Cerebellar morphological alterations in rats induced by prenatal ozone exposure

Rivas-Manzano, Patricia; Paz, Carlos

doi:10.1016/s0304-3940(99)00777-6

Cited by 12 publications

(7 citation statements)

References 19 publications

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“…Thus, it is possible that animals prenatally exposed may show some alterations in Purkinje cell modulation of GABA-mediated inhibition, leading to such symptoms as ataxia. This is consistent with the observation of important morphological alterations in the cerebellum, mainly in Purkinje cells, during development [13] and into adulthood [14] of prenatally exposed animals. On the other hand, some lines of evidence strongly suggest that cerebellar NE is involved in functional recovery after motor brain injury [26,27,28].…”

Section: Discussionsupporting

confidence: 92%

“…Morphological studies have been conducted focusing on the cerebellum of offspring whose mothers were exposed to O3 during pregnancy. It has been described that rat pups show cerebellar necrotic signs at postnatal day 0, diminishment of the molecular layer at day 12 and unusual clumps of chromatin in the nucleus periphery of purkinje cells at postnatal day 60 [13], as well as a reduction in the number of purkinje cells at postnatal day 90 [14]. Due to the important morphological changes produced by prenatal O3 exposure in the cerebellum, it is expected that some neurotransmitter systems could be disrupted by prenatal O3 exposure.…”

Section: Introductionmentioning

confidence: 99%

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Prenatal Exposure to Ozone Disrupts Cerebellar Monoamine Contents in Newborn Rats

et al. 2007

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Ozone (O3) is widely distributed in environments with high levels of air pollution. Since cerebellar morphologic disruptions have been reported with prenatal O3 exposure, O3 may have an effect on some neurotransmitter systems, such as monoamines. In order to test this hypothesis, we used 60 male rats taken from either, mothers exposed to 1 ppm of O3 during the entire pregnancy, or from mothers breathing filtered and clean air during pregnancy. The cerebellum was extracted at 0, 5, and 10 postnatal days. Tissues were processed in order to analyze by HPLC, dopamine (DA) levels, 3,4 dihydroxyphenilacetic acid (DOPAC) and homovanillic acid (HVA), norepinephrine (NA), serotonin, and 5-hydroxy-indole-acetic acid (5-HIAA) contents. Results showed a decrease of DA, NA, DOPAC and HVA mainly in 0 and 5 postnatal days. There were no changes in 5-HT levels, and 5-HIAA showed an increase after 10 postnatal days. DOPAC + HVA/DA ratio showed changes in 0 and 10 postnatal days, while 5-HIAA/5-HT ratio showed a slight decrease in 0 days. The data suggest that prenatal O3 exposure disrupts the cerebellar catecholamine system rather than the indole-amine system. Disruptions in cerebellar NA could lead to ataxic symptoms and also could limit recovery after cortical brain damage in adults. These finding are important given that recovery mechanisms observed in animals are also observed in humans.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Prenatal Exposure to Ozone Disrupts Cerebellar Monoamine Contents in Newborn Rats

et al. 2007

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“…Prenatal ozone exposure leads to permanent damage of the cerebellum [118] and disruption of the cerebellar monoaminergic system [119]. In addition, prolonged prenatal ozone exposure altered the levels neurotrophic factor in the brain.…”

Section: Air Pollution and Neurological Diseasementioning

confidence: 99%

The Adverse Effects of Air Pollution on the Nervous System

Genç

Zadeoğluları

Fuss

et al. 2012

Journal of Toxicology

516

334

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Exposure to ambient air pollution is a serious and common public health concern associated with growing morbidity and mortality worldwide. In the last decades, the adverse effects of air pollution on the pulmonary and cardiovascular systems have been well established in a series of major epidemiological and observational studies. In the recent past, air pollution has also been associated with diseases of the central nervous system (CNS), including stroke, Alzheimer's disease, Parkinson's disease, and neurodevelopmental disorders. It has been demonstrated that various components of air pollution, such as nanosized particles, can easily translocate to the CNS where they can activate innate immune responses. Furthermore, systemic inflammation arising from the pulmonary or cardiovascular system can affect CNS health. Despite intense studies on the health effects of ambient air pollution, the underlying molecular mechanisms of susceptibility and disease remain largely elusive. However, emerging evidence suggests that air pollution-induced neuroinflammation, oxidative stress, microglial activation, cerebrovascular dysfunction, and alterations in the blood-brain barrier contribute to CNS pathology. A better understanding of the mediators and mechanisms will enable the development of new strategies to protect individuals at risk and to reduce detrimental effects of air pollution on the nervous system and mental health.

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“…In animal studies, prenatal exposure to nitrogen dioxide (NO 2 ) affected neuromuscular coordination and caused functional deficits in the developing offspring of mice [3] and prenatal sulfur dioxide (SO 2 ) exposure reduced the levels of several mouse social/agonistic behaviors, such as tail rattling, freezing, and defensive postures [4] impaired neuromuscular coordination [5] and impaired the coordination and locomotor development of their offspring [6]. Exposure to high ozone (O 3 ) concentrations during gestation induces permanent cerebellar damage in rats and negatively impacts activity/exploration and social behavior [7,8]. It is also found the significant increase in freezing and defensive postures, decreases in nose-sniffing behavior and decreased nerve growth factor (NGF) levels in the hippocampus [9].…”

Section: Introductionmentioning

confidence: 99%

Multilevel Analysis of Air Pollution and Early Childhood Neurobehavioral Development

Lin

Yang

Lin

et al. 2014

IJERPH

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To investigate the association between the ambient air pollution levels during the prenatal and postnatal stages and early childhood neurobehavioral development, our study recruited 533 mother-infant pairs from 11 towns in Taiwan. All study subjects were asked to complete childhood neurobehavioral development scales and questionnaires at 6 and 18 months. Air pollution, including particulate matter ≤10 μm (PM10), carbon monoxide (CO), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), and hydrocarbons, was measured at air quality monitoring stations in the towns where the subjects lived. Multilevel analyses were applied to assess the association between air pollution and childhood neurobehavioral development during pregnancy and when the children were 0 to 6 months, 7 to 12 months, and 13 to 18 months old. At 18 months, poor subclinical neurodevelopment in early childhood is associated with the average SO2 exposure of prenatal, during all trimesters of pregnancy and at postnatal ages up to 12 months (first trimester β = −0.083, se = 0.030; second and third trimester β = −0.114, se = 0.045; from birth to 12 months of age β = −0.091, se = 0.034). Furthermore, adverse gross motor below average scores at six months of age were associated with increased average non-methane hydrocarbon, (NMHC) levels during the second and third trimesters (β = −8.742, se = 3.512). Low-level SO2 exposure prenatally and up to twelve months postnatal could cause adverse neurobehavioral effects at 18 months of age. Maternal NMHC exposure during the 2nd and 3rd trimesters of pregnancy would be also associated with poor gross motor development in their children at 6 months of age.

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Cerebellar morphological alterations in rats induced by prenatal ozone exposure

Cited by 12 publications

References 19 publications

Prenatal Exposure to Ozone Disrupts Cerebellar Monoamine Contents in Newborn Rats

Prenatal Exposure to Ozone Disrupts Cerebellar Monoamine Contents in Newborn Rats

The Adverse Effects of Air Pollution on the Nervous System

Multilevel Analysis of Air Pollution and Early Childhood Neurobehavioral Development

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