The effect of pesticides on telomere length and mitochondrial DNA copy number variation in human gingival mesenchymal stem cells

Pesticides are chemical constituents which may represent a significant hazard to the environment and public health, especially considering their permanence in water, food and soil. Pesticides are also known to contribute to mitochondrial dysfunction and telomere damage, promoting oxidative damage and pathological conditions. For this reason, our aim was to comprehend the effect of pesticides on telomere length (TL) and mitochondrial DNA copy number variation (mtDNA CNV) in human gingival mesenchymal stem cells (hGMSCs), which have been established as some of the first cells that pesticides come in contact with after the consumption of fruits and vegetables. hGMSCs were cultured alone or with pesticides Boscalid (B), Propamocarb (PR), Pyraclostrobin (PY) and Lambda-cialotrina (LC) for 10 days. Then, DNA was manually isolated from each cell sample and quantified. To evaluate the average TL and mtDNA CNV in the hGMSCs exposed to the single pesticides or combinations of them compared to the control group, each DNA was analyzed in triplicate through qPCR by employing the Absolute Human Telomere Length and Mitochondrial DNA Copy Number Dual Quantification qPCR Assay Kit (ScienCell). Our results highlighted that the relative TL of hGMSCs treated with pesticides compared to the hGMSCs control group, was significantly (p-value < 0,05) decreased in the totality of treatments with pesticides, suggesting a possible TL shortening and a consequent premature replicative senescence. Moreover, hGMSCs treated with B, LC, PY, B+PY, B+PY+PR and B+PY+LC compared to the controls, showed a decrease in the mtDNA CN, indicating a potential impairment of mitochondrial function which exceeds the mitochondrial capacity to make up for the damage and then reduces the mtDNA content. hGMSCs treated with PR+LC and PR compared to controls, displayed an increase in mtDNA CN in order to compensate for mtDNA damage and mitochondrial dysfunction. Further experiments are currently underway in human umbilical vein endothelial cells (HUVEC). Investigating the impact of environmental toxicants, such as pesticides, on TL and mtDNA CNV in human cells may be of vital importance to better clarify the mechanisms at play and develop prevention strategies protecting systemic health.