Lovastatin attenuates glyoxal-induced toxicity on rat liver mitochondria.
A HosseinzadehSaeed MehrzadiM RezaeiM BadaviA NesariMehdi GoudarziPublished in: Human & experimental toxicology (2021)
Alpha-dicarbonyls such as glyoxal (GO) trigger mitochondrial dysfunction resulting in the development of different diabetic complications. The present study investigated the effects of lovastatin against GO-induced toxicity on rat liver mitochondria. The rat liver mitochondria (0.5 mg protein/mL) were treated with various concentrations of lovastatin (1, 5, 10 µM) at 37°C for 30 min and then exposed to GO (3 mM) at 37°C for 30 min. Oxidative stress markers including MDA, reactive oxygen species (ROS), glutathione (GSH) and protein carbonylation (PC) level were measured. Mitochondrial complex II activity and mitochondrial membrane potential (MMP) were assessed for evaluating mitochondrial function. Glyoxal significantly increased the level of ROS, PC and MDA. This effect was associated with the reduction of MMP, complex II activity and GSH content. Pre-treatment with lovastatin potentially reversed GO-induced mitochondrial toxicity. These results suggest that lovastatin have a protective effect against GO-induced toxicity in isolated rat liver mitochondria.
Keyphrases
- oxidative stress
- diabetic rats
- reactive oxygen species
- dna damage
- cell death
- high glucose
- ischemia reperfusion injury
- induced apoptosis
- type diabetes
- drug induced
- endothelial cells
- cell proliferation
- endoplasmic reticulum
- small molecule
- fluorescent probe
- newly diagnosed
- cell cycle arrest
- risk assessment
- mass spectrometry
- stress induced
- pi k akt
- combination therapy
- wound healing