Open AccessHuman lipoprotein lipase deficiency: does chronic dyslipidemia lead to increased oxidative stress and mitochondrial DNA damage in blood cells?
Author(s) -
M.R.V. Murthy,
Pierre Julien,
Preman J. Singh,
Émile Lévy
Publication year - 1996
Publication title -
acta biochimica polonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.452
H-Index - 78
eISSN - 1734-154X
pISSN - 0001-527X
DOI - 10.18388/abp.1996_4580
Subject(s) - dyslipidemia , lipoprotein lipase , oxidative stress , enzyme , mitochondrial dna , mitochondrion , population , biology , endocrinology , medicine , gene , chemistry , biochemistry , diabetes mellitus , environmental health
Lipoprotein lipase (LPL) is a key enzyme in the metabolism of lipoproteins and their balanced distribution in the plasma. A deficiency of this enzyme due to gene mutations leads to severe dyslipidemia. In this report, we describe the major LPL gene mutations that are prevalent in the French-Canadian population of Québec and the nature of dyslipidemia caused by the resulting enzyme deficiency. We discuss the possibility that dyslipidemia caused by LPL deficiency may enhance oxidative stress in the blood cells, bring about increased fluidity of the membrane components of these cells and increase the susceptibility of their mitochondrial DNA to structural alterations. Some preliminary experimental results in verification of this hypothesis are presented.