Developmental Neurotoxicity of Arsenic: Involvement of Oxidative Stress and Mitochondrial Functions

Chandravanshi, Lalit P.; Gupta, Richa; Shukla, Rohit

doi:10.1007/s12011-018-1286-1

Cited by 84 publications

(38 citation statements)

References 62 publications

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“…One study demonstrated that As has a direct effect on oxidative stress and the imbalances of defensive anti-oxidative mechanism and neurotransmitter metabolism in the hippocampus [40]. In addition, perinatal As exposure has a developmental neurotoxicity with abrupt changes in the reactive oxygen species (ROS), oxidative stress, mitochondrial functions and apoptosis in the developing brain [41].…”

Section: Discussionmentioning

confidence: 99%

Blood heavy metals and brain-derived neurotrophic factor in the first trimester of pregnancy among migrant workers

Zaw

Taneepanichskul

2019

PLoS ONE

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Background Lead, mercury, cadmium and arsenic are the priority heavy metals of major public health concern in industrialized countries. Exposure to them can cause cognitive impairment and depressive disorders through an effect on Brain-derived neurotrophic factor (BDNF) which is an important biomarker of pregnancy. Despite a number of prior studies on heavy metals pollution, there is few of studies on the effect of heavy metals on BDNF during early pregnancy. This study aims to examine the association between maternal blood heavy metals concentrations and BDNF during the first trimester pregnancy among Myanmar migrants in Thailand. Methodology This cross sectional study, a part of ongoing birth cohort was conducted at the antenatal care clinic from June to October 2018. A total of 108 with Myanmar migrant pregnancy with a single viable fetus of 0 to 14 gestation weeks who stayed within the industrial plant at least 3 months before were recruited. Socio-demographic characteristics and health behaviors were accessed using a self-report questionnaire. Maternal blood heavy metals (lead (Pb), mercury (Hg), cadmium (Cd) and arsenic (As)) were measured using an inductively coupled plasma mass spectrometer and plasma BDNF was measured using an enzyme-linked immunosorbent assay. Multivariate binary logistic regression were modeled to access the association. Results Median (interquartile rank: IQR) concentrations were: BDNF (6.49 (1.79) μg/ml), Pb (2.77 (1.46) μg/dL), Hg (0.62 (0.54) μg/dL), Cd (0.93(0.86) μg/L) and As (0.40 (0.11) μg/dL) respectively. We categorized BDNF concentrations into high (> median) (n = 54) and low (≤ median) (n = 54) groups. After adjusting for potential confounders, high blood total arsenic concentration had 2.6-fold increased odds (aOR = 2.603, 95% CI: 1.178, 5.751) of low plasma BDNF level as compared with low blood total arsenic group. However, there was no significant association between BDNF and Pb, Hg and Cd. Conclusions The present findings demonstrate higher blood total arsenic level were more likely to have lower BDNF in early pregnancy. Our study suggested that heavy metal could be worsen BDNF level which plays its important role on biological effect of maternal depressive disorder and newborn neurodevelopment.

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Section: Discussionmentioning

confidence: 99%

Blood heavy metals and brain-derived neurotrophic factor in the first trimester of pregnancy among migrant workers

Zaw

Taneepanichskul

2019

PLoS ONE

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“…One of the most important mechanisms involved in the neurotoxicity of As is its ability to cause oxidative stress and mitochondrial dysfunction [29,30]. Arsenic decreased the activities of mitochondrial complexes I, II-III, and IV in the rat brain and increased the levels of reactive oxygen species (ROS) [31].…”

Section: Toxic Mechanismsmentioning

confidence: 99%

Arsenic Neurotoxicity in Humans

Mochizuki

2019

IJMS

152

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Arsenic (As) contamination affects hundreds of millions of people globally. Although the number of patients with chronic As exposure is large, the symptoms and long-term clinical courses of the patients remain unclear. In addition to reviewing the literature on As contamination and toxicity, we provide useful clinical information on medical care for As-exposed patients. Further, As metabolite pathways, toxicity, speculated toxicity mechanisms, and clinical neurological symptoms are documented. Several mechanisms that seem to play key roles in As-induced neurotoxicity, including oxidative stress, apoptosis, thiamine deficiency, and decreased acetyl cholinesterase activity, are described. The observed neurotoxicity predominantly affects peripheral nerves in sensory fibers, with a lesser effect on motor fibers. A sural nerve biopsy showed the axonal degeneration of peripheral nerves mainly in small myelinated and unmyelinated fibers. Exposure to high concentrations of As causes severe central nervous system impairment in infants, but no or minimal impairment in adults. The exposure dose–response relationship was observed in various organs including neurological systems. The symptoms caused by heavy metal pollution (including As) are often nonspecific. Therefore, in order to recognize patients experiencing health problems caused by As, a multifaceted approach is needed, including not only clinicians, but also specialists from multiple fields.

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“…Since hippocampus plays a pivotal role in learning and memory modulation [39], learning and memory deficits in arsenic-treated animals might be associated with an impaired cholinergic system. Evidence produced by other studies have suggested that arsenic can disturb anti-oxidants, causing oxidative stress in the brain [40][41][42]. Oxidative stress has been shown to inhibit or decrease acetylcholine receptors in the hippocampus and frontal cortex in animals treated with arsenic [43].…”

Section: Discussionmentioning

confidence: 98%

The Protective Effects of Nicotine and Bucladesine on Impaired Avoidance Memory Caused by Sodium Arsenate Toxicity in Mice

Najafi

Hashemzaei

Sadeghi

et al. 2021

IJT

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Background: The toxic effect of sodium arsenate on nervous system has been shown; but the protective effects of several compounds against sodium arsenate are not clear. This study aimed to investigate the protective effects of nicotine and bucladesine, two positive modulators of neuronal function, on sodium arsenate toxicity against avoidance memory impairment. Methods: Male mice (N=154) were assigned to 22 groups (12 experimental and 10 control) of seven animals each and were treated as follows: sodium arsenate (2.5, 5, or 10 mg/kg) for 28 days, nicotine (1 mg/kg) for either 1, 2, or 4 days, bucladesine (600 nM/mouse) for either 1, 2, or 4 days, and nicotine (1 mg/kg)+bucladesine (600 nM/mouse)+sodium arsenate (2.5 mg/kg). The last group was treated with 2.5 mg/kg sodium arsenate first, and then received the combination of nicotine and bucladesine for 1, 2, or 4-days. The corresponding control groups did not receive any drug but either saline, deionized water, or combination of deionized water and DMSO, but went through the same procedure as other animals. All mice were trained 24 h in the step-through passive avoidance task. The avoidance memory retention was assessed at 24, 48, 96, and 168 h after the training period by measuring the time they stayed in a dark chamber. Results: All sodium arsenate doses significantly reduced the time stayed in the dark chamber regardless of the treatment duration (24, 48, 96 & 168 h) after training. Both nicotine and bucladesine, whether used singly or combined for 1, 2, and 4 days significantly enhanced the time latency compared to the controls at all of the experimental timepoints following the training. Conclusion: Nicotine and bucladesine showed synergistic effects and reversed the sodium arsenate-induced avoidance memory deficits in mice.

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Developmental Neurotoxicity of Arsenic: Involvement of Oxidative Stress and Mitochondrial Functions

Cited by 84 publications

References 62 publications

Blood heavy metals and brain-derived neurotrophic factor in the first trimester of pregnancy among migrant workers

Blood heavy metals and brain-derived neurotrophic factor in the first trimester of pregnancy among migrant workers

Arsenic Neurotoxicity in Humans

The Protective Effects of Nicotine and Bucladesine on Impaired Avoidance Memory Caused by Sodium Arsenate Toxicity in Mice

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