Melatonin protects against maternal diabetes-associated meiotic defects by maintaining mitochondrial function
Maternal diabetes has been widely reported to adversely affect oocyte quality. Although various molecules and pathways may be involved in this process, strategies to prevent maternal diabetes-induced deterioration of oocyte quality remain unexplored. Melatonin is synthesized by the pineal gland and...
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| Published in | Free radical biology & medicine Vol. 188; pp. 386 - 394 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Elsevier Inc
01.08.2022
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| Online Access | Get full text |
| ISSN | 0891-5849 1873-4596 1873-4596 |
| DOI | 10.1016/j.freeradbiomed.2022.06.243 |
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| Abstract | Maternal diabetes has been widely reported to adversely affect oocyte quality. Although various molecules and pathways may be involved in this process, strategies to prevent maternal diabetes-induced deterioration of oocyte quality remain unexplored. Melatonin is synthesized by the pineal gland and has been shown to have beneficial effects on oocyte quality owing to its antioxidative function. In the present study, we found that the exposure of oocytes of diabetic mice to melatonin, in vitro, alleviated aberrant oocyte maturation competence. Notably, melatonin supplementation attenuated defects in spindle organization and chromosome alignment by mediating the expression of TPX2 and pericentrin localization. Importantly, melatonin eliminated the accumulation of reactive oxygen species and increased the cytosolic Ca2+ levels in diabetic oocytes by maintaining mitochondrial function. Moreover, the occurrence of autophagy and apoptosis was reversed in diabetic oocytes after melatonin exposure via decreased LC3β expression. Collectively, our findings provide evidence that melatonin supplementation can protect oocytes from maternal diabetes-related meiotic defects and poor egg quality, providing a potential strategy for improving oocyte quality in assisted reproductive technologies.
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•Melatonin restores the maternal diabetes-induced deterioration of oocyte quality.•Melatonin improves the oocyte maturation competency of diabetic oocytes.•Melatonin alleviates maternal diabetes-induced mitochondrial dysfunction.•Melatonin suppresses the oxidative stress-induced DNA damage and apoptosis of diabetic oocytes. |
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| AbstractList | Maternal diabetes has been widely reported to adversely affect oocyte quality. Although various molecules and pathways may be involved in this process, strategies to prevent maternal diabetes-induced deterioration of oocyte quality remain unexplored. Melatonin is synthesized by the pineal gland and has been shown to have beneficial effects on oocyte quality owing to its antioxidative function. In the present study, we found that the exposure of oocytes of diabetic mice to melatonin, in vitro, alleviated aberrant oocyte maturation competence. Notably, melatonin supplementation attenuated defects in spindle organization and chromosome alignment by mediating the expression of TPX2 and pericentrin localization. Importantly, melatonin eliminated the accumulation of reactive oxygen species and increased the cytosolic Ca2+ levels in diabetic oocytes by maintaining mitochondrial function. Moreover, the occurrence of autophagy and apoptosis was reversed in diabetic oocytes after melatonin exposure via decreased LC3β expression. Collectively, our findings provide evidence that melatonin supplementation can protect oocytes from maternal diabetes-related meiotic defects and poor egg quality, providing a potential strategy for improving oocyte quality in assisted reproductive technologies.
[Display omitted]
•Melatonin restores the maternal diabetes-induced deterioration of oocyte quality.•Melatonin improves the oocyte maturation competency of diabetic oocytes.•Melatonin alleviates maternal diabetes-induced mitochondrial dysfunction.•Melatonin suppresses the oxidative stress-induced DNA damage and apoptosis of diabetic oocytes. Maternal diabetes has been widely reported to adversely affect oocyte quality. Although various molecules and pathways may be involved in this process, strategies to prevent maternal diabetes-induced deterioration of oocyte quality remain unexplored. Melatonin is synthesized by the pineal gland and has been shown to have beneficial effects on oocyte quality owing to its antioxidative function. In the present study, we found that the exposure of oocytes of diabetic mice to melatonin, in vitro, alleviated aberrant oocyte maturation competence. Notably, melatonin supplementation attenuated defects in spindle organization and chromosome alignment by mediating the expression of TPX2 and pericentrin localization. Importantly, melatonin eliminated the accumulation of reactive oxygen species and increased the cytosolic Ca2+ levels in diabetic oocytes by maintaining mitochondrial function. Moreover, the occurrence of autophagy and apoptosis was reversed in diabetic oocytes after melatonin exposure via decreased LC3β expression. Collectively, our findings provide evidence that melatonin supplementation can protect oocytes from maternal diabetes-related meiotic defects and poor egg quality, providing a potential strategy for improving oocyte quality in assisted reproductive technologies.Maternal diabetes has been widely reported to adversely affect oocyte quality. Although various molecules and pathways may be involved in this process, strategies to prevent maternal diabetes-induced deterioration of oocyte quality remain unexplored. Melatonin is synthesized by the pineal gland and has been shown to have beneficial effects on oocyte quality owing to its antioxidative function. In the present study, we found that the exposure of oocytes of diabetic mice to melatonin, in vitro, alleviated aberrant oocyte maturation competence. Notably, melatonin supplementation attenuated defects in spindle organization and chromosome alignment by mediating the expression of TPX2 and pericentrin localization. Importantly, melatonin eliminated the accumulation of reactive oxygen species and increased the cytosolic Ca2+ levels in diabetic oocytes by maintaining mitochondrial function. Moreover, the occurrence of autophagy and apoptosis was reversed in diabetic oocytes after melatonin exposure via decreased LC3β expression. Collectively, our findings provide evidence that melatonin supplementation can protect oocytes from maternal diabetes-related meiotic defects and poor egg quality, providing a potential strategy for improving oocyte quality in assisted reproductive technologies. |
| Author | Wang, Yi Liu, Yu Niu, Dong Li, Xiao-Qing Duan, Xing Ma, Xiang Li, Si-Hong Yang, Shu-Jie Liu, Lu |
| Author_xml | – sequence: 1 givenname: Xiao-Qing surname: Li fullname: Li, Xiao-Qing – sequence: 2 givenname: Yi surname: Wang fullname: Wang, Yi – sequence: 3 givenname: Shu-Jie surname: Yang fullname: Yang, Shu-Jie – sequence: 4 givenname: Yu surname: Liu fullname: Liu, Yu – sequence: 5 givenname: Xiang surname: Ma fullname: Ma, Xiang – sequence: 6 givenname: Lu surname: Liu fullname: Liu, Lu – sequence: 7 givenname: Si-Hong surname: Li fullname: Li, Si-Hong – sequence: 8 givenname: Dong surname: Niu fullname: Niu, Dong email: dniu@zafu.edu.cn – sequence: 9 givenname: Xing orcidid: 0000-0002-0538-9102 surname: Duan fullname: Duan, Xing email: duanxing@zafu.edu.cn |
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