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<p>Paraquat dichloride (PQ) is a widely used, fast-acting nonselective herbicide extensively applied in agriculture for weed control and crop desiccation. Despite regulatory bans in several countries, PQ remains in use in many regions due to its affordability and effectiveness, raising environmental and occupational health concerns. Agricultural workers and surrounding communities may be exposed through dermal contact, inhalation, and contaminated soil or water, and PQ is well known to induce toxicity via redox cycling and excessive reactive oxygen species (ROS) generation. While pulmonary and renal toxicity are well established, the impact of PQ on female reproductive physiology and estrogen receptor signaling remains incompletely defined. This study evaluated the dose-dependent effects of PQ (25, 50, and 150&#xa0;mg/kg b.w.) on systemic parameters, oxidative stress biomarkers, endocrine function, and ovarian <i>Esr1</i> expression in adult female mice over 14&#xa0;days, with estradiol (0.001&#xa0;mg/kg b.w.) as a positive control. High-dose PQ significantly reduced body, ovarian, and uterine weights and disrupted estrous cyclicity, characterized by prolonged diestrus and shortened estrus. Histological analysis revealed progressive follicular atresia, stromal collapse, and uterine structural degeneration. Oxidative stress assessment demonstrated significant increases in lipid peroxidation (MDA) and depletion of reduced glutathione (GSH), along with suppression of superoxide dismutase (SOD) and catalase (CAT) at 150&#xa0;mg/kg, indicating antioxidant exhaustion. Hormonal analysis showed reduced estradiol with maintained progesterone at high dose. Quantitative PCR revealed significant upregulation of ovarian <i>Esr1</i> in estradiol-treated mice and marked downregulation (≈78%) following high-dose PQ exposure. These findings indicate that PQ induces oxidative stress–mediated endocrine disruption and reproductive toxicity, identifying suppression of <i>Esr1</i> expression as a key molecular mechanism linking environmental herbicide exposure to impaired female reproductive function.</p>

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Studies on the toxicological responses of Paraquat dichloride in the reproductive health of female albino mice

  • 期刊论文

  • 发表日期：

    2026年3月24日

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  • Bhaswat Ranjan Borah,
  • Jogen Chandra Kalita,
  • Manas Das

摘要

Paraquat dichloride (PQ) is a widely used, fast-acting nonselective herbicide extensively applied in agriculture for weed control and crop desiccation. Despite regulatory bans in several countries, PQ remains in use in many regions due to its affordability and effectiveness, raising environmental and occupational health concerns. Agricultural workers and surrounding communities may be exposed through dermal contact, inhalation, and contaminated soil or water, and PQ is well known to induce toxicity via redox cycling and excessive reactive oxygen species (ROS) generation. While pulmonary and renal toxicity are well established, the impact of PQ on female reproductive physiology and estrogen receptor signaling remains incompletely defined. This study evaluated the dose-dependent effects of PQ (25, 50, and 150 mg/kg b.w.) on systemic parameters, oxidative stress biomarkers, endocrine function, and ovarian Esr1 expression in adult female mice over 14 days, with estradiol (0.001 mg/kg b.w.) as a positive control. High-dose PQ significantly reduced body, ovarian, and uterine weights and disrupted estrous cyclicity, characterized by prolonged diestrus and shortened estrus. Histological analysis revealed progressive follicular atresia, stromal collapse, and uterine structural degeneration. Oxidative stress assessment demonstrated significant increases in lipid peroxidation (MDA) and depletion of reduced glutathione (GSH), along with suppression of superoxide dismutase (SOD) and catalase (CAT) at 150 mg/kg, indicating antioxidant exhaustion. Hormonal analysis showed reduced estradiol with maintained progesterone at high dose. Quantitative PCR revealed significant upregulation of ovarian Esr1 in estradiol-treated mice and marked downregulation (≈78%) following high-dose PQ exposure. These findings indicate that PQ induces oxidative stress–mediated endocrine disruption and reproductive toxicity, identifying suppression of Esr1 expression as a key molecular mechanism linking environmental herbicide exposure to impaired female reproductive function.