Abstract
Women over 35 have higher rates of infertility, largely due to deterioration of oocyte quality characterized by fragmentation, abnormal meiotic spindle-chromosome complexes, and oxidative stress. C-phycocyanin (PC) is a biliprotein enriched in Spirulina platensis that is known to possess antioxidant, anti-inflammatory, and radical-scavenging properties. D-galactose-induced aging acceleration in mice has been extensively used to study aging mechanisms and for pharmaceutical screening. In this study, adult female B6D2F/1 mice injected with D-galactose were used as a model to test the age-reversing effects of PC on degenerated reproductive ability. Our results show that PC can prevent oocyte fragmentation and aneuploidy by maintaining cytoskeletal integrity. Moreover, PC can reverse the expression of antioxidant genes, increase superoxide dismutase (SOD) activity and decrease methane dicarboxylic aldehyde (MDA) content, and normalize mitochondria distribution. PC exerts its benefit by inhibiting reactive oxygen species (ROS) production, which decreases apoptosis. Finally, we observe a significant increase in litter size after PC administration to D-galactose-induced aging mice. Our study demonstrates for the first time that D-galactose-induced impaired female reproductive capability can be partially rescued by the antioxidant effects of PC.
Highlights
The human female reproductive system ages more rapidly than most other body systems, and reproductive capacity is negatively correlated with age [1, 2]
We examined the age-reversing effect of PC in the reproductive system of D-gal-induced aging mice
We investigated the ability of PC to reverse D-gal-induced reproduction impairments in mice
Summary
The human female reproductive system ages more rapidly than most other body systems, and reproductive capacity is negatively correlated with age [1, 2]. Poor oocyte quality is characterized by meiotic spindle anomalies, chromosome misalignment, oxidative stress, gene expression changes, shortened telomeres, and loss of cohesion [1, 4,5,6]. Germ cells initiate meiosis and arrest at the dictyate stage of prophase I in the fetal ovary; these postnatal germ cells remain arrested for weeks to months in mice and 10-50 years in humans [9]. During this prolonged interval, reactive oxygen species (ROS) accumulate and decrease oocyte quality and quantity [10]. Previous reports demonstrated that ROS accumulation in cells can lead to cytoskeletal derangement [13], shortened telomeres [14], impaired telomerase activity [15], antioxidant system dysfunction [16, 17], disturbances of ATP levels [18] and mitochondrial distribution [19], and cell apoptosis [20]
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