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Lysosomal acid phosphatase decrease in nutritional encephalopathy in chicks
Nutrition and Metabolism
|January 1, 1980
Insights
Vitamin E deficiency in chicks induced encephalopathy, significantly reducing bound acid phosphatase activity in the cerebellum. This highlights vitamin E
Area of Science:
- Biochemistry
- Neuroscience
- Nutritional Science
Background:
- Vitamin E is crucial for neurological health.
- Oxidized oils can impact nutrient availability and health.
- Acid phosphatase is an enzyme involved in cellular processes.
Purpose of the Study:
- To investigate the effects of vitamin E deficiency and thermally oxidized safflower oil on chick encephalopathy.
- To examine the activity of acid phosphatase in the cerebellum, cerebrum, and liver of affected chicks.
Main Methods:
- Inducing encephalopathy in 14-day-old chicks using a vitamin E-deficient diet with 15% thermally oxidized safflower oil.
- Measuring bound and free acid phosphatase activity in the cerebellum, cerebrum, and liver of deficient and control chicks.
Main Results:
- Chicks fed a vitamin E-deficient diet exhibited encephalopathy.
- Markedly lower bound acid phosphatase activity was observed in the cerebellum of deficient chicks compared to controls.
- Free acid phosphatase activity also showed a tendency to be lower in the cerebellum of deficient chicks.
- No significant differences in enzyme activities were found in the cerebrum and liver.
Conclusions:
- Vitamin E deficiency, exacerbated by thermally oxidized safflower oil, leads to encephalopathy in chicks.
- Cerebellar bound acid phosphatase activity is significantly reduced in vitamin E-deficient encephalopathic chicks.
- The cerebellum appears to be a primary target for the enzymatic changes associated with this induced neurological condition.
Abstract:
Encephalopathy was induced in 14-day-old chicks by a vitamin E-deficient diet containing 15% thermally oxidized safflower oil. Bound acid phosphatase activity in the cerebellum was markedly lower in affected chicks than in vitamin E-supplied control chicks. Free activity also tended to be lower in the deficient group. There were no differences in enzyme activities of cerebrum and liver between deficient and control chicks.