Match!
Sergiy I. Musiyenko
University of South Alabama
4Publications
4H-index
360Citations
Publications 4
Newest
#1Larysa V. Yuzefovych (USA: University of South Alabama)H-Index: 7
#2Sergiy I. Musiyenko (USA: University of South Alabama)H-Index: 4
Last.Lyudmila I. Rachek (USA: University of South Alabama)H-Index: 16
view all 4 authors...
Background Recent studies showed a link between a high fat diet (HFD)-induced obesity and lipid accumulation in non-adipose tissues, such as skeletal muscle and liver, and insulin resistance (IR). Although the mechanisms responsible for IR in those tissues are different, oxidative stress and mitochondrial dysfunction have been implicated in the disease process. We tested the hypothesis that HFD induced mitochondrial DNA (mtDNA) damage and that this damage is associated with mitochondrial dysfunc...
134 CitationsSource
#1Lyudmila I. Rachek (USA: University of South Alabama)H-Index: 16
#2Sergiy I. Musiyenko (USA: University of South Alabama)H-Index: 4
Last.Glenn L. Wilson (USA: University of South Alabama)H-Index: 48
view all 4 authors...
A major characteristic of type 2 diabetes mellitus (T2DM) is insulin resistance in skeletal muscle. A growing body of evidence indicates that oxidative stress that results from increased production of reactive oxygen species and/or reactive nitrogen species leads to insulin resistance, tissue damage, and other complications observed in T2DM. It has been suggested that muscular free fatty acid accumulation might be responsible for the mitochondrial dysfunction and insulin resistance seen in T2DM,...
103 CitationsSource
#1Valentina I. Grishko (USA: University of South Alabama)H-Index: 20
#2Lyudmila I. Rachek (USA: University of South Alabama)H-Index: 16
Last.Glenn L. Wilson (USA: University of South Alabama)H-Index: 48
view all 5 authors...
Abstract A growing body of evidence indicates that free fatty acids (FFA) can have deleterious effects on β-cells. It has been suggested that the β-cell dysfunction and death observed in diabetes may involve exaggerated activation of the inducible form of nitric oxide synthase (iNOS) by FFA, with the resultant generation of excess nitric oxide (NO). However, the cellular targets with which NO interact have not been fully identified. We hypothesized that one of these targets might be mitochondria...
45 CitationsSource
#1Lyudmila I. Rachek (IU: Indiana University)H-Index: 16
#2Valentina I. Grishko (IU: Indiana University)H-Index: 20
Last.Glenn L. Wilson (IU: Indiana University)H-Index: 48
view all 6 authors...
Abstract Oxidative damage to mitochondrial DNA (mtDNA) has been suggested to be a key factor in the etiologies of many diseases and in the normal process of aging. Although the presence of a repair system to remove this damage has been demonstrated, the mechanisms involved in this repair have not been well defined. In an effort to better understand the physiological role of recombinant 8-oxoguanine DNA glycosylase/apurinic lyase (OGG1) in mtDNA repair, we constructed an expression vector contain...
78 CitationsSource
1