DOI: 10.26650/iujhsr2026-1818384 ISSN: 3149-9724

Effects of Low-Dose Mercury Exposure During Pregnancy and Lactation on Pancreatic Tissue in Epileptic Rats

Duygu Aydemir, Sabriye Karadenizli Taşkın, Ayşe Akdemir, Şule Beyhan Özdaş, Fatma Kaya - Dağıstanlı, Deniz Şahin
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Objective: This study aimed to evaluate the effects of chronic low-dose mercury exposure during gestation and lactation on the pancreatic endocrine architecture and function in epileptic WAG/Rij rats, elucidating the potential link between developmental toxicant exposure and later metabolic-neural comorbidity.Materials and Methods: Pregnant WAG/Rij rats received intramuscular injections of mercuric chloride (initial dose, 4.6 μg/kg; maintenance dose, 0.07 μg/kg/day) throughout gestation and lactation. The offspring were assessed at postnatal month 5. Body weight and fasting blood glucose were measured. Pancreatic tissues were harvested for histopathological assessment, immunohistochemistry (insulin, glucagon, somatostatin), and Western blotting for quantitative protein expression. Statistical analyses were performed using the Student’s t-test (GraphPad Prism 9.0).Results: Mercury-exposed offspring exhibited significantly elevated body weight (p<0.05) and fasting blood glucose levels (p<0.0001) relative to controls. Immunohistochemical analysis revealed a marked reduction in insulin-positive increase in the numbers of glucagon- and somatostatin-positive cells within the islets. Western blot data confirmed decreased β-actin-normalised insulin expression alongside increased glucagon and somatostatin protein levels. These results indicate pronounced endocrine disruption and β-cell dysfunction following exposure to mercury during the perinatal period.Conclusion: Chronic developmental exposure to low-dose mercury profoundly disrupts pancreatic endocrine homeostasis in epileptic rats, characterized by β-cell depletion and systemic hyperglycemia. These findings support the developmental origins of the health and disease framework and address that early-life mercury exposure may predispose patients to long-term metabolic and neurological comorbidities. Further investigations should focus on the molecular mechanisms, particularly oxidative stress, mitochondrial dysfunction, and the perturbation of calcium signalling, that mediate mercury-induced cell injury.

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