Human lipoprotein lipase deficiency: does chronic dyslipidemia lead to increased oxidative stress and mitochondrial DNA damage in blood cells?

Abstract

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.

Nicarbazin Induce Oxidative Response and Colony Stimulating Factor Production in Mouse lung Cells In Vitro

“…It can be highlighted that the mechanism of action of Nicarbazin and its ingredients in alternation of oxidative stress level may have different pathway because there are lots of structures proposed but none is precisely approved. As it said NCZ can increase the action of some enzymes in the metabolism of body, like lipoprotein lipase 8 , and variation in the activity of these enzymes can consequently impress the antioxidative defense system [15][16][17][18][19][20][21][22] . In conclusion lipoprotein lipase activation may be the most effective pathway in calling Nicarbazin as sources for oxidative stress.…”

“…Unfortunately, by the best of literature review, no evidence was found which can illustrate the long term effects of this drug. But if we consider that NCZ can activate lipoprotein lipase 8 , and take into account the relationships between lipoprotein lipase expression and oxidative stress, concluded from different studies [15][16][17][18][19][20][21][22] , it may hypothesized that Nicarbazin can affect the oxidative situation of cells.…”

LDLR C1725T Gene Polymorphism Frequency in Type 2 Diabetes Mellitus Patients With Dyslipidemia

“…Due to the high morbidity and mortality in these patients, the prevention of cardiovascular complications has become a primary objective in the management of diabetes [ 7 ]. In addition to insulin resistance, other cardiovascular risk factors include dyslipidemia, hypertension, susceptibility to coagulation, obesity, hyperinsulinemia and inflammation [ 8 , 9 ]. Dyslipidemia, one of the most important risk factors, includes various pathologic conditions involving abnormal concentration, composition and distribution of lipids.…”