Summary.
Chicks fed vitamin E deficient diets containing 5 per cent cod liver oil developed peroxides in the adipose tissue during the period in which the known symptoms of exudation, and particularly brown coloration of the same tissue occurred. The relation between the peroxidation and the symptoms is discussed.
Subcutaneous injection of 0.3 ml of cod liver oil with a peroxide value of 16 to chicks receiving a normal diet, resulted in very marked peroxidation at the site of injection accompanied by a progressive deposition of yellow to brown fibrous material. This local peroxidation was not prevented by the incorporation of 2.4 mg of free natural alpha‐tocopherols in the injected oil.
Rats reared on vitamin E deficient diets containing 20 per cent cod liver oil from weaning developed peroxides in the adipose tissue preceding the visible yellow‐brown coloration which appeared first in the paraepididymal fat, then in the intraperitoneal, and finally in the subcutaneous fat. When females together with their offspring were given the same diet from the time of delivery, the symptoms in the young developed earlier than in weanling rats and were more marked.
The yellow‐brown color of the adipose tissue is due to two substances, one of which is extractable with fat solvents, while the other, which occurs in larger quantity, is soluble in dilute alkali. A further, preliminary, characterization of this latter substance is given.
Vitamin E has no influence on the lowering of hemoglobin caused by feeding high cod liver oil diets to young rats.
Background: Biomarkers are essential for identification of individuals at high risk of mild cognitive impairment (MCI) for potential prevention of dementia. We investigated DNA methylation in the APOE gene and apolipoprotein E (ApoE) plasma levels as MCI biomarkers in Colombian subjects with MCI and controls. Methods: In total, 100 participants were included (71% women; average age, 70 years; range, 43–91 years). MCI was diagnosed by neuropsychological testing, medical and social history, activities of daily living, cognitive symptoms and neuroimaging. Using multivariate logistic regression models adjusted by age and gender, we examined the risk association of MCI with plasma ApoE and APOE methylation. Results: MCI was diagnosed in 41 subjects (average age, 66.5 ± 9.6 years) and compared with 59 controls. Elevated plasma ApoE and APOE methylation of CpGs 165, 190, and 198 were risk factors for MCI (p < 0.05). Higher CpG-227 methylation correlated with lower risk for MCI (p = 0.002). Only CpG-227 was significantly correlated with plasma ApoE levels (correlation coefficient = −0.665; p = 0.008). Conclusion: Differential APOE methylation and increased plasma ApoE levels were correlated with MCI. These epigenetic patterns require confirmation in larger samples but could potentially be used as biomarkers to identify early stages of MCI.
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