Nitric oxide synthase activity in mitochondria

TL;DR: Melatonin preserves mitochondrial function by preventing cardiolipin oxidation and this may explain, at least in part, the protective role of this compound in mitochondrial physiopathology and aging.

TL;DR: A growing body of evidence suggests that a mitochondrial defect might cause the impairement of differentiation and invasion of the trophoblast that leads to pre-eclampsia.

TL;DR: Experimental evidence that a mammalian ortholog of AtNOS1 protein functions in the cellular context of mitochondria is presented, suggesting that a candidate for mammalian mitochondrial nitric oxide synthase contributes to multiple physiological processes during embryogenesis.

TL;DR: How Ca2+ regulates several metabolic programs in T cells such as the activation of AMPK and the PI3K-AKT-mTORC1 pathway, aerobic glycolysis, mitochondrial metabolism including tricarboxylic acid (TCA) cycle function and oxidative phosphorylation (OXPHOS), as well as lipid metabolism is discussed.

TL;DR: The cage mechanism can explain the residual yield of nitrate that appears to be formed even in the presence of high concentrations of all of the scavengers studied to date, since scavengers capture only free HO. and .NO2 and not caged radicals.

TL;DR: Results indicate that nitric oxide is capable of rapidly and reversibly inhibiting the mitochondrial respiratory chain and may be implicated in the cytotoxic effects of Nitric oxide in the CNS and other tissues.

TL;DR: It is assumed, given the monooxygenase-like activity of NOS and the heavy iso- tope labeling studies, that H20 is the ultimate fate of the other oxygen atom.