Study of polychlorinated biphenyls as potential modifiers of developmental neurotoxicity of methylmercury

Teresa Coccini, Anna F. Castoldi, Elisa Roda, Dimosthenis A. Sarigiannis, Luigi Manzo

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The developing brain is the most susceptible target for methylmercury (MeHg) toxicity. Typical features of developmental MeHg neurotoxicity include the delayed onset of symptoms and the persistency of dysfunction. One of the factors which may modulate MeHg neurotoxicity is co-exposure to other neurotoxic pollutant, e.g. polychlorinated biphenyls (PCBs) from the same dietary sources. Because PCBs themselves can induce subtle neurodevelopmental deficiencies, recent epidemiological and research studies have focused on the potential hazard resulting from mixtures of PCBs and MeHg. This work summarizes our experimental findings on several endpoints of the cholinergic and aminergic systems in the developing rat brain, following two distinct perinatal co-exposure protocols involving low to moderate doses of MeHg and PCB153 or PCB126. The neurochemical modifications induced by either agent, alone or combined, involved monoamine oxidase type-B activity, biogenic amine levels (e.g., serotonin and dopamine), total cholinergic muscarinic receptors (MRs) and M1, M2 and M3 subtypes. The effects were brain region-, age- and gender-dependent. Some early-onset changes (weaning) persisted until puberty, while other alterations became manifest only at the advanced time point, when the brain levels of Hg, PCB153, and PCB126 had declined. The results of the combined exposure ruled out synergistic interactions between MeHg and PCB153 or PCB126 on every neurochemical endpoint tested. This applied to all pups regardless of the (i) regimen of exposure, (ii) gender, (iii) age, and (iv) brain area. The co-treatment with either PCB153 or PCB126 sometimes masked MeHg-induced changes on selected neurochemical endpoints. Nevertheless, this cannot be viewed as a protective effect. The final health effect may be masked at early time-points, but may become manifest later during life time.

Original languageEnglish
Pages (from-to)1432-1438
Number of pages7
JournalFresenius Environmental Bulletin
Volume17
Issue number9 B
Publication statusPublished - 2008

Fingerprint

Polychlorinated Biphenyls
methylmercury
Polychlorinated biphenyls
brain
PCB
Brain
Cholinergic Agents
gender
Muscarinic M1 Receptors
Biogenic Amines
weaning
Monoamine Oxidase
Toxicity
Rats
Amines
Dopamine
Serotonin
Hazards
neurotoxicity
Health

Keywords

  • Brain
  • MeHg
  • Mixture
  • Offspring
  • PCB126
  • PCB153

ASJC Scopus subject areas

  • Pollution
  • Waste Management and Disposal
  • Environmental Chemistry

Cite this

Study of polychlorinated biphenyls as potential modifiers of developmental neurotoxicity of methylmercury. / Coccini, Teresa; Castoldi, Anna F.; Roda, Elisa; Sarigiannis, Dimosthenis A.; Manzo, Luigi.

In: Fresenius Environmental Bulletin, Vol. 17, No. 9 B, 2008, p. 1432-1438.

Research output: Contribution to journalArticle

Coccini, Teresa ; Castoldi, Anna F. ; Roda, Elisa ; Sarigiannis, Dimosthenis A. ; Manzo, Luigi. / Study of polychlorinated biphenyls as potential modifiers of developmental neurotoxicity of methylmercury. In: Fresenius Environmental Bulletin. 2008 ; Vol. 17, No. 9 B. pp. 1432-1438.
@article{291bc584d9a84f02a2727eb36cc6fb57,
title = "Study of polychlorinated biphenyls as potential modifiers of developmental neurotoxicity of methylmercury",
abstract = "The developing brain is the most susceptible target for methylmercury (MeHg) toxicity. Typical features of developmental MeHg neurotoxicity include the delayed onset of symptoms and the persistency of dysfunction. One of the factors which may modulate MeHg neurotoxicity is co-exposure to other neurotoxic pollutant, e.g. polychlorinated biphenyls (PCBs) from the same dietary sources. Because PCBs themselves can induce subtle neurodevelopmental deficiencies, recent epidemiological and research studies have focused on the potential hazard resulting from mixtures of PCBs and MeHg. This work summarizes our experimental findings on several endpoints of the cholinergic and aminergic systems in the developing rat brain, following two distinct perinatal co-exposure protocols involving low to moderate doses of MeHg and PCB153 or PCB126. The neurochemical modifications induced by either agent, alone or combined, involved monoamine oxidase type-B activity, biogenic amine levels (e.g., serotonin and dopamine), total cholinergic muscarinic receptors (MRs) and M1, M2 and M3 subtypes. The effects were brain region-, age- and gender-dependent. Some early-onset changes (weaning) persisted until puberty, while other alterations became manifest only at the advanced time point, when the brain levels of Hg, PCB153, and PCB126 had declined. The results of the combined exposure ruled out synergistic interactions between MeHg and PCB153 or PCB126 on every neurochemical endpoint tested. This applied to all pups regardless of the (i) regimen of exposure, (ii) gender, (iii) age, and (iv) brain area. The co-treatment with either PCB153 or PCB126 sometimes masked MeHg-induced changes on selected neurochemical endpoints. Nevertheless, this cannot be viewed as a protective effect. The final health effect may be masked at early time-points, but may become manifest later during life time.",
keywords = "Brain, MeHg, Mixture, Offspring, PCB126, PCB153",
author = "Teresa Coccini and Castoldi, {Anna F.} and Elisa Roda and Sarigiannis, {Dimosthenis A.} and Luigi Manzo",
year = "2008",
language = "English",
volume = "17",
pages = "1432--1438",
journal = "Fresenius Environmental Bulletin",
issn = "1018-4619",
publisher = "Parlar Scientific Publications",
number = "9 B",

}

TY - JOUR

T1 - Study of polychlorinated biphenyls as potential modifiers of developmental neurotoxicity of methylmercury

AU - Coccini, Teresa

AU - Castoldi, Anna F.

AU - Roda, Elisa

AU - Sarigiannis, Dimosthenis A.

AU - Manzo, Luigi

PY - 2008

Y1 - 2008

N2 - The developing brain is the most susceptible target for methylmercury (MeHg) toxicity. Typical features of developmental MeHg neurotoxicity include the delayed onset of symptoms and the persistency of dysfunction. One of the factors which may modulate MeHg neurotoxicity is co-exposure to other neurotoxic pollutant, e.g. polychlorinated biphenyls (PCBs) from the same dietary sources. Because PCBs themselves can induce subtle neurodevelopmental deficiencies, recent epidemiological and research studies have focused on the potential hazard resulting from mixtures of PCBs and MeHg. This work summarizes our experimental findings on several endpoints of the cholinergic and aminergic systems in the developing rat brain, following two distinct perinatal co-exposure protocols involving low to moderate doses of MeHg and PCB153 or PCB126. The neurochemical modifications induced by either agent, alone or combined, involved monoamine oxidase type-B activity, biogenic amine levels (e.g., serotonin and dopamine), total cholinergic muscarinic receptors (MRs) and M1, M2 and M3 subtypes. The effects were brain region-, age- and gender-dependent. Some early-onset changes (weaning) persisted until puberty, while other alterations became manifest only at the advanced time point, when the brain levels of Hg, PCB153, and PCB126 had declined. The results of the combined exposure ruled out synergistic interactions between MeHg and PCB153 or PCB126 on every neurochemical endpoint tested. This applied to all pups regardless of the (i) regimen of exposure, (ii) gender, (iii) age, and (iv) brain area. The co-treatment with either PCB153 or PCB126 sometimes masked MeHg-induced changes on selected neurochemical endpoints. Nevertheless, this cannot be viewed as a protective effect. The final health effect may be masked at early time-points, but may become manifest later during life time.

AB - The developing brain is the most susceptible target for methylmercury (MeHg) toxicity. Typical features of developmental MeHg neurotoxicity include the delayed onset of symptoms and the persistency of dysfunction. One of the factors which may modulate MeHg neurotoxicity is co-exposure to other neurotoxic pollutant, e.g. polychlorinated biphenyls (PCBs) from the same dietary sources. Because PCBs themselves can induce subtle neurodevelopmental deficiencies, recent epidemiological and research studies have focused on the potential hazard resulting from mixtures of PCBs and MeHg. This work summarizes our experimental findings on several endpoints of the cholinergic and aminergic systems in the developing rat brain, following two distinct perinatal co-exposure protocols involving low to moderate doses of MeHg and PCB153 or PCB126. The neurochemical modifications induced by either agent, alone or combined, involved monoamine oxidase type-B activity, biogenic amine levels (e.g., serotonin and dopamine), total cholinergic muscarinic receptors (MRs) and M1, M2 and M3 subtypes. The effects were brain region-, age- and gender-dependent. Some early-onset changes (weaning) persisted until puberty, while other alterations became manifest only at the advanced time point, when the brain levels of Hg, PCB153, and PCB126 had declined. The results of the combined exposure ruled out synergistic interactions between MeHg and PCB153 or PCB126 on every neurochemical endpoint tested. This applied to all pups regardless of the (i) regimen of exposure, (ii) gender, (iii) age, and (iv) brain area. The co-treatment with either PCB153 or PCB126 sometimes masked MeHg-induced changes on selected neurochemical endpoints. Nevertheless, this cannot be viewed as a protective effect. The final health effect may be masked at early time-points, but may become manifest later during life time.

KW - Brain

KW - MeHg

KW - Mixture

KW - Offspring

KW - PCB126

KW - PCB153

UR - http://www.scopus.com/inward/record.url?scp=55549091453&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=55549091453&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:55549091453

VL - 17

SP - 1432

EP - 1438

JO - Fresenius Environmental Bulletin

JF - Fresenius Environmental Bulletin

SN - 1018-4619

IS - 9 B

ER -