Impact of endocrine-disrupting chemicals on neural development and the onset of neurological disorders.
Journal Title: Pharmacological Reports - Year 2013, Vol 65, Issue 6
Abstract
Even though high doses of organic pollutants are toxic, relatively low concentrations have been reported to cause long-term alterations in functioning of individual organisms, populations and even next generations. Among these pollutants are dioxins, polychlorinated biphenyls, pesticides, brominated flame retardants, plasticizers (bisphenol A, nonylphenol, and phthalates) as well as personal care products and drugs. In addition to toxic effects, they are able to interfere with hormone receptors, hormone synthesis or hormone conversion. Because these chemicals alter hormone-dependent processes and disrupt functioning of the endocrine glands, they have been classified as endocrine-disrupting chemicals (EDCs). Because certain EDCs are able to alter neural transmission and the formation of neural networks, the term neural-disrupting chemicals has been introduced, thus implicating EDCs in the etiology of neurological disorders. Recently, public concern has been focused on the effects of EDCs on brain function, concomitantly with an increase in neuropsychiatric disorders, including autism, attention deficit and hyperactivity disorder as well as learning disabilities and aggressiveness. Several lines of evidence suggest that exposure to EDCs is associated with depression and could result in neural degeneration. EDCs act via several classes of receptors with the best documented mechanisms being reported for nuclear steroid and xenobiotic receptors. Low doses of EDCs have been postulated to cause incomplete methylation of specific gene regions in the young brain and to impair neural development and brain functions across generations. Efforts are needed to develop systematic epidemiological studies and to investigate the mechanisms of action of EDCs in order to fully understand their effects on wildlife and humans.
Authors and Affiliations
Małgorzata Kajta, Anna Wójtowicz
Early co-administration of vitamin E acetate and methylcobalamin improves thermal hyperalgesia and motor nerve conduction velocity following sciatic nerve crush injury in rats.
Our previous studies have shown that early administration of vitamin E acetate (50 mg/kg, ip (VEA)) and methylcobalamin (500 microg/kg, ip (MCA)) for 30 days improved conduction velocity and neuropathic pain behavior. He...
Pharmacokinetics of sunitinib in combination with fluoroquinolones in rabbit model.
Background: Fluoroquinolones are widely prescribed antibiotics. Ciprofloxacin is a well-known inhibitor of cytochrome P450 CYP3A4 and causes numerous drug interactions that are not found for levofloxacin and moxifloxacin...
Heme oxygenase (HO-1) is involved in the negative regulation of contact sensitivity reaction.
Cutaneous contact sensitivity (CS) is a subtype of delayed-type sensitivity and is mediated by either CD4(+) or CD8(+) CS-effector T cells. CS can be induced by skin painting with haptens like trinitrophenyl chloride (TN...
Synthesis, anticonvulsant activity and 5-HT(1A)/5-HT(7) receptors affinity of 1-[(4-arylpiperazin-1-yl)-propyl]-succinimides.
Background: Epilepsy is the most prevalent neurological disorder, affecting approximately 50 million people worldwide. Even though significant advances have been made in epilepsy research, convulsions in about 30% of epi...
Anxiolytic-like effects of group III mGlu receptor ligands in the hippocampus involve GABA(A) signaling.
Recent literature data and the results of our earlier pharmacological studies, have provided evidence that antagonists of group I metabotropic glutamate receptors (mGluRs) and agonists of group II mGluRs show anxiolytic-...