Resveratrol Inhibits Oxidative Stress and Prevents Mitochondrial Damage Induced by Zinc Oxide Nanoparticles in Zebrafish (Danio rerio)
Abstract
Despite their wide industrial use, Zinc oxide (ZnO) nanoparticles (NPs) exhibit a high
toxic potential while concerns of their health-related risks are still present, urging additional in vivo
clarification studies. Oxidative stress is recognized as the primary trigger of NP-associated toxicity,
suggesting antioxidants as a promising counteractive approach. Here, we investigated the
protective effect of the natural antioxidant resveratrol against ZnO NP-induced toxicity in vivo
using the zebrafish model. Our findings demonstrate that resveratrol counteracts ZnO NP-induced
zebrafish lethality preventing cardiac morphological and functional damage. NP-induced vascular
structural abnormalities during embryonic fish development were significantly counteracted by
resveratrol treatment. Mechanistically, we further showed that resveratrol inhibits ROS increase,
prevents mitochondrial membrane potential dysfunction, and counteracts cell apoptosis/necrosis
elicited by ZnO NP. Overall, our data provide further evidence demonstrating the primary role of
oxidative stress in NP-induced damage, and highlight new insights concerning the protective
mechanism of antioxidants against nanomaterial toxicity.
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