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How The Herbicide Paraquat Decreases Male Fertility

Feb 26, 20246 min read


‘The use of chemicals in agriculture does not affect human health’ is the claim that will be disproved throughout this report. As the European Environmental Union states, “Human exposure to chemical pesticides is linked to chronic illnesses such as cancer, and heart, respiratory and neurological diseases.” This article discusses the many negative effects that pesticides have on humans and provides valuable data such as graphs and surveys as evidence. Subsequently, after initial research had been completed, a broad research question was developed based on the original claim, “How does the herbicide paraquat used in agriculture affect human health?” This was further refined to consider how the herbicide paraquat affects male fertility. Below, you will find a comprehensive account of this refinement and an elaboration of the specific research question at hand.

 

Paraquat plays a crucial role in mitigating the adverse impacts of climate change by aiding in soil erosion reduction, safeguarding soil health, and supporting regenerative agricultural methods like no- and minimum-till practices (Syngenta Global, 2023). As such, this herbicide is utilized often in agriculture throughout the world. Yet this chemical can have many effects on living organisms, specifically humans. This widely used nonselective dipyridyl herbicide poses a significant threat to human and animal well-being due to its detrimental effects. The lungs, specifically, are the primary organ affected by Paraquat, leading to severe lung inflammation and interstitial fibrosis, which are major contributors to respiratory failure and mortality (Chen, Et al, 2016). However, there has been limited research regarding the impact of this chemical on reproductive organs. All the few studies that have been performed on the effects of paraquat on reproductive organs state the same general idea, that the presence of paraquat leads to a reduction in the number of reproductive cells and can also induce deformities in these cells, which is mainly seen in males (Ranjbar, et al, 2015). Therefore, this report proposes the specific research question:

 

How does the agriculturally used paraquat herbicide decrease male fertility through testicular histomorphometry (i.e., spermatogonia, Spermatocytes, Spermatid, Sertoli, Leydig mean numbers) and testicular cell apoptosis


Background:

Paraquat, alternatively referred to as N, N'-dimethyl-4,4'-bipyridinium dichloride or methyl viologen, is an organic compound known by the chemical formula [(C₆H₇N)₂]Cl₂. This compound falls under the classification of viologens, which are a group of heterocycles with a similar redox-active structure (Laboratories of The Rockefeller Institute for Medical Research, 1933). This chemical is extremely toxic, therefore it is used as a herbicide in agriculture, primarily for grass and weed control. When ingested by humans or animals it can have many fatal complications such as acute respiratory distress syndrome, renal failure, and hepatotoxicity, which affect the lungs, kidneys, and liver respectively (National Library of Medicine, 2019). Not only does paraquat affect many major organs as previously stated, but it also affects the reproductive systems as the chemical is known to stimulate critical damage in male reproductive organs (Mustafa, et al, 2023). Testicular histomorphometry involves the quantitative analysis of the microscopic structure and composition of testicular tissue, providing insights into cellular changes, tissue architecture, and composition. It is a valuable approach for understanding the characteristics of the testes at a cellular level. Testicular cell apoptosis is a type of cell death in which a series of molecular steps in a cell lead to its death in the testes (National Cancer Institute, 2023). Paraquat's toxicity affects testicular cells through redox cycling, generating reactive oxygen species (ROS) and causing oxidative stress. Testicular cells (spermatogonia, Spermatocytes, Spermatid, Sertoli, Leydig), involved in essential functions like cell division and hormone production, are highly susceptible to ROS damage. Excessive ROS production disrupts the balance between ROS and antioxidant defenses, resulting in cellular damage, including DNA, lipid, and protein oxidation. These effects impair cell viability, proliferation, hormonal regulation, and sperm production. The disruption of normal testicular cell functioning has adverse effects on testicular histomorphometry and male fertility. Paraquat also increases the activities of caspase -3 and -9, they are a part of the Caspase family of protease enzymes which play an essential role in programmed cell death. Consequently, the independent variable of paraquat has some type of effect on the dependent variable of testicular cell apoptosis and testicular histomorphometry.

 

Study 1 Evidence:


10 male Wistar rats were split into two groups, the controlled and group ad paraquat-treated group. The right testes were fixed in a 10% formalin solution, embedded in paraffin, and cut into 3µm slices. These slices were mounted on microscope slides coated with a salinized substance. After staining with hematoxylin and eosin, the sections (3 per animal) were examined under light microscopy. Using random selection, 25 tubules with a visible circular cross-section were chosen for each animal. The counts of spermatogonia, spermatocytes, spermatids, Leydig cells, and Sertoli cells were performed. There can be seen a trend that when paraquat was added to the experimental group there was a decrease in the means for all types of cells found in the process of sperm production compared to the control group, which demonstrates a significant difference. There was a significant increase seen in the p values for Leydig, spermatid, and spermatocytes (P=0.015, P<0.001, P<0.001 respectively) but there was no significant difference for Sertoli and spermatogonia (no asterisk beside data). The standard error as a percentage of the mean was calculated to indicate uncertainty, (Spermatogonia: 0.8009%, Spermatocytes: 0.6445%, spermatid: 0.3315%, Sertoli: 1.5192%, Leydig: 1.6142%) as all of them were under 10% all of them are highly accurate. This data is highly useful in answering the research question as it provides clear evidence of a decrease in all cell types that are used in the process of sperm production due to paraquat.

 

Study 2 evidence:



PQ (paraquat) induced testicular cell apoptosis through the mitochondrial pathway. PQ led to an increase in the activities of caspase-3 and -9 in the testis tissues. The results were expressed as the mean ± SD (n = 8 rats per group). P < 0.05, * P < 0.01 versus the control

 

This study used a total of 32 male Wistar rats that were 8 weeks old and were randomly divided into groups of four, they collected the data about the activity of caspase -9 and -3 with a colorimetric assay kit according to the manufacturer’s protocol. As seen in the graph, there is a trend that when the mg of paraquat is increased so did the activities of caspase -9 and -3 in the testis tissue which shows a significant difference due to paraquat. Caspase -9 starts at 0.3 (mean) when no paraquat is added but then increases up to 0.5 (mean) when 8mg of paraquat is added. The same can be seen in catalase -3, it starts at 0.3 (mean) when 0 paraquat is added yet it increases to 0.9 (mean) when 8 mg of paraquat is added. All images of paraquat had a p-value < 0.01, except for 0.5 which had a p-value < 0.05. As the standard deviation bars do not overlap it indicates that a significant difference does exist and shows how the data is precise. Notably, caspase -3 had more of an increase due to the paraquat compared to caspase -9. This data and the trend that it shows to answer the research question as it specifically gives insight into how paraquat decreases male fertility as it increases caspase -9 and -3 which then increase testicular cell apoptosis (cell death).

 

Conclusion:

 Paraquat decreases male fertility through testicular histomorphometry by directly decreasing the different types of sperm cells that are used in the process of sperm production and also through testicular cell apoptosis, by increasing caspase -3 and -9 which then starts the process of executing cell death. The evidence that has been gathered displays sufficient accuracy and reliability to partially support this answer to the research question. Limitations such as both studies focusing on rats and the sample size of both studies have reduced the ability to fully support an answer to the research question. Although this investigation answers the research question it cannot be generalised to support the claim. This is because only the chemical paraquat and its effects on the male reproductive system were studied, this could be extended by studying the effects of other chemicals (Thiram, Atrazine, Chlordane, Chlordecone) on all parts of the body to accurately answer the claim.

 
Author Emily Spong is a 16 year old student living in Australia with a passion for how the human body works on a mental and physical level. In her free time, she enjoys playing with her two cats, reading and writing

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