Blueberry Polyphenol May Relieve Plastic-Caused Sperm Damage

Nanoplastics seem to activate ROS production, causing DNA damage in cells.


Environmental PolystyreneEnvironmental Polystyrene

A recent paper has investigated the impact of polystyrene nanoplastics on the molecular processes of male reproductive tissues in mice [1].

Health risks of micro- and nanoplastics

Microplastic and nanoplastic contamination is a worldwide public health concern for a good reason. Numerous research papers have associated microplastics with multiple health risks in the respiratory, immune, digestive, nervous, and reproductive systems, with nanoparticles especially dangerous for reproductive and nervous systems [2-8] due to their ability to “infiltrate biological barriers and have longer retention in tissue”, as the authors point out.

Humans are exposed to microplastics and nanoplastics primarily through food but also through skin contact and air [9, 10]. Studies have reported the presence of microplastics in human blood, the placenta, and the testes [6, 11, 12].

The authors of this study specifically focused on polystyrene nanoplastics and their impact on the male reproductive system. They mentioned that there are some previous studies that have already investigated polystyrene nanoplastics’ impact on reproductive health, showing that polystyrene nanoplastic exposure can lead to changes in sperm count, motility, and morphology [13] and can lead to a reduction in male fertility, including complete infertility [14]. Some studies have noted that an excess of reactive oxygen species (ROS) and premature senescence are part of the toxic effects of polystyrene nanoplastics [15].

Adverse effects of nanoplastics

The researchers exposed the mice to polystyrene nanoplastics for 60 days by delivering them directly to their stomachs. When they analyzed the animals’ tissue morphology after this treatment, they observed changes to male reproductive organ cells and accumulation of exogenous particles in spermatogenic cells. The researchers also referred to their previous, similar study, in which they observed a reduction in reproductive capacity and lower semen quality [16].


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The authors also analyzed gene expression in testicular tissues. They noted that in mice exposed to polystyrene nanoplastics, molecular indicators connected to undifferentiated male germ cells (spermatogonia) were downregulated, and the number of spermatogonia was reduced in the group of mice that received a higher nanoplastics dose.

The researchers further evaluated mouse spermatogonia-derived cultured cells by exposing them to various concentrations of polystyrene nanoplastics. They observed suppressed cell proliferation and dose-dependent cell cycle arrest, which can lead to cellular apoptosis or senescence. Through measuring biomarkers, gene expression, and protein levels, the authors demonstrated elevated levels of cellular senescence in mouse spermatogonia that were exposed to polystyrene nanoplastics.

The damage from reactive oxygen species

The researchers aimed to determine exactly how polystyrene nanoplastic exposure leads to cellular senescence. Analysis of gene expression data indicated a role of reactive oxygen species (ROS) metabolism and ROS synthesis processes. Experimental exposure of mouse spermatogonia-derived cultured cells to polystyrene nanoplastics resulted in a dose-dependent increase in ROS levels.

To further investigate the role of ROS, the authors treated the cells with N-acetyl-L-cysteine (NAC), a ROS inhibitor. Exposing cells to NAC reduced the effects of polystyrene nanoplastic-induced changes in senescent biomarkers, gene and protein levels, and cell cycle arrest.

Further investigation into the molecular mechanism behind polystyrene nanoplastics’ impact on male fertility involved extracting data from the male health atlas (MHA) database and other gene expression databases along with a series of experiments. The authors arrived at the conclusion that Sirt1 is, at least partly, responsible for activating polystyrene nanoplastic-induced ROS generation. This “excessive ROS triggers DNA damage response in spermatogenic cells.”


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The authors also discuss previous studies that implicated ROS as inducers of senescence and add that their results confirm that suppressing excessive ROS production can blunt the related effects of polystyrene nanoplastics. Taken together, they believe that polystyrene nanoplastic exposure causes excessive ROS production, which leads to a DNA damage response that causes spermatogenic cell senescence.

Potential of pterostilbene

After identifying the problem, the researchers tested pterostilbene as a potential remedy for it. Pterostilbene is a resveratrol-related polyphenol derived from blueberries, and it has potent antioxidant activity and a higher bioavailability than resveratrol.

Similar to the NAC treatment, using pterostilbene to treat polystyrene nanoplastic-exposed, mouse spermatogonia-derived cultured cells reduced ROS levels, cell cycle arrest, senescent cell levels, and expression of senescence-associated molecular markers. It also decreased the levels of a critical DNA damage marker.

The researchers concluded that “pterostilbene can alleviate the spermatogenic cell senescence induced by polystyrene nanoplastics.” Pterostilbene achieves this by reducing the detrimental effects of oxidative stress-mediated DNA damage.

Further research into protecting reproductive functions

The authors emphasize the importance of studying environmental pollutants on male reproductive ability. Their results linking polystyrene nanoplastics to cellular senescence align with previous research linking this particular type of nanoplastic to senescence in different types of cells.


Our study provides a scientific foundation for assessing the male reproductive health risks associated with nanoplastics exposure and identifies a promising intervention drug to mitigate the detrimental health effects of nanoplastics on male reproductive health. However, the impact of PS-NPs on male reproductive health still requires further exploration of the specific mechanism by which Sirt1 leads to ROS outbreaks, and further research is needed to combine epidemiological evidence to better explain the impact of PS-NPs on the spermatogenic process.

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About the author
Anna Drangowska-Way

Anna Drangowska-Way

Anna graduated from the University of Virginia, where she studied genetics in a tiny worm called C. elegans. During graduate school, she became interested in science communication and joined the Genetics Society of America’s Early Career Scientist Leadership Program, where she was a member of the Communication and Outreach Subcommittee. After graduation, she worked as a freelance science writer and communications specialist mainly with non-profit organizations.