Date Created
8-2026
Document Type
Thesis
Degree Name
Master of Science
Department
College of Natural and Health Sciences, Biological Sciences, Biological Sciences Student Work
First Advisor
Patrick Burns
First Committee Member
James Haughian
Second Committee Member
Andrea James
Abstract
The bovine corpus luteum (CL) is a transient endocrine gland that forms after ovulation and produces progesterone, a hormone crucial for early pregnancy. The cattle industry faces tremendous losses annually due to early embryonic mortality within the first 100 days of gestation, where approximately 16% occur during a critical timeframe known as the maternal recognition of pregnancy (MRP). In a normal estrous cycle, if no viable embryo is present, the uterus secretes prostaglandin F2α (PGF2α) during the late luteal phase, triggering luteal regression. One key action of PGF2α is reducing luteal blood flow, leading to hypoxia. This hypoxic state induces mitochondrial stress, ultimately decreasing progesterone production and promoting cellular apoptosis. In the presence of a viable, yet slow-developing embryo, the embryo produces insufficient amounts of MRP signal, Interferon Tau (IFNτ), to mitigate pulses of PGF2α. This can result in regression of the CL and loss of pregnancy. However, dietary fish meal supplementation has been shown to mitigate the luteolytic effects of PGF2α, though the precise mechanism remains unclear. This study aimed to 1) establish a reliable model for studying steroidogenic luteal cell function under hypoxic stress and 2) investigate whether steroidogenic cells cultured in serum from fish meal-supplemented cows, high in omega-3 fatty acids, maintain mitochondrial membrane potential, indicative of health, during acute hypoxia. We show that the Percoll gradient enrichment protocol effectively isolated functionally steroidogenic small and large luteal cells from whole tissue, as set by NTT assays for steroidogenic cells. Mitochondrial membrane potential (ΔΨm) was comparable across luteal cell subtypes (small and large luteal cells) under basal conditions, demonstrating consistent mitochondrial integrity in vitro. Hypoxia induced a decline in mitochondrial depolarization in steroidogenic MA-10 cells cultured in medium supplemented with fetal bovine serum, emphasizing the susceptibility of steroidogenic cells to oxygen deprivation. Using two-way ANOVA analysis revealed cross-row comparison of mitochondrial membrane potential in cells cultured in serum obtained from fish meal-supplemented cows, delayed mitochondrial depolarization at 15 minutes, suggesting prolongation of ATP production despite oxygen deficiency. This research provides a foundation for understanding how omega-3 fatty acids influence mitochondrial membrane potential in steroidogenic cells during hypoxia, a luteolytic mechanism downstream of PGF2α. This research bridges gaps in our current understanding of steroidogenic mitochondrial physiology and potential innovation for providing luteoprotection during MRP.
Abstract Format
html
Keywords
Mitochondria; corpus luteum; omega 3; MA- 10; Bovine; Reproductive; reproduction; CL
Language
English
Extent
123 pages
Rights Statement
Copyright is held by the author.
Digital Origin
Born digital
Recommended Citation
Goodluck, Tyra Marie, "Fish Meal Serum Modulates Mitochondrial Membrane Potential in Steroidogenic Cells: Implications for Luteoprotection in Cattle" (2026). Master's Theses. 372.
https://digscholarship.unco.edu/theses/372