Tissue & cell · 2026
Maternal tocotrienol supplementation protects early embryo mitochondria from allergic asthma stress.
СтатьяНазвание и аннотация: Перевод в очереди
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Wafriy Che Ismail, Kamsani Yuhaniza Shafinie, Muid Suhaila Abd, Sarbandi Mimi Sophia, Nor-Ashikin Mohamed Noor Khan
Аннотация
BACKGROUND: To determine whether maternal tocotrienol-rich fraction supplementation restores mitochondrial-volume, -fusion, and -interaction with lipid droplets in 2-cell embryos of ovalbumin-induced allergic asthma mice.
METHOD: Female BALB/c mice were sensitised and challenged with ovalbumin to induce allergic asthma and subsequently supplemented with tocotrienol-rich fraction. Two-cell embryos were collected for ultrastructural evaluation using transmission electron microscopy (TEM) and for gene expression analysis using Fluidigm qPCR including developmental potential thru microscopic analysis. Mitochondrial relative volume, mitochondrial clusters volume (fusion), lipid droplet volume and peridroplet mitochondria formation together with gene expression of mitochondrial fusion (Mfn1, Mfn2, Opa1) and ATP synthesis (Atp5e, Cox4i1) were studied.
RESULTS: Ovalbumin-induced allergic asthma significantly reduced total mitochondrial relative volume, mitochondrial fusion activity, lipid droplet volume and peridroplet mitochondria formation in 2-cell embryos. However, maternal tocotrienol-rich fraction supplementation partially restored mitochondrial relative volume and significantly enhanced mitochondrial clusters and peridroplet mitochondria relative volume. Tocotrienol-rich fraction supplementation also upregulated Mfn1, Mfn2, Opa1, Atp5e and Cox4i1 genes expression beyond control levels indicating improved mitochondrial fusion activity and ATP synthesis capacity. Microscopic analysis revealed low developmental potential in asthmatic group which was reversed by maternal supplementation of tocotrienol-rich fraction.
CONCLUSION: Maternal allergic asthma disrupts mitochondrial dynamics and metabolic interactions essential for early embryonic development. Tocotrienol-rich fraction supplementation mitigates these impairments by restoring mitochondrial fusion, enhancing mitochondria-lipid droplet interactions and preserving ATP synthesis which lead to improve developmental potential. These findings highlight the therapeutic potential of tocotrienol-rich fraction in improving reproductive outcomes under maternal inflammatory stress.
METHOD: Female BALB/c mice were sensitised and challenged with ovalbumin to induce allergic asthma and subsequently supplemented with tocotrienol-rich fraction. Two-cell embryos were collected for ultrastructural evaluation using transmission electron microscopy (TEM) and for gene expression analysis using Fluidigm qPCR including developmental potential thru microscopic analysis. Mitochondrial relative volume, mitochondrial clusters volume (fusion), lipid droplet volume and peridroplet mitochondria formation together with gene expression of mitochondrial fusion (Mfn1, Mfn2, Opa1) and ATP synthesis (Atp5e, Cox4i1) were studied.
RESULTS: Ovalbumin-induced allergic asthma significantly reduced total mitochondrial relative volume, mitochondrial fusion activity, lipid droplet volume and peridroplet mitochondria formation in 2-cell embryos. However, maternal tocotrienol-rich fraction supplementation partially restored mitochondrial relative volume and significantly enhanced mitochondrial clusters and peridroplet mitochondria relative volume. Tocotrienol-rich fraction supplementation also upregulated Mfn1, Mfn2, Opa1, Atp5e and Cox4i1 genes expression beyond control levels indicating improved mitochondrial fusion activity and ATP synthesis capacity. Microscopic analysis revealed low developmental potential in asthmatic group which was reversed by maternal supplementation of tocotrienol-rich fraction.
CONCLUSION: Maternal allergic asthma disrupts mitochondrial dynamics and metabolic interactions essential for early embryonic development. Tocotrienol-rich fraction supplementation mitigates these impairments by restoring mitochondrial fusion, enhancing mitochondria-lipid droplet interactions and preserving ATP synthesis which lead to improve developmental potential. These findings highlight the therapeutic potential of tocotrienol-rich fraction in improving reproductive outcomes under maternal inflammatory stress.