“Brand New Paradigm” – Scientists Discover How Human Eggs Remain Healthy for Decades



Immature human egg cells skip a crucial metabolic pathway thought to be important for generating energy, according to research from the Center for Genomic Regulation (CRG) that was published in the journal Nature.

The metabolism of the cells is altered to halt the production of reactive oxygen species, which are harmful chemicals that can build up, harm DNA, and result in cell death. The study reveals how human egg cells can remain fertile while latent in the ovaries for up to 50 years.

"Humans are born with their entire lifetime's worth of egg cells. Humans are the only terrestrial mammals who live the longest, thus egg cells must preserve their immaculate state while avoiding a lifetime of wear and tear. We demonstrate that this issue can be resolved by omitting a crucial metabolic process that is also the primary cause of cell damage. It functions similarly to turning on standby mode on batteries as a long-term maintenance method. The study's first author, Dr. Aida Rodriguez, a postdoctoral researcher at the CRG, calls this a paradigm shift never before observed in animal cells.

An oocyte is supported by granulosa cells on the outer layer of a human follicle, which can be seen by live cell imaging. Red indicates the activity of reactive oxygen species. The activity of ROS was seen by the researchers in the granulosa cells, but it was almost completely absent in the oocyte. Aida Rodriguez/Nature is the author.

During fetal development, human eggs are first generated in the ovaries and proceed through various phases of maturation. Oocytes, or immature egg cells, enter cellular arrest at the earliest stages of this process and remain dormant in the ovaries for up to 50 years. Oocytes have mitochondria, or cell batteries, like all other eukaryotic cells, which they use to generate energy for their requirements during this dormant stage.

The researchers found that mitochondria in both human and Xenopus oocytes use alternative metabolic pathways to make energy, not previously seen in other animal cell types, by combining live imaging, proteomic, and biochemical techniques.

The typical "gatekeeper" that starts the reactions needed to generate energy in mitochondria is complex I, a complex protein and enzyme. This protein is essential because it functions in the cells of all living things, from yeast to blue whales. But the scientists discovered that complex I is essentially missing in oocytes. Only the cells that make up the parasitic plant mistletoe are known to be able to live with low complex I levels.

The study's authors claim that their findings explain why some women with complex I-related mitochondrial diseases, like Leber's Hereditary Optic Neuropathy, do not have lower fertility than women with diseases affecting other mitochondrial respiratory complexes.

The research findings might potentially inspire the development of fresh tactics for keeping cancer patients' ovarian reserves intact. Complex I inhibitors have been recommended as a cancer treatment in the past. Dr. Elvan Böke, senior author of the work and Group Leader in the Cell & Developmental Biology program at the CRG, notes that if these inhibitors demonstrate promise in subsequent trials, they may be able to target malignant cells while sparing oocytes.

Oocytes must combine longevity with function, which makes them very distinct from other types of cells. With one of the goals being to comprehend how nutrition affects female fertility, the researchers intend to carry on with this line of inquiry and discover the energy source oocytes use throughout their protracted dormancy in the absence of complex I.

There is a significant knowledge gap in our understanding of female reproduction, as evidenced by the one in four cases of female infertility that are unsolved. Our goal is to understand the mechanisms that oocytes use to maintain their health over a long period of time in order to understand why these mechanisms inevitably break down as people get older.

Oocytes maintain ROS-free mitochondrial metabolism by decreasing complex I, according to a study published in Nature on July 20, 2022, by Aida Rodriguez-Nuevo, Ariadna Torres-Sanchez, Juan M. Duran, Cristian De Guirior, Maria Angeles Martnez-Zamora, and Elvan Böke.

By CENTER FOR GENOMIC REGULATION 

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