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The Impact of Air Pollution on Male Fertility

Air pollution harms male reproductive health, with vitamins offering potential support.

Cao Wang, Yingchi Zhao, Bin Liu, Zhen Luo, Guangxu Zhou, Kaiyi Mao

― 7 min read


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Table of Contents

Lately, male infertility is a growing problem around the globe, and one of the main reasons behind it is the drop in Sperm Quality. It seems that as air pollution gets worse, more men are having trouble with fertility. While we know that pollution can harm sperm, we still don't fully understand how this happens.

One of the big culprits in urban areas, especially in China, is fine particulate matter, known as PM2.5. This nasty stuff comes mainly from car exhaust and is a real danger because it carries harmful materials into our bodies when we breathe. Most research on PM2.5 has focused on how it affects things like the lungs and heart, but the impact on male reproductive health hasn't received as much attention.

PM2.5 creates reactive oxygen species (ROS) in our bodies, which leads to Oxidative Stress. Simply put, oxidative stress is like having too many party crashers at a gathering; it causes chaos and can even lead to cell death. The specific ways that PM2.5 damages cells, especially in the male reproductive system, are still a bit of a mystery.

Fortunately, our cells do have a backup plan when things get rough: the mitochondrial unfolded protein response (UPRmt). This is like a superhero for our mitochondria, helping them survive tough times by cleaning up damaged proteins. However, how PM2.5 affects UPRmt in germ cells, which are vital for sperm production, remains unclear.

This study looks at how PM2.5 impacts oxidative stress, UPRmt, and cell death in rats exposed to different amounts of this pollutant. It also examines whether adding vitamins could help improve reproductive health. The goal is to reveal how PM2.5 causes damage and what can be done to fight back.

How We Gathered the Pollutant

To study PM2.5, we collected it from busy highways in Zunyi City, China, over a few months. Once we had the particulate matter, we treated it to create a suspension for testing. This involved cutting up the filter we collected from, soaking it, and using some fancy lab equipment to ensure it was ready for use. The PM2.5 was then kept at very low temperatures to preserve it until we needed it.

The Animal Study

For our experiments, we used laboratory rats. They were kept in a controlled environment and given a variety of treatments. We divided them into four groups: one group received just saline (like a very boring water), another got vitamins C and E, a third was given PM2.5, and the last group received both PM2.5 and vitamins.

The rats received their treatments for four weeks, and at the end of that period, we looked at their weight, reproductive organs, and sperm quality.

Weighing the Rats

After our treatments, we weighed the rats and took out their testis and epididymis. These are fancy names for parts of the male reproductive system where sperm is produced and stored. We weighed these organs to see if any changes brought on by PM2.5 and vitamins had an effect.

Sperm Quality Assessment

One crucial part of this study was to look at sperm quality. To do this, we prepared sperm samples from the rats' epididymis and counted the sperm under a microscope.

We measured total sperm counts, viable (living) sperm, and looked for any abnormal shapes. Bad shapes include sperm with two heads or tails, or a bent neck. This let us calculate how well the sperm were performing.

Looking at Testis Structures

We also examined the testis tissue under a microscope to see how PM2.5 affected it. In healthy rats, we expect to see lots of layers of healthy sperm-producing cells. However, in the rats exposed to PM2.5, those layers were fewer, and there were signs of damage.

Mitochondrial Changes

Mitochondria are the tiny powerhouses in our cells, and they can get hurt by PM2.5. We used a special electron microscope to look at the mitochondria in the testis cells. In healthy rats, the mitochondria looked great, but in those exposed to PM2.5, they appeared damaged and swollen.

Cell Death in Testes

Since oxidative stress can lead to cell death, we also examined the rate of apoptosis, which is just a fancy way of saying "cell death." We used a special dye that highlights dead cells so we could see how many were present in the testis tissue. We found that being exposed to PM2.5 increased cell death, while vitamins seemed to help reduce it.

Results After Exposure

After four weeks of exposure to PM2.5, the rats had gained some unwanted effects. Their body weights and the weights of their reproductive organs dropped. Their sperm counts plummeted, and the number of abnormal sperm increased. Basically, it looked like PM2.5 threw a wrench in the works of male reproduction.

But, there’s a silver lining! The vitamin-treated rats showed improvements in body weight and sperm quality. The vitamins seemed to act like a shield, helping to protect against some of the negative effects of pollution.

Oxidative Stress and Rat Health

To figure out how PM2.5 causes harm, we looked at oxidative stress. After exposure to PM2.5, there was a decrease in protective proteins and an increase in harmful substances in the testis tissue. Essentially, the rats were dealing with a mess in their bodies due to pollution.

Speaking of messes, we saw that the combination of vitamins helped balance things out, leading to better health results.

Mitochondrial Damage

Looking at the mitochondria again, we found that PM2.5 exposure led to significant damage, but the vitamins helped restore some of that damage. Mitochondria that were once swollen and in disarray started to show improvement after vitamin treatment.

UPRmt Function in Trouble

The UPRmt is our biological backup plan when mitochondria are stressed. However, in the rats exposed to PM2.5, we saw a decline in the protective proteins involved in UPRmt. This indicated that PM2.5 not only damaged mitochondria but also impaired their ability to cope with stress.

Just like a fire drill keeps things safe in a building, UPRmt helps keep our cells stable during tough times. PM2.5 exposure, however, caused a delay in this response, leading to increased cell death.

The Apoptosis Story

When examining apoptosis, we found that the levels of proteins that promote cell death increased after PM2.5 exposure. Meanwhile, the proteins that help cells survive were reduced. This showed that PM2.5 is like an unwanted guest that overstayed its welcome, leading to a chaotic scene.

Interestingly, vitamin treatment seemed to reverse some of these effects, bringing balance back to the apoptosis process in the testis.

Summing It All Up

What we’ve learned from this study is pretty eye-opening. PM2.5 from car exhaust isn't just bad for the environment; it's also harmful to male reproductive health. The pollutants create oxidative stress, which leads to mitochondrial damage and, ultimately, cell death.

However, the good news is that combining vitamins can help combat some of these negative effects. It’s a reminder that while pollution might be tough, we can still fight back and protect our health in smart ways.

So, if you ever thought that vitamins are just for boosting your immune system, think again! They might just be the heroes our sperm need when fighting off the bad guys from air pollution.

Next time you’re stuck in traffic, remember: your health might just depend on your next vitamin boost!

Conclusion

In conclusion, this study sheds light on the harmful effects of PM2.5 on male reproductive health. It shows a clear link between air pollution and declining sperm quality, which can lead to male infertility. The combination of vitamins C and E offers a potential solution to help counteract these effects, making it a win for reproductive health.

As we move forward, it’s crucial to continue raising awareness about the impact of pollution and explore new ways to protect our health. After all, a little knowledge today can make a big difference tomorrow!

Original Source

Title: PM2.5 from Automobile Exhaust Induces Apoptosis in Male Rat Germ Cells via the ROS-UPRmt Signaling Pathway

Abstract: ObjectiveTo explore the underlying mechanism behind the fine particulate matters (PM2.5)-mediated regulation of reproductive function in male rats, and to determine the role of vitamins in this process. MethodsIn all, 32 male SD rats were randomized to a control cohort (normal saline), a Vit cohort (vitamin C at 100 mg/kg + vitamin E at 50 mg/kg), a PM2.5 cohort (PM2.5 10 mg/kg), and a PM2.5+Vit cohort (PM2.5 exposure + vitamin C at 100 mg/kg + vitamin E at 50 mg/kg), with eight rats in each cohort. After four weeks of exposure, mating experiments were carried out. Thereafter, rats were euthanized, and the testis and epididymis tissues were excised for hematoxylin-eosin (HE) staining and sperm quality analysis. Apoptosis of testis tissues was quantified via a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the testicular oxidative stress (OS)-, apoptosis- and mitochondrial unfolded protein response (UPRmt)-related essential protein expressions were measured via western blotting (WB). ResultsAfter PM2.5 exposure, the sperm count and motility decreased, while sperm abnormality and the apoptosis index increased. HE staining showed that the number of spermatogenic cells decreased. WB showed that the PM2.5 group had decreased expressions of superoxide dismutase (SOD), nuclear factor E2-related factor 2 (Nrf2), and B-cell lymphoma-2 (Bcl-2) (p < 0.05), increased expressions of malondialdehyde (MDA), Bcl-2 associated X protein (Bax), and Caspase3 (p < 0.05), and downregulated expressions of C/EBP homologous protein (CHOP), heat shock protein 60 (HSP60), and activating transcription factor 5 (ATF5) (p < 0.05). These were all reversed by vitamin intervention. ConclusionPM2.5 from automobile exhaust disrupts male reproductive function. A combination of vitamins may protect reproductive function via the reactive oxygen species (ROS)-UPRmt signaling pathway. HighlightsO_LIPM2.5 from vehicle exhaust can cause apoptosis of male germ cells. C_LIO_LIPM2.5 from vehicle exhaust induces germ cell apoptosis through the ROS-UPRmt signaling pathway. C_LIO_LICombined vitamin C and E can enhance UPRmt activity to alleviate the germ cell apoptosis caused by PM2.5 from vehicle exhaust. C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=134 SRC="FIGDIR/small/621651v1_ufig1.gif" ALT="Figure 1"> View larger version (30K): [email protected]@1b6daa1org.highwire.dtl.DTLVardef@1cba0b4org.highwire.dtl.DTLVardef@1a3c9f1_HPS_FORMAT_FIGEXP M_FIG C_FIG

Authors: Cao Wang, Yingchi Zhao, Bin Liu, Zhen Luo, Guangxu Zhou, Kaiyi Mao

Last Update: 2024-11-04 00:00:00

Language: English

Source URL: https://www.biorxiv.org/content/10.1101/2024.11.02.621651

Source PDF: https://www.biorxiv.org/content/10.1101/2024.11.02.621651.full.pdf

Licence: https://creativecommons.org/licenses/by/4.0/

Changes: This summary was created with assistance from AI and may have inaccuracies. For accurate information, please refer to the original source documents linked here.

Thank you to biorxiv for use of its open access interoperability.

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