作者: Giuseppina Barrera , Fabrizio Gentile , Stefania Pizzimenti , Rosa Canuto , Martina Daga
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摘要: In several human diseases, such as cancer and neurodegenerative the levels of reactive oxygen species (ROS), produced mainly by mitochondrial oxidative phosphorylation, is increased. cells, increase ROS production has been associated with mtDNA mutations that, in turn, seem to be functional alterations bioenergetics biosynthetic state cells. Moreover, overproduction can enhance peroxidation fatty acids membranes. particular, phospholipid cardiolipin leads formation aldehydes, 4-hydroxynonenal (HNE) malondialdehyde (MDA), which are able react proteins DNA. Covalent modifications products lipid (LPO) course cell stress involved dysfunctions observed diseases. Such appear affect negatively integrity function, particular energy metabolism, adenosine triphosphate (ATP) production, antioxidant defenses responses. indirect confirmation for pathogenetic relevance LPO-dependent comes from disease phenotypes their genetic alterations.