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Background. Epidemiological studies indicate that by consuming 6-14 mg lutein daily, the risk of acquiring eye diseases like age-related macular degeneration (AMD) or cataracts becomes reduced. Their symptoms can also by such means be alleviated and treatment improved. Objectives. To estimate dietary intakes of lutein obtained from foodstuffs and supplements along with determining its main sources in selected groups of adults suffering from eye disease and healthy controls. Material and Methods. The study was performed in Warsaw and its neighbourhoods during 2008-12. Subjects were 375 adults aged 50-97 years, of whom half had been diagnosed with AMD and/or cataracts; constituting the test group. Dietary intakes of lutein were assessed by Food Frequency Questionnaire Method whilst interview questionnaires assessed the intake of supplements. Results. Overall, the average dietary intake of lutein from foodstuffs was 2.5 mg daily, with the test group being significantly higher than healthy controls (2.9 vs 2.1 mg daily). Women’s intakes were also higher than in men (2.9 vs 2.1 mg daily), as were those possessing higher or secondary education compared to the others with primary or vocational education (2.7 vs 2.3 mg daily). Fresh vegetables were found to be the main dietary sources of lutein that included green leafy vegetables and frozen vegetables, constituting respectively 63% and 13% of the dietary intake. Dietary supplements containing lutein were taken by 109 subjects of whom most had eye disease (over 80%); where the average daily consumption of lutein from this source was 6.5 mg. Conclusions. For older people, the dietary intake of lutein from foodstuffs may be insufficient to prevent eye disease. Taking daily dietary supplements would thus be indicated to make up such deficiencies of lutein.
Sphingolipid deregulation may be an important factor of age-related neuronal stress vulnerability. Current data suggests potential links between sphingosine kinases (SphK1&2), their product sphingosine1-phosphate (S1P) and age-related protein conformation diseases. The aim of this study was to investigate a possible role of SphKs in alpha-synuclein (ASN) and amyloid beta (ABeta) precursor protein (APP) level and secretion. The studies were carried out using human SH-SY5Y neuroblastoma cell line stably transfected with the human gene for α-synuclein (ASNwt). Sphingosine kinase inhibitor (SKI) significantly increased ASN secretion in concentration-dependent manner. S1P also displayed similar influence. Neither compound exerted any significant effect on the ASN protein level. S1P may act via cell surface receptors or as an intracellular second messenger. The similar effect of S1P and SphK inhibitors on ASN secretion may suggest that the regulation of its release is critically dependent on the varied (intra)cellular targets of SphKs and downstream signaling pathways. We have found that stable human ASNwt expression in SH-SY5Y cells caused a three-fold, significant increase of the cellular APP level. In ASN-transfected cells S1P enhanced APP secretion and reduced its intracellular level. This could be linked to the recently reported effect of S1P on secretase beta activity. Inhibition of SphKs significantly decreased APP secretion. In summary our data indicates that endogenous ASN regulates APP level in SH-SY5Y cells and that sphingolipids play a crucial role in the secretion of ASN and APP. These processes may have significant impact on neuronal survival and health.
Aging is a complex process involving morphologic and biochemical changes in single cells and in the whole organism. One of the most popular explanations of how aging occurs at the molecular level is the oxidative stress hypothesis. Oxidative stress leads in many cases to an age-dependent increase in the cellular level of oxidatively modified macromolecules including DNA, and it is this increase which has been linked to various pathological conditions, such as aging, carcinogenesis, neurodegenerative and cardiovascular diseases. It is, however, possible that a number of short-comings associated with gaps in our knowledge may be responsible for the failure to produce definite results when applied to understanding the role of DNA damage in aging and age-related diseases.
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