Curcumin maintains cardiac and mitochondrial function in chronic kidney disease

Phloretin ameliorates arsenic trioxide induced mitochondrial dysfunction in H9c2 cardiomyoblasts mediated via alterations in membrane permeability and ETC complexes

“…The activity of aconitase was significantly reduced in ATO treated cells and it has been reported that reduced activity of aconitase is an indicator of increased mitochondrial superoxide production (Correa et al, 2013). ATO is a potent mitochondrial toxin capable of inducing reactive oxygen species production that mainly originates in the intracellular mitochondrial respiratory chain and further toxic byproducts subsequently produced could lead to mitochondrial damage.…”

Aconitase post-translational modification as a key in linkage between Krebs cycle, iron homeostasis, redox signaling, and metabolism of reactive oxygen species

“…Aconitase protection by certain pharmacological approaches such as the application of a natural pigment with antioxidant activity, curcumin, may be promising in prevention of specific disorders. 76 It seems that Aco may be a convenient sensor to evaluate the redox status of both the cytosolic and mitochondrial cell compartments, but the question of correct measurement of its activity and prevention of experimental artifacts will need especial attention because up to now this is virtually not resolved and extensively debated. an anonymous referee for very professional analysis of the paper and giving valuable suggestions resulting in better and more clear presentation of the material.…”

The beneficial role of curcumin on inflammation, diabetes and neurodegenerative disease: A recent update

“…The pathophysiological mechanisms linked to oxidative stress and mitochondrial dysfunctions were reported to be reduced by treatment with curcumin (Correa et al, 2013). In a rat model of renal injury, curcumin post-treatment reversed 5/6NX-induced glomerular hypertension, hyperfiltration and oxidative stress.…”