AI Article Synopsis
- Mitochondrial dysfunction from high levels of reactive oxygen species (ROS) during embryonic development can cause growth issues.
- This study investigates if maternal zinc (Zn) can protect against oxidative stress affecting mitochondrial function, using an avian model.
- Results show that Zn supplementation improves mitochondrial health by boosting ATP production and reducing oxidative damage, suggesting it can safeguard offspring from oxidative stress through Nrf2/PGC-1α signaling activation.
Article Abstract
Background: Mitochondrial dysfunction induced by excessive mitochondrial reactive oxygen species (ROS) damages embryonic development and leads to growth arrest.
Objective: The purpose of this study is to elucidate whether maternal zinc (Zn) exert protective effect on oxidative stress targeting mitochondrial function using an avian model.
Result: In ovo injected tert-butyl hydroperoxide (BHP) increases (P < 0.05) hepatic mitochondrial ROS, malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine (8-OHdG), and decreases (P < 0.05) mitochondrial membrane potential (MMP), mitochondrial DNA (mtDNA) copy number and adenosine triphosphate (ATP) content, contributing to mitochondrial dysfunction. In vivo and in vitro studies revealed that Zn addition enhances (P < 0.05) ATP synthesis and metallothionein 4 (MT4) content and expression as well as alleviates (P < 0.05) the BHP-induced mitochondrial ROS generation, oxidative damage and dysfunction, exerting a protective effect on mitochondrial function by enhancing antioxidant capacity and upregulating the mRNA and protein expressions of Nrf2 and PGC-1α.
Conclusions: The present study provides a new way to protect offspring against oxidative damage by maternal Zn supplementation through the process of targeting mitochondria involving the activation of Nrf2/PGC-1α signaling.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10091542 | PMC |
| http://dx.doi.org/10.1186/s40104-023-00852-1 | DOI Listing |
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