XXXX and hepatosteatosis in @entity19 with enhanced oxidative DNA damage processing in mitochondria.

@entity1 @entity25469 @entity249 @entity844 @entity6 @entity28 @entity5 @entity19 @entity7298 @entity706 @entity179 @entity9814 @entity209 @entity9552
Mitochondria play critical roles in oxidative phosphorylation and energy metabolism. Increasing evidence supports that mitochondrial DNA (mtDNA) damage and dysfunction play vital roles in the development of many mitochondria-related diseases, such as @entity28 , @entity6 , @entity249 , @entity179 , and @entity5 in @entity1 . @entity1 @entity25469 -DNA glycosylase 1 ( @entity9552 ) transgenic (TG) @entity19 were produced by nuclear microinjection. Transgene integration was analyzed by PCR. Transgene expression was measured by RT-PCR and Western blot analysis. Mitochondrial DNA damage was analyzed by mutational analyses and measurement of mtDNA copy number. Total fat content was measured by a whole-body scan using dual-energy X-ray absorptiometry. The @entity9552 overexpression in mitochondria increased the abundance of intracellular free radicals and major deletions in mtDNA. @entity28 in @entity9552 TG @entity19 resulted from increased fat content in tissues, produced by @entity7298 . The molecular mechanisms of @entity28 involved overexpression of genes in the central orexigenic (appetite-stimulating) pathway, peripheral lipogenesis, down-regulation of genes in the central anorexigenic (appetite-suppressing) pathway, peripheral adaptive thermogenesis, and @entity844 oxidation. Diffuse hepatosteatosis, @entity9814 , and increased frequency of @entity706 were also seen in these @entity9552 TG @entity19 . High levels of @entity9552 expression in mitochondria, resulting in enhanced oxidative DNA damage processing, may be an important factor in @entity1 @entity209 , @entity249 , and @entity5 .
