Abstract

Simple SummaryIn sheep farming, ovarian inflammation caused by bacterial infections often leads to infertility and economic losses. Bacterial toxins damage the ovarian cells that support egg development, but whether selenium, a trace mineral with recognized anti-inflammatory properties, can protect these cells remains unclear. In this study, we exposed sheep ovarian cells to bacterial toxin to induce inflammation and then treated them with selenium. Using high-resolution microscopy and functional assays, we found that the toxin severely damaged the mitochondria—the energy-producing compartments of the cells—causing them to shrink and fragment. Selenium treatment restored these structures to a healthy state. This structural repair, in turn, reduced inflammation and cell death, alleviated oxidative stress, and improved the production of reproductive hormones by the cells. Our findings provide direct evidence that selenium protects sheep ovarian cells by preserving their internal structures, suggesting that selenium supplementation could serve as a practical nutritional strategy for safeguarding sheep fertility against inflammation-related disorders.Lipopolysaccharide (LPS) impairs the function of ovine follicular granulosa cells (GCs), representing a primary cause of follicular atresia. Selenium (Se), an essential trace element, possesses anti-inflammatory and cytoprotective properties; however, its effects on GC ultrastructure remain largely unknown. In this study, primary ovine GCs were exposed to LPS (10 µg/mL) and treated with sodium selenite (25 nM). Transmission electron microscopy (TEM), JC-1 staining, enzyme-linked immunosorbent assay (ELISA), reactive oxygen species (ROS) detection, flow cytometry, and quantitative real-time PCR (qRT-PCR) were employed to evaluate cellular ultrastructure, mitochondrial membrane potential (ΔΨm), and downstream physiological processes. LPS induced severe mitochondrial pyknosis, cristae loss, and reduced ΔΨm, accompanied by inf