Lipid oxidation products and chick nutritional encephalopathy

Area of Science:

• Nutritional biochemistry
• Animal nutrition
• Lipid oxidation

Background:

• Vitamin E deficiency can lead to nutritional encephalopathy (NE) in animals.
• Dietary lipids, particularly polyunsaturated fatty acids, are susceptible to oxidation.
• The role of oxidized lipids and their byproducts in NE is not fully understood.

Purpose of the Study:

• To investigate the effect of thermally oxidized safflower oil and its methyl esters on nutritional encephalopathy (NE) in vitamin E deficient chicks.
• To identify specific lipid components responsible for exacerbating NE.
• To explore potential protective agents against NE.

Main Methods:

• Safflower oil and its methyl esters were thermally oxidized.
• These oxidized lipids were fed to vitamin E deficient young chicks at a 10% dietary level.
• Polar lipid extracts and synthetic keto-fatty acids were tested for NE-inducing effects.
• The impact of Dicumarol as a potential protective agent was evaluated.

Main Results:

• Dietary oxidized lipids at 10% significantly worsened NE compared to unoxidized methyl esters.
• A polar lipid extract from oxidized methyl esters accelerated NE induction.
• Synthetic methyl esters of keto-octadecenoic and keto-octadecadienoic acids also accelerated NE.
• Dicumarol demonstrated a protective effect against NE.

Conclusions:

• Factors beyond dietary linoleic acid and vitamin E contribute to NE development.
• Conjugated keto-polyenoic fatty acids, potentially from oxidized oils or endogenous formation, may play a causative role in NE.
• Further research into these specific lipid oxidation products is warranted for understanding and preventing NE.