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Hyperhomocysteinemia Induced Mitochondrial Dysfunction Disrupting the Eye Development
Manuela Sozo Cecchini1, Gilian Fernando Bourckhardt1, Madson Silveira de Melo1
1Departamento de Biologia Celular, Embriologia e Genética, Universidade Federal de Santa Catarina, Florianópolis, 88040-900, Brazil.
Neurotoxicity Research
|October 19, 2025
Summary
Hyperhomocysteinemia (HHcy) significantly reduces embryo survival and damages mitochondria, impairing eye development. This study reveals HHcy disrupts mitochondrial dynamics and integrity, impacting neural cell function.
Area of Science:
- Developmental biology
- Neuroscience
- Metabolic disorders
Background:
- Mitochondrial dynamics (fusion/fission) are crucial for neural development and energy-intensive processes like eye formation.
- Hyperhomocysteinemia (HHcy), marked by elevated homocysteine (Hcy), can disrupt normal embryonic development.
Purpose of the Study:
- To investigate the impact of HHcy on embryonic eye development in Gallus domesticus.
- To analyze HHcy-induced changes in mitochondrial structure, dynamics, and autophagy.
Main Methods:
- Fertilized eggs treated with homocysteine (Hcy) at embryonic day 2 (E2).
- Analyses at E6 and E10 included survival rates, transmission electron microscopy, flow cytometry, and cell viability assays.
- Evaluated mitochondrial proteins (Drp1, Mfn1, Mfn2) and autophagy markers.
Main Results:
- HHcy exposure caused a 40% reduction in embryo survival.
- Ultrastructural analysis revealed mitochondrial damage (membrane rupture, cristae disorganization).
- Increased fission (Drp1) and decreased fusion (Mfn1, Mfn2) proteins were observed, alongside increased cytoplasmic vesicles and autophagy.
Conclusions:
- Mitochondria are primary targets of HHcy toxicity during embryonic development.
- HHcy disrupts mitochondrial dynamics and ultrastructural integrity, negatively affecting eye formation.
- Elevated Hcy levels pose significant risks to embryonic development and ocular health.
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