# Induction of Cellular Senescence by Pesticide Exposure in Human Umbilical Vein Endothelial Cells (HUVECs): Impacts on Telomerase Length, Cellular Morphology, and mtDNA Variation

## TL;DR

This study shows that pesticide exposure causes aging-like changes in human blood vessel cells, affecting their structure and function.

## Contribution

The study demonstrates that specific pesticides induce cellular senescence in endothelial cells through multiple biomarkers.

## Key findings

- Pesticide exposure reduced cell viability and disrupted tube formation in endothelial cells.
- Pesticides caused mitochondrial DNA changes and telomere shortening, signs of cellular aging.
- Increased p21 and reduced Ki67 and TERT expression were observed, indicating senescence.

## Abstract

Chronic exposure to pesticides represents a substantial risk to human health; however, their role in promoting cellular senescence remains poorly understood. It's well known that endothelial dysfunction is an early hallmark of aging‐related vascular damage. We employed Human Umbilical Vein Endothelial Cells (HUVECs) as an in vitro model for vascular endothelium to investigate whether pesticide exposure accelerates cellular senescence. The pesticides Boscalid (B), Pyraclostrobin (PY), Propamocarb (PR), and Lambda‐cyhalothrin (LC) were tested individually and in combination. Following pesticide exposure, we evaluated cell viability through MTS assay, Endothelial Tube Formation by Scanning Electron Microscopy (SEM), alteration in mitochondria through Mitochondrial DNA Copy Number (mtDNA) variation, and TOM20 evaluation, Telomere Length reduction, expression of p21, reduced Ki67, and TERT through Immunofluorescence. Our findings suggest that pesticides accelerate senescence in endothelial cells.