenium protects chickens against exudative diathesis (Patterson et al, 1957;Schwarz et al, 1957) but not against encephalomalacia Ames and Swanson, 1958); dietary linoleic or arachidonic acid is necessary for the development of encephalomalacia (Dam et al, 1958b;Machlin and Gordon, 1960a); and that the synthetic antioxidant, Santoquin, 1 will prevent encephalomalacia, muscular degeneration and exudative diathesis even when added to purified diets which are essentially free of vitamin E (Machlin et al, 1959) . Accordingly it has been difficult to produce one E-deficiency symptom uncomplicated by the presence of another.…”

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confidence: 99%

Etiology of Exudative Diathesis, Encephalomalacia, and Muscular Degeneration in the Chicken

Machlin

Gordon

1962

Poultry Science

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“…E NCEPHALOMALACIA usually occurs in young chicks receiving vitamin E-deficient diets which also contain a certain amount of linoleic acid (Dam et al, 1958;Century and Horwitt, 1959;Machlin and Gordon, 1960). The effect of various oils on the incidence of this disease is well documented (Singsen et al, 1954;Mokadi and Budowski, 1963;Dam et al, 1966;and Pudelkiewicz et al, 1970).…”

Section: Introductionmentioning

confidence: 99%

Nutritional Factors Affecting the Occurrence of Experimental Encephalomalacia in Chicks

Bartov

Bornstein

1972

Poultry Science

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Potato starch used as an ingredient in a semi-synthetic vitamin E-deficient diet containing oxidized safflower oil, with or without BHT supplementation, caused a higher incidence of encephalomalacia than did corn starch. Oxidized safflower oil was most effective in promoting the disease followed by oxidized soybean oil, fresh safflower oil and oxidized soybean-oil soapstock. Cod liver oil, either fresh or oxidized, caused relatively few cases of this disease. Fresh soybean oil or soybean soapstock did not induce encephalomalacia. Yellow corn or soybean soapstock, when added to an encephalomalacia-inducing diet, lowered the incidence of the disease in proportion to the amount of a-tocopherol or total reducing substances which they supplied. Dietary non a-tocopherol reducing substances markedly decreased mortality due to encephalomalacia in the presence of relatively low levels of dietary a-tocopherol.at Serials Acq (Law) on May 24, 2015 http://ps.oxfordjournals.org/ Downloaded from

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Linoleic Acid as Causative Agent of Encephalomalacia in Chickens Fed Oxidized Fats.

Cited by 56 publications

References 1 publication

Morphological Studies on Nutritional Encephalomalacia in Chicks, with Special Reference to Mineralized Deposits in the Cerebellum

Morphological Studies on Nutritional Encephalomalacia in Chicks, with Special Reference to Mineralized Deposits in the Cerebellum

Etiology of Exudative Diathesis, Encephalomalacia, and Muscular Degeneration in the Chicken

Nutritional Factors Affecting the Occurrence of Experimental Encephalomalacia in Chicks

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