Gestational exposure to cadmium alters crucial offspring rat brain enzyme activities: The role of cadmium-free lactation

Liapi, Charis; Stolakis, Vasileios; Ζάρρος, Απόστολος; Zissis, Konstantinos M.; Botis, John; Al-Humadi, Hussam; Tsakiris, Stylianos

doi:10.1016/j.etap.2013.07.014

Cited by 23 publications

(3 citation statements)

References 15 publications

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“…The abnormalities in offspring include decreased locomotor activity, disruption in the expression of neurotransmitters and decreased neuromotor maturation (Tian et al, 2020 ; Zhao et al, 2015 ). Moreover, perinatal exposure to Cd and exposure during lactation have been proved to increase the activity of the sodium–potassium adenosine triphosphatase (Na + /K + ‐ATPase) in the brain (Liapi et al, 2013 ; Stolakis et al, 2013 ).…”

Section: D As a Neurotoxic Factormentioning

confidence: 99%

Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data

Ruczaj

Brzóska

2022

J of Applied Toxicology

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Nowadays, more and more attention has been focused on the risk of the neurotoxic action of cadmium (Cd) under environmental exposure. Due to the growing incidence of nervous system diseases, including neurodegenerative changes, and suggested involvement of Cd in their aetiopathogenesis, this review aimed to discuss critically this element neurotoxicity. Attempts have been made to recognize at which concentrations in the blood and urine Cd may increase the risk of damage to the nervous system and compare it to the risk of injury of other organs and systems. The performed overview of the available literature shows that Cd may have an unfavourable impact on the human's nervous system at the concentration >0.8 μg Cd/L in the urine and >0.6 μg Cd/L in the blood. Because such concentrations are currently noted in the general population of industrialized countries, it can be concluded that environmental exposure to this xenobiotic may create a risk of damage to the nervous system and be involved in the aetiopathogenesis of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, as well as worsening cognitive and behavioural functions. The potential mechanism of Cd neurotoxicity consists in inducing oxidative stress, disrupting the activity of enzymes essential to the proper functioning of the nervous system and destroying the homoeostasis of bioelements in the brain. Thus, further studies are necessary to recognize accurately both the risk of nervous system damage in the general population due to environmental exposure to Cd and the mechanism of this action.

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Section: D As a Neurotoxic Factormentioning

confidence: 99%

Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data

Ruczaj

Brzóska

2022

J of Applied Toxicology

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“…To address these outstanding questions, we have established a mouse model of maternal Cd exposure (Fig. 1) using a low, environmentally relevant Cd dose and a high dose of Cd that has been used in previous rodent studies 22–24 . We generated F 1 mice from matings between two genetically divergent inbred strains to study allele-specific epigenetic and transcriptional responses to maternal Cd exposure.…”

Section: Introductionmentioning

confidence: 99%

Maternal cadmium exposure in the mouse leads to increased heart weight at birth and programs susceptibility to hypertension in adulthood

Hudson

Belcher

Cowley

2019

Sci Rep

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cadmium (cd) is a toxic heavy metal ubiquitous in the environment. Maternal exposure to cd is associated with fetal growth restriction, trace element deficiencies, and congenital malformations. Cd exposure during adulthood is associated with cardiovascular disease (CVD); however, the effects of maternal Cd exposure on offspring cardiovascular development and disease are not well-understood. Utilizing a mouse model of maternal Cd exposure, we show that offspring born to Cd-exposed mothers have increased heart weights at birth and susceptibility to hypertension during adulthood. Despite inefficient maternal-fetal transfer of Cd, maternal Cd alters fetal levels of essential trace elements including a deficiency in iron, which is required for cardiovascular system development, oxygen homeostasis, and cellular metabolism. RNA-seq on newborn hearts identifies differentially expressed genes associated with maternal Cd exposure that are enriched for functions in CVD, hypertension, enlarged hearts, cellular energy, and hypoxic stress. We propose that a maternal Cd exposure-induced iron deficiency leads to altered cellular metabolic pathways and hypoxic conditions during fetal development; this stress may contribute to increased heart weight at birth and the programming of susceptibility to hypertension in adulthood. these studies will give insights into potential mechanisms through which maternal cd exposure impacts cardiovascular development and disease.

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“…Other studies shown that Cd is implicated in the induction of developmental neurotoxicity and cognitive dysfunction in both humans [41] and animals [42]. Additionally, gestational Cd exposure induced a decrease in brain enzymes activity, including AChE activity, in the offspring [14], [43].…”

Section: Discussionmentioning

confidence: 95%

Gestational Exposure to Cadmium and Dimethoate Mixture Modifies Fetal Programming in Rats During Development

Anselmo

Horta

Godinho

2020

EJMED

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The combined effects of environmental agents, as metals and pesticides, on human health, need be evaluated because human exposition occurs generally through mixtures, while regulatory assessment of neurotoxicity by these compounds is currently performed only on selected single substances. In the present study the effects of maternal exposure to 10 mg cadmium/l (as cadmium acetate) in drinking water and dimethoate 4 mg/kg (via gavage) during gestation on the development of motor activity (locomotion and motor coordination) and social behavior (anxiety-like behavior and aggressivity) were studied. The importance of the cholinergic system in the modulation of behaviors was studied using acetylcholinesterase (AChE) activity as a biomarker of effect. Cadmium (Cd) and dimethoate (DM) single exposition modified fetal programing for motor activity and social behavior at childhood and adulthood and leads to disturbs of the AChE activity. Exposition to the mixture of Cd and DM enhanced effects on fetal programing and AChE activity. The present results provide, for the ﬁrst time, direct experimental evidence supporting that joint exposure to cadmium and dimethoate in uterus of rats seems additive and it is perturbs offspring development leading to harmful consequences on motor activity and social behavior, probably related to modulation of the cholinergic system. Our data suggest that added precautions regarding gestational exposure to metals and pesticide mixtures would be prudent to avoid the possibility of fetal programming.

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Gestational exposure to cadmium alters crucial offspring rat brain enzyme activities: The role of cadmium-free lactation

Cited by 23 publications

References 15 publications

Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data

Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data

Maternal cadmium exposure in the mouse leads to increased heart weight at birth and programs susceptibility to hypertension in adulthood

Gestational Exposure to Cadmium and Dimethoate Mixture Modifies Fetal Programming in Rats During Development

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