Not exact matches
High PI and DBI equals short lifespan MLSP despite mitochondrial Glutathione and Thioredoxin trying its best to scavenge membrane
Hydroperoxides formation from hydroxyl radical stealing hydrogen atom from unsaturated fatty acids (initiating
lipid peroxidation propagation forming highly mutational reactive aldehydes (MDA, MDA - TBARS), alkenals (4 - HNE), methylglyoxals (creating glucosepane, MDA - Lys, CML, pentosidine, CEL, furosine from Amadori).
But more importantly this old study (by mitochondrial membrande phospholipid fatty acids composition remodeling towards a low perodizable index PI and double bond unsaturation index DBI by genetically reduced desaturase (essentially switching perodizable polyunsaturates with monounsaturates / saturates, rendering membranes
lipid peroxidation resistant / blocking
hydroperoxide formation by DHA n - 3 and lowering mitochondrial DNA lesions formation by membrane
lipid peroxidation chain propagation), It's true though that these effects are due to transcriptional
lipid genes regulation (so the genes are the reason of this dramatic effect and this is also a gene therapy, that hit the key points) this old study showed
The blood glucose, plasma insulin, hemoglobin, glycated hemoglobin, activities of the various antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase) and
lipid peroxidation markers (malondialdehyde,
hydroperoxides and conjugated dienes) were evaluated in all the groups.