Abstract
We investigated this hypothesis that methamphetamine could directly cause mitochondrial dysfunction and calcitriol could reduce its adverse effects in rat heart isolated mitochondria. Results indicated that 250 µM methamphetamine caused a deleterious alteration in mitochondrial functions, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) collapse, mitochondrial swelling, oxidative stress and lipid peroxidation. While our results indicated that calcitriol (5 µM) can reduce methamphetamine-induced toxicity in isolated cardiac mitochondria. Altogether, the results of the current study showed that methamphetamine directly induce mitochondrial dysfunction through oxidative stress in isolated cardiac mitochondria, which were ameliorated by calcitriol with its antioxidant potential.
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