Elsevier

Neurotoxicology and Teratology

Volume 18, Issue 6, November–December 1996, Pages 691-696
Neurotoxicology and Teratology

Article
Central nervous system myelin deficit in rats exposed to 2,4-dichlorophenoxyacetic acid throughout lactation

https://doi.org/10.1016/S0892-0362(96)00087-6Get rights and content

Abstract

Our results show that 2,4-dichlorophenoxyacetic acid (2,4-D) exposure through mother's milk during the period of rapid myelination (from the 15th to the 25th postnatal days) results in a myelin deficit in the pup's brain and demonstrates the vulnerability of the developing central nervous system (CNS) to 2,4-D. After 100 mg/kg 2,4-D administration to dams, brains of male and female rats show a significant diminution of myelin markers such as monohexosylceramide as well as phospholipids and free fatty acids (FFA) and an increase of cholesteryl esters. Histological studies revealed myelin deficit in some brain regions after 2,4-D treatment. These data indicate that 2,4-D, through the mother's milk, alters the myelination process during a specific postnatal period.

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    Treatment with DZN did not have an overall effect on myelin gene expression, but elicited a statistically significant reduction in individual myelin-related gene expression (Slotkin and Seidler, 2007). Similarly, neonatal exposure to 2,4-D resulted in myelin deficits in the rat pup brain, as measured by protein expression (Duffard et al., 1996; Konjuh et al., 2008) and electron microscopy (Konjuh et al., 2008; Rosso et al., 2000), and alterations in behavior (Rosso et al., 2000). Taken together, these studies indicate that exposure to CPF, DZN, or 2,4-D during the developmental period corresponding to the onset of myelination can induce negative effects on myelin-related gene expression and function and myelination in the brain.

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