Key result
Plastomitin administration suppressed the 26% increase in the production rate of short-lived reactive oxygen species induced by doxorubicin in rat heart tissue homogenates.
Why the study?
The study evaluated the protective effects of the mitochondrial-targeted antioxidant plastomitin during hyperproduction of short-lived reactive oxygen species induced by doxorubicin.
Does plastomitin reduce the production rate of short-lived reactive oxygen species in rat heart homogenates following doxorubicin injection?
Does plastomitin reduce the production rate of short-lived reactive oxygen species in rat heart homogenates following doxorubicin injection?
Plastomitin mitigates doxorubicin-induced oxidative stress in rat heart tissue by suppressing the generation of short-lived reactive oxygen species.
The protective effects of the mitochondrial-targeted antioxidant plastomitin (Skulachev ions (SkQs)) were studied upon hyperproduction of short-lived reactive oxygen species (ROS) in animals. The integral production rate of highly toxic oxygen radicals was assessed in oxidative stress induced in rats by doxorubicin injection, and the protective effect of plastomitin was evaluated. Experiments were carried out with rat heart tissue homogenates by EPR spectroscopy. Doxorubicin injection in rats was shown to significantly (by 26%) increase the production rate of short-lived ROS in the homogenate. The effect was suppressed to a great extent when plastomitin was administered together with doxorubicin.
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Timoshin et al. (2023) studied Doxorubicin-induced oxidative stress. Plastomitin vs. Doxorubicin alone was evaluated on Production rate of short-lived reactive oxygen species (ROS) in heart tissue homogenate. Plastomitin administration suppressed the 26% increase in the production rate of short-lived reactive oxygen species induced by doxorubicin in rat heart tissue homogenates.
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