Heart tissue of harlequin (hq)/Big Blue mice has elevated reactive oxygen species without significant impact on the frequency and nature of point mutations in nuclear DNA.

摘要: Abstract Age is a major risk factor for heart disease, and cardiac aging characterized by elevated mitochondrial reactive oxygen species (ROS) with compromised nuclear DNA integrity. To assess links between increased ROS levels mutations, we examined in situ of cII mutation frequency, pattern spectrum the harlequin ( hq )/Big Blue ® mice. The mouse model premature dysfunction oxidative stress-induced disease means vivo detection. produces significant downregulation X-linked apoptosis-inducing gene Aif ) impairing both antioxidant phosphorylation functions AIF. Brain skin mice have frequencies point mutations histopathology cell loss. Reports associated elevations brain mixed results. Herein, were compared to AIF-proficient p carrier Heart also assessed 15 days following an acute exposure exogenous inducer (10 mg paraquat/kg). Acute paraquat short mutant manifestation period was insufficient elevate frequency or alter post-mitotic tissue Paraquat induction requires complex I thus likely Results this preliminary survey context recent literature suggest that determining causal AIF deficiency phenotypes specific tissues better addressed assay large-scale changes types.