Neonatal exposure to 3,3′,4,4′-tetrachlorobiphenyl: changes in spontaneous behaviour and cholinergic muscarinic receptors in the adult mouse

Eriksson, Per; Lundkvist, Ulrika; Fredriksson, Anders

doi:10.1016/0300-483x(91)90150-y

Cited by 94 publications

(30 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, it has been shown that exposure of mice to BDE-47 and BDE-99 during the critical neonatal period causes neurotoxic effects in adult animals (Eriksson et al 2001;Viberg et al 2002). Similar effects have previously been reported for certain coplanar and ortho-substituted PCBs (Eriksson and Fredriksson 1996a, 1996bEriksson et al 1991). In addition, effects of prenatal and postnatal exposure to PCBs, such as lower gestational age and birth weight (Fein et al 1984;Rylander et al 2000;Taylor et al 1984), delayed development (Guo et al 1994), and intellectual impairment (Jacobson and Jacobson 1996), have been reported in humans.…”

supporting

confidence: 65%

Human prenatal and postnatal exposure to polybrominated diphenyl ethers, polychlorinated biphenyls, polychlorobiphenylols, and pentachlorophenol.

Guvenius

Aronsson

Ekman-Ordeberg

et al. 2003

Environ Health Perspect

327

160

View full text Add to dashboard Cite

The aim of this study was to determine human prenatal and postnatal exposures to polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), hydroxylated metabolites of PCBs (polychlorobiphenylols; OH-PCBs), and pentachlorophenol (PCP). The median PBDE fresh-weight concentrations in maternal and cord blood plasma and in breast milk were 24, 4.3, and 75 pg/g, respectively. The PCB concentrations were approximately 60 times higher in each compartment (1,560, 277, and 4,310 pg/g, respectively). Calculated on a lipid weight basis, the levels were comparable in maternal blood plasma and breast milk. In contrast to PCBs, differences were found between PBDE congener distribution in maternal and cord blood plasma. The OH-PCBs constituted up to 26% of the PCB levels in maternal blood plasma and 53% in cord blood plasma, with levels of 120 and 88 pg/g fresh weight, respectively, and in breast milk 3 pg/g. The corresponding concentrations for PCP were 2,830, 1,960, and 20 pg/g. The ratios of PCB to OH-PCB were 13, 3, and 1,400 in maternal, cord plasma, and breast milk, respectively. It is evident that prenatal exposures occur for all the analytes. Moreover, the exposure continues after birth via breast milk. However, levels of OH-PCBs and PCP in breast milk are low compared with levels in blood plasma. Exposures to both PCBs and PBDEs, and in particular to the endocrine-active halogenated phenolic compounds, are of concern and implicate a potential risk for developmental disturbances.

show abstract

supporting

confidence: 65%

Human prenatal and postnatal exposure to polybrominated diphenyl ethers, polychlorinated biphenyls, polychlorobiphenylols, and pentachlorophenol.

Guvenius

Aronsson

Ekman-Ordeberg

et al. 2003

Environ Health Perspect

327

160

View full text Add to dashboard Cite

show abstract

“…Increased activity is a well-known effect caused by PCB mixtures, ortho-substituted and coplanar congeners in rats (Hany et al, 1999b;Holene et al, 1995;Jacobson and Jacobson, 1997;Lilienthal et al, 1990;Schantz et al, 1995). Also in mice, increased locomotor activity has been reported to occur in adult animals after prenatal and postnatal exposure to Aroclor 1254 (Storm et al, 1981), or neonatal exposure to coplanar PCBs (Eriksson et al, 1991;Eriksson and Fredriksson, 1998) and ortho-chlorinated PCBs (Eriksson and Fredriksson, 1996). Agrawal et al (1981) showed that elevated levels of locomotor activity induced by developmental exposure of mice to a high dose of 3,3 0 ,4,4 0 -tetrachlorobiphenyl was associated with decreased dopamine concentrations in the corpus striatum.…”

Section: Discussionmentioning

confidence: 99%

Developmental Exposure to 4-hydroxy-2,3,3',4',5-pentachlorobiphenyl (4-OH-CB107): Long-Term Effects on Brain Development, Behavior, and Brain Stem Auditory Evoked Potentials in Rats

Meerts

Lilienthal²,

Hoving³

et al. 2004

Toxicological Sciences

View full text Add to dashboard Cite

In the present study the developmental neurotoxic effects of the PCB metabolite 4-OH-2,3,3 0 ,4 0 ,5-pentachlorobiphenyl (4-OH-CB107) were compared with effects caused by a mixture of parent polychlorinated biphenyl (PCB) congeners (Aroclor 1254). Pregnant female Wistar rats were exposed to 0.5 or 5 mg 4-OH-CB107, or 25 mg Aroclor 1254 per kg body weight from gestation days 10 to 16. Plasma thyroid hormone levels were significantly decreased in the offspring of all treatment groups at postnatal day 4 (PND 4). Behavioral experiments using an open field paradigm revealed an impaired habituation in male offspring of all treatment groups at PND 130. Passive avoidance experiments indicated significant influences on the time course of step-down latencies across trials in exposed male rats. Catalepsy induced by haloperidol showed increases in latencies to movement onset in female offspring exposed to 0.5 mg 4-OH-CB107 compared to Aroclor 1254 treated offspring at PND 168-175. Male offspring exposed to 4-OH-CB107 or Aroclor 1254 showed decreases in latencies compared to control animals. Brain stem auditory evoked potentials (BAEPs) measured at PND 300-310 showed significant increases in auditory thresholds in the low frequency range between Aroclor 1254 and 4-OH-CB107 (5 mg/kg bw) treated animals. Measurements of neurotransmitter levels revealed effects of Aroclor 154 exposure on both the dopaminergic and the serotonergic systems, whereas 4-OH-CB107 exposure affected dopaminergic and noradrenergic systems, with slight but not significant effects on the serotonergic system. These results indicate that 4-OH-CB107 is able to induce long-term effects on behavior and neurodevelopment. The observed effects for 4-OH-CB107 are similar to, but in some aspects different from, the effects observed after Aroclor 1254 exposure.

show abstract

“…It has been reported that maternal administration of dioxinlike isomer PCB 77 (TEF = 0.0001) (32 mg/kg/day, then 3.2 µg TEQ/kg/day, on GD10 to 16) to CD-1 mice induced the hyperactivity, reduction of front leg gripping, the disturbance in the vision replacement and disruption of the passive avoidance in their offspring 120) , and that these behavioral changes are accompanied by the inhibition of synaptic formation in the nucleus accumbens 121) and by decrease in dopamine contents and its receptor binding in the striatum 122) . Eriksson et al (1991) reported that postnatal exposure to PCB 77 (41 mg/kg, then 4.1 µg TEQ/kg) to male NMRI mice on PND10 affected locomotion in adulthood, i.e. the decrease in the initial stage of the test and the increase in the final stage of the test, suggesting that PCB inhibited habituation to the test environment 123) .…”

Section: Impairment Of Learning Performance By Pcbsmentioning

confidence: 99%

“…Eriksson et al (1991) reported that postnatal exposure to PCB 77 (41 mg/kg, then 4.1 µg TEQ/kg) to male NMRI mice on PND10 affected locomotion in adulthood, i.e. the decrease in the initial stage of the test and the increase in the final stage of the test, suggesting that PCB inhibited habituation to the test environment 123) . Recently, Roegge et al (2000) reported that maternal administration of Aroclor 1254 (6 mg/kg/day, given i.p.)…”

Section: Impairment Of Learning Performance By Pcbsmentioning

confidence: 99%

Developmental Neurotoxicity of Dioxin and Its Related Compounds.

Kakeyama

Tohyama

2003

INDUSTRIAL HEALTH

View full text Add to dashboard Cite

This manuscript reviewed the neurotoxicity of dioxins and related compounds with an emphasis on maternal exposure. The brain during developmental period is thought to be highly sensitive to dioxin and its related compounds that affect a broad range of brain functions from the advanced brain function to the reproduction-controlling function, even at low doses. It is suggested that dioxins exhibit endocrine-disrupting action on the gonadal and thyroid hormone axes, as well as the 'neural-disrupting action' on neural transmission and neural network formation. From behavioral toxicological studies as well as studies on the underlying mechanisms of dioxins' toxicity, dioxins affect some specific functions in particular regions or cells of the brain at critical windows during the developmental period.

show abstract

Neonatal exposure to 3,3′,4,4′-tetrachlorobiphenyl: changes in spontaneous behaviour and cholinergic muscarinic receptors in the adult mouse

Cited by 94 publications

References 27 publications

Human prenatal and postnatal exposure to polybrominated diphenyl ethers, polychlorinated biphenyls, polychlorobiphenylols, and pentachlorophenol.

Human prenatal and postnatal exposure to polybrominated diphenyl ethers, polychlorinated biphenyls, polychlorobiphenylols, and pentachlorophenol.

Developmental Exposure to 4-hydroxy-2,3,3',4',5-pentachlorobiphenyl (4-OH-CB107): Long-Term Effects on Brain Development, Behavior, and Brain Stem Auditory Evoked Potentials in Rats

Developmental Neurotoxicity of Dioxin and Its Related Compounds.

Contact Info

Product

Resources

About