Exposure to acrylamide decreases noradrenergic axons in rat brain

Zhang, Lingyi; Hara, Satoshi; Ichinose, Hiroshi; Nagashima, Daichi; Morita, Kyo; Sakurai, ﻿Toshihiro; Ichihara, Sahoko; Ichihara, Gaku

doi:10.1016/j.neuro.2020.03.001

Cited by 21 publications

(9 citation statements)

References 26 publications

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“…To our knowledge, this study was the first to explore the relationship between ACR and depression and the possible role of AQP4 in depression in rats. Some studies have observed changes in brain monoamine levels and depressive symptoms comorbid with anxiety behavior in rodents after exposure to ACR [ 21 , 22 ]. A population-based cross-sectional study evaluated the association between ACR levels in the hemoglobin adducts and depressive symptoms in US adults by using data from the National Health and Nutrition Examination Survey [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

AQP4 Attenuated TRAF6/NFκB Activation in Acrylamide-Induced Neurotoxicity

et al. 2022

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Acrylamide (ACR) is present in high-temperature-processed high-carbohydrate foods, cigarette smoke, and industrial pollution. Chronic exposure to ACR may induce neurotoxicity from reactive oxygen species (ROS); however, the mechanisms underlying ACR-induced neurotoxicity remain unclear. We studied 28-day subacute ACR toxicity by repeatedly feeding ACR (0, 15, or 30 mg/kg) to rats. We conducted RNA sequencing and Western blot analyses to identify differences in mRNA expression in the blood and in protein expression in the brain tissues, respectively, of the rats. AQP4 transient transfection was performed to identify potential associations with protein regulation. The rats treated with 30 mg/kg ACR exhibited hind-limb muscle weakness. Matrix metalloproteinase (MMP9) expression was higher in the ACR-treated group than in the control group. ACR induced MMP-9 and AQP4 protein expression in the brain tissues of the rats, which subsequently presented with neurotoxicity. In the in vitro study, Neuro-2a cells were transiently transfected with AQP4, which inhibited MMP-9 and TNF receptor-associated factor 6 (TRAF6) expression, and inhibited ACR induced expression of TRAF6, IκBα, and nuclear factor κB (NFκB). Using a combination of in vivo and in vitro experiments, this study revealed that depressive symptoms associated with ACR-induced neurotoxicity are associated with downregulation of AQP4 and induction of the TRAF6 pathway.

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Section: Discussionmentioning

confidence: 99%

AQP4 Attenuated TRAF6/NFκB Activation in Acrylamide-Induced Neurotoxicity

et al. 2022

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“…An elevated concentration of serum malondialdehyde and superoxide dismutase was found in patients with major depression. , The deficiency of monoamine neurotransmitters was also associated with a higher risk of depression . The experimental animal studies indicated that AA-induced oxidative stress in nervous tissue enhanced lipid peroxidation and reduced the antioxidative capacity, as well as enzymatic and nonenzymatic antioxidants. , Moreover, changes in relevant brain proteins of the presynaptic vesicle cycling and depression-like behavior with monoamine neurotransmitters’ depletion were observed in AA-treated animals. ,,, …”

Section: Discussionmentioning

confidence: 99%

“…AA-induced oxidative stress is involved in the pathology of neurodegeneration , and may play roles in depression . Furthermore, depletion, impaired synthesis, and regulation of monoamine neurotransmitters (5-hydroxytryptamine, noradrenaline, and dopamine) may be associated with a higher risk of depression. , Several studies observed changed levels of monoamines in animal brains and depression phenotype comorbid with anxiety behavior after exposure to AA. − However, to date, an association between depressive symptoms and AA has not been reported in epidemiologic studies in the general population. Therefore, we conducted this population-based cross-sectional study to evaluate the association between HbAA, HbGA, HbGA/HbAA, and depressive symptoms using US adults (≥18 years) from the National Health and Nutrition Examination Survey (NHANES) 2013–2016.…”

Section: Introductionmentioning

confidence: 99%

Association between Acrylamide Hemoglobin Adduct Levels and Depressive Symptoms in US Adults: NHANES 2013–2016

Sun

Zhang

2021

J. Agric. Food Chem.

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Acrylamide (AA) is widely present in heat-processed carbohydrate-rich food, cigarette smoke, and the environment. Prolonged exposure to AA may cause central nervous system damage. However, few epidemiologic studies assessed the association between hemoglobin adduct levels of AA or its metabolite glycidamide (GA) and depressive symptoms. We included 3595 US adults (≥18 years) from the National Health and Nutrition Examination Survey (NHANES) 2013−2016. Data for hemoglobin adduct levels from AA and GA (HbAA and HbGA) were used as a measure of internal dose. Depressive symptom data were from mental health questionnaires and measured by nine-item Patient Health Questionnaire (PHQ-9) scores. Results of logistic regression models showed a positive association between HbAA in quartile 4 and depressive symptoms with ORs and 95% CI of 2. 47 (1.29, 4.77) [OR continuous HbAA and 95% CI: 1.006 (1.000, 1.013)], but an inverse association was detected in quartiles 2 and 3 of HbGA/ HbAA [0.62 (0.38, 0.99) and 0.54 (0.32, 0.92), respectively]. Especially, an association between HbAA and depressive symptoms was strengthened in smokers, in age 18−39 and 40−59 years and BMI 25−30 kg/m 2 groups. Further explorations are needed to study the found associations between HbAA, HbGA, and depressive symptoms.

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“…Both chemicals are classified as soft electrophiles and share similar reaction mechanisms; for instance, neurotoxicity of both 1-BP 34 and acrylamide 35 was reported to have a similar underlying mechanism in animal studies. 34,35 Whether prenatal acrylamide induced DNT remains to be fully determined, since only the toxicity to body weight increase was reproducible. 36,37 In contrast, longer exposure until weaning exhibited DNT.…”

Section: Discussionmentioning

confidence: 99%

Exposure to 1-bromopropane vapors during pregnancy enhances the development of hippocampal neuronal excitability in rat pups during lactation

Fueta

Ueno

Ishidao

et al. 2020

Journal of Occupational Health

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Objectives Although 1‐Bromopropane (1‐BP) exposure has been reported to cause neurotoxicity in adult humans and animals, its effects on the development of the central nervous system remain unclear. Recently, we reported delayed developmental neurotoxicity (DNT) upon 1‐BP exposure in rats. Here we aimed to study the effect of prenatal 1‐BP exposure on the hippocampal excitability in the juvenile offspring. Methods Pregnant Wistar rats were exposed to vaporized 1‐BP for 20 days (6 h/d) with concentrations of 0 (control), 400, or 700 ppm. Hippocampal slices were prepared from male offspring during postnatal days (PNDs) 13, 14, and 15. Field excitatory postsynaptic potential (fEPSP) and population spike (PS) were recorded simultaneously from the CA1 region. Results In the exposed groups, the stimulation/response relationships of fEPSP slope and PS amplitude were enhanced more than in the control group at PND 14. Analysis of fEPSP‐spike coupling demonstrated increased values of Top and Eslope50 in the exposed groups. Real‐time PCR analysis showed a significant increase in the mRNA levels of the adult type Na v 1.1 Na + channel subunit and the GluR1 glutamate receptor subunit in the hippocampus of the 700 ppm group at PND 14. Conclusions Our results provide evidence that prenatal exposure to 1‐BP accelerates developmental enhancement of hippocampal excitability in the pups before eye‐opening. The current study suggests that our evaluation method of DNT is applicable to the industrial chemical 1‐BP.

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Exposure to acrylamide decreases noradrenergic axons in rat brain

Cited by 21 publications

References 26 publications

AQP4 Attenuated TRAF6/NFκB Activation in Acrylamide-Induced Neurotoxicity

AQP4 Attenuated TRAF6/NFκB Activation in Acrylamide-Induced Neurotoxicity

Association between Acrylamide Hemoglobin Adduct Levels and Depressive Symptoms in US Adults: NHANES 2013–2016

Exposure to 1-bromopropane vapors during pregnancy enhances the development of hippocampal neuronal excitability in rat pups during lactation

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