In vivo studies on the toxic effects of microcystins on mitochondrial electron transport chain and ion regulation in liver and heart of rabbit

Oxidative stress response after prolonged exposure of domestic rabbit to a lower dosage of extracted microcystins

“…It has also been supposed that under MCs exposure a block in electron flow along the respiratory chain results in an increased production of free radicals, and LPO products (Turrens, 2003). Recently, our researches have shown the obvious oxidative stress response followed the mitochondrial damage induced by extracted MC in rabbits (Zhao et al, 2008). In our present study, the oxidative stress response showed obviously in different organs.…”

The profound effects of microcystin on cardiac antioxidant enzymes, mitochondrial function and cardiac toxicity in rat

“…It is reported that 3-nitropropionic acidinduced bradycardia in isolated atria is associated with inhibition of mitochondrial respiration and subsequent decreased cardiac ATP content (Lopez et al, 1998). Previous studies identified the binding of ATP synthase by MC in vitro (Mikhailov et al, 2003) and the mitochondrial electron transport chain dysfunction after MC treatment (Zhao et al, 2008), while intracellular ATP depletion was confirmed in microcystin-LR treated lymphocytes from Carassius auratus (Zhang et al, 2007). Therefore, obvious inhibition of mitochondrial respiration in the present study might have resulted in the impairment of ATP generation and thereby depletion of the intracellular ATP, consequently leading to bradycardia.…”

A review of reproductive toxicity of microcystins

“…As GSH is the first line of defense against ROS, its cell efflux should increase ROS generation. Moreover, mitochondria do not have the enzymatic pool associated with GSH synthesis and depends on cytoplasmatic GSH, so the depletion of cytosol GSH could reflect in a decreased GSH concentration inside mitochondria, a situation that favours ROS production and electron transport chain (ETC) disruption [33,103,107,108]. MCs can bind to the beta subunit of ATP-synthase [109], which could disturb oxidative phosphorylation (OXPHOS) system [33,108], reduce ATP synthesis and contribute to the intensification of the mitochondrial membrane depolarization, disruption of ETC and ROS generation.…”