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Abstract <p>Although teratogenic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD) are well documented, its effects at low doses remain poorlycharacterized. In this work we examined the impact of a low-dose TCDDexposure (0.1 µg/kg body weight)—a level not previously linked tostructural brain defects—on cortical development and function inmale rat offspring. Notably, this low dose was sufficient to cause significantfunctional deficits, including reduced body weight and a severelyimpaired placing reflex, pointing to sensorimotor cortex dysfunction.Biochemical analysis confirmed that the underlying pathology causedby TCDD exposure was linked to the elevated activity of the pro-apoptoticenzyme caspase-3, and electron microscopy demonstrated a delay inneural tissue development (e.g. increased extracellular space, immaturesynapses, delayed myelination) as well as neuronal damage (cytoplasmicvacuolization). Therefore, this study provides critical evidencethat TCDD exposure at doses once considered sub-toxic can disruptbrain development by triggering apoptosis and impairing neurogenesis, leadingto significant functional neurological deficits.</p>

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The Effect of Administration of a Low Dose of 2,3,7,8-Tetrachlorodibenzo-P-Dioxin to Pregnant Rats on the Ultrastructure of the Parietal Cortex and Neurodevelopmental Behavior of the Offspring in Early Ontogenesis

  • 期刊论文

  • 发表日期：

    2025年12月19日

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  • D. S. Vasilev,
  • N. L. Tumanova,
  • N. M. Dubrovskaya,
  • K. V. Pakhomov,
  • V. E. Sobolev

摘要

Abstract

Although teratogenic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD) are well documented, its effects at low doses remain poorlycharacterized. In this work we examined the impact of a low-dose TCDDexposure (0.1 µg/kg body weight)—a level not previously linked tostructural brain defects—on cortical development and function inmale rat offspring. Notably, this low dose was sufficient to cause significantfunctional deficits, including reduced body weight and a severelyimpaired placing reflex, pointing to sensorimotor cortex dysfunction.Biochemical analysis confirmed that the underlying pathology causedby TCDD exposure was linked to the elevated activity of the pro-apoptoticenzyme caspase-3, and electron microscopy demonstrated a delay inneural tissue development (e.g. increased extracellular space, immaturesynapses, delayed myelination) as well as neuronal damage (cytoplasmicvacuolization). Therefore, this study provides critical evidencethat TCDD exposure at doses once considered sub-toxic can disruptbrain development by triggering apoptosis and impairing neurogenesis, leadingto significant functional neurological deficits.