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The mechanisms of mitochondrial dysfunction and glucose intake decrease induced by Microcystin-LR in ovarian
Jinling Zhu1, Kunyang Liu1, Ligang Pei2
1Immunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing 210093, China; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing 210093, China.
Abstract:
Microcystin-LR (MC-LR) is a cyclic heptapeptide; it is an intracellular toxin released by cyanobacteria that exhibits strong reproductive toxicity. Previous studies have demonstrated that MC-LR induces oxidative stress in granulosa cells by damaging the mitochondria, which eventually leads to follicle atresia and female subfertility. In the present study, granulosa cells were exposed to 0, 0.01, 0.1 and 1 μM MC-LR. After 24 h, we observed changes in mitochondrial cristae morphology and dynamics by analyzing the results of mitochondrial transmission electron microscopy and detecting the expression of DRP1. We also evaluated glucose intake using biochemical assays and expression of glucose transport related proteins. MC-LR exposure resulted in mitochondrial fragmentation and glucose intake decrease in granulosa cells, as shown by increasing mitochondrial fission via dynamin-related protein 1 (DRP1) upregulation and decreasing glucose transporter 1 and 4 (GLUT1 and GLUT4). Furthermore, the expression levels of forkhead box protein M1 (FOXM1) significantly increased due to the overproduction of reactive oxygen species (ROS) after MC-LR exposure. Our results proved that MC-LR exposure causes mitochondrial fragmentation and glucose intake decrease in granulosa cells, which provides new insights to study the molecular mechanism of female reproductive toxicity induced by MC-LR.
Insights
Microcystin-LR toxin causes mitochondrial damage and reduces glucose uptake in female reproductive cells. This cellular damage, driven by increased mitochondrial fission and oxidative stress, contributes to female subfertility.
Area of Science:
- Reproductive Toxicology
- Cellular Biology
- Environmental Health
Background:
- Microcystin-LR (MC-LR) is a cyanobacterial toxin known for reproductive toxicity.
- MC-LR induces oxidative stress and mitochondrial damage in granulosa cells, leading to follicle atresia and subfertility.
Purpose of the Study:
- To investigate the effects of MC-LR on mitochondrial morphology and glucose metabolism in granulosa cells.
- To elucidate the molecular mechanisms underlying MC-LR-induced female reproductive toxicity.
Main Methods:
- Granulosa cells were exposed to varying concentrations of MC-LR (0-1 μM).
- Mitochondrial morphology and dynamics were assessed using transmission electron microscopy and DRP1 expression analysis.
- Glucose uptake and glucose transporter (GLUT1, GLUT4) expression were evaluated.
- Reactive oxygen species (ROS) and FOXM1 levels were measured.
Main Results:
- MC-LR exposure led to mitochondrial fragmentation, characterized by increased DRP1-mediated mitochondrial fission.
- Glucose intake and expression of GLUT1 and GLUT4 were significantly decreased in MC-LR-treated cells.
- MC-LR exposure elevated ROS production and increased FOXM1 expression.
Conclusions:
- MC-LR exposure induces mitochondrial fragmentation and impairs glucose uptake in granulosa cells.
- Increased mitochondrial fission and oxidative stress are key mechanisms in MC-LR's reproductive toxicity.
- These findings offer new insights into the molecular pathways of MC-LR-induced female subfertility.
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