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. 2018 Aug 18;19(8):2439. doi: 10.3390/ijms19082439

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Reactive oxygen species (ROS) levels in oocytes of normal control (NO) and obese (OB) mice (A) and mean spindle/chromosomal defects (B) of the oocytes (values are means ± SEM). Obesity was associated with an increase in ROS and elevated molecular damage in oocytes. Melatonin (MEL) treatment reduced both parameters. When SIRT3 was silenced (with siRNA) the actions of melatonin were negated. This suggests that the antioxidant action of melatonin in oocytes depends on stimulation (deacetylation) of SIRT3 which enhances the activity of the antioxidant enzyme, superoxide dismutase. Figure drawn from the data of Han et al. [210]. * p > 0.001.

Reactive oxygen species (ROS) levels in oocytes of normal control (NO) and obese (OB) mice (A) and mean spindle/chromosomal defects (B) of the oocytes (values are means ± SEM). Obesity was associated with an increase in ROS and elevated molecular damage in oocytes. Melatonin (MEL) treatment reduced both parameters. When SIRT3 was silenced (with siRNA) the actions of melatonin were negated. This suggests that the antioxidant action of melatonin in oocytes depends on stimulation (deacetylation) of SIRT3 which enhances the activity of the antioxidant enzyme, superoxide dismutase. Figure drawn from the data of Han et al. [210]. * p > 0.001.