Age-related changes in retinoic, docosahexaenoic and arachidonic acid modulation in nuclear lipid metabolism

被引:3
作者
Gaveglio, Virginia L. [1 ]
Pascual, Ana C. [1 ]
Giusto, Norma M. [1 ]
Pasquare, Susana J. [1 ]
机构
[1] Univ Nacl Sur, Inst Invest Bioquim Bahia Blanca, CONICET, RA-8000 Bahia Blanca, Buenos Aires, Argentina
关键词
Diacylglycerol; Monoacylglycerol; Nuclei; Retinoic acid; Docosahexaenoic acid; Aging; PROLIFERATOR-ACTIVATED RECEPTORS; POLYUNSATURATED FATTY-ACIDS; LA-N-1; NEUROBLASTOMA-CELLS; ALZHEIMERS-DISEASE; PHOSPHATIDIC-ACID; NERVOUS-SYSTEM; SIGNALING PATHWAY; BOVINE RETINA; BRAIN; PHOSPHOLIPIDS;
D O I
10.1016/j.abb.2016.06.017
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The aim of this work was to study how age-related changes could modify several enzymatic activities that regulate lipid mediator levels in nuclei from rat cerebellum and how these changes are modulated by all-trans retinoic acid (RA), docosahexaenoic acid (DHA) and arachidonic acid (AA). The higher phosphatidate phosphohydrolase activity and lower diacylglycerol lipase (DAGL) activity observed in aged animals compared with adults could augment diacylglycerol (DAG) availability in the former. Additionally, monoacylglycerol (MAC) availability could be high due to an increase in lysophosphatidate phosphohydrolase (LPAPase) activity and a decrease in monocylglycerol lipase activity. Interestingly, RA, DHA and AA were observed to modulate these enzymatic activities and this modulation was found to change in aged rats. In adult nuclei, whereas RA led to high DAG and MAC production through inhibition of their hydrolytic enzymes, DHA and AA promoted high MAC production by LPAPase and DAGL stimulation. In contrast, in aged nuclei RA caused high MAC generation whereas DHA and AA diminished it through LPAPase activity modulation. These results demonstrate that aging promotes a different nuclear lipid metabolism as well as a different type of non-genomic regulation by RA, DHA and AA, which could be involved in nuclear signaling events. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码:121 / 127
页数:7
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