Abstract
Recent studies have revealed a notable connection between pesticide exposure and Recurrent Pregnancy Loss (RPL), yet the precise molecular underpinning of this toxicity remains elusive. Through the alignment of Differentially Expressed Genes (DEGs) of healthy and RPL patients with the target genes of 9 pesticide components, we identified a set of 12 genes responsible for RPL etiology. Interestingly, biological process showed that besides RPL, those 12 genes also associated with preeclampsia and cardiovascular disease. Enrichment analysis showed the engagement of these genes associated with essential roles in the molecular transport of small molecules, as well as the aldosterone-regulated sodium reabsorption, endocrine and other factor-regulated calcium reabsorption, mineral absorption, ion homeostasis, and ion transport by P-type ATPases. Notably, the crosstalk targets between pesticide components played crucial roles in influencing RPL results, suggesting a role in attenuating pesticide agents that contribute to RPL. It is important to note that non-significant concentration of the pesticide components observed in both control and RPL samples should not prematurely undermine the potential for pesticides to induce RPL in humans. This study emphasizes the complexity of pesticide induced RPL and highlights avenues for further research and precautionary measures.
Acknowledgments
Many thanks are addressed to Ecology and Evolutionary Genomics and Bioinformatics (EEG) Laboratory, Kaohsiung Medical University for supporting and facilitating this study.
Author contributions
M.L. performed computational experiments and interpreted the data, M.L. and P.S. wrote the main manuscript text and prepared all figures, YC.S. and R.B.P. provided critical discussions and valuable intellectual input. All authors reviewed the manuscript.
Informed consent statement
As the data were already deposited in a public repository, there was no direct involvement with human subjects.
Disclosure statement
No potential conflict of interest was reported by the author(s). The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.