Long-term acrylamide exposure exacerbates brain and lung pathology in a mouse malaria model

Ngo-Thanh, Ha; Thuy, Trang Dam; Suzue, Kazutomo; Kamitani, Wataru; Yokoo, Hideaki; Isoda, Koji; Shimokawa, Chikako; Hisaeda, Hajime; Imai, Takashi

doi:10.1016/j.fct.2021.112132

Cited by 6 publications

(4 citation statements)

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“…In our study, the rats treated with ACR for 28 days exhibited symptoms of neurotoxicity, including muscle weakness, difficulty in walking, limb numbness, decreased tactile sensation, and disappearance of tendon reflexes. ACR is toxic to the nervous systems of both humans and animals [ 7 ]. It causes swelling at the ends of axons of both the central and peripheral nervous systems and induces paralysis of the cerebrospinal system in humans.…”

Section: Discussionmentioning

confidence: 99%

“…Among the types of ACR-induced toxicity, neurotoxicity is the earliest to present and has been studied the most thoroughly. Several studies have reported that ACR-induced oxidative stress may contribute to neurotoxicity; common symptoms exhibited by rats exposed to ACR have included hind-limb foot splay, ataxia, and skeletal muscle weakness [ 7 ]. The early symptoms exhibited by workers exposed to ACR are skin peeling on the hands, impairment of vibration sensation in the toes, weakness in the leg muscles, and numbness in the hands and legs; workers with long-term ACR exposure experience limb weakness, anorexia, truncal ataxia, and horizontal nystagmus [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

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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%

Section: Introductionmentioning

confidence: 99%

AQP4 Attenuated TRAF6/NFκB Activation in Acrylamide-Induced Neurotoxicity

et al. 2022

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“…2,59 AA leads to central and peripheral axonopathy/myopathy and neuropathy or encephalopathy. 47,60,61 In this study, experimental AA toxicity in rats was planned, and the pathological effects of AA on both central and peripheral nervous systems were tried to be elucidated in the light of histopathological/immunohistochemical data, behavioural tests and various biochemical and molecular tests. In addition, considering the need to develop alternative therapeutic natural agents in the treatment of disorders caused by neurotoxic substances, 62,63 The neuromodulatory property of CRV as a protector against AA-induced neurodegeneration was also investigated for the first time to our knowledge.…”

Section: Discussionmentioning

confidence: 99%

“…AA, an environmental and industrial pollutant, is a potent toxicant to the nervous system of humans and animals 2,59 . AA leads to central and peripheral axonopathy/myopathy and neuropathy or encephalopathy 47,60,61 . In this study, experimental AA toxicity in rats was planned, and the pathological effects of AA on both central and peripheral nervous systems were tried to be elucidated in the light of histopathological/immunohistochemical data, behavioural tests and various biochemical and molecular tests.…”

Section: Discussionmentioning

confidence: 99%

Metabolomic modelling and neuroprotective effects of carvacrol against acrylamide toxicity in rat's brain and sciatic nerve

Durmus,

Burak,

Goktug

et al. 2024

Clin Exp Pharma Physio

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The study aimed to investigate the harmful effects of acrylamide (AA), which forms in carbohydrate‐rich foods at temperatures above 120°C, on the central and peripheral nervous systems and to evaluate the potential neuroprotective effects of carvacrol (CRV). Male Wistar Albino rats were subjected to AA (40 mg/kg/bw/day) and CRV (50 mg/kg/bw/day) for 15 days. Following the last administration, evaluations revealed disrupted gait, heightened thermal sensitivity and altered paw withdrawal thresholds in AA‐exposed rats. Notably, AA reduced glutathione (GSH) and raised malondialdehyde (MDA) levels in both brain and sciatic nerve tissues. AA raised nuclear factor erythroid 2‐related factor 2 (Nrf2), caspase 3 and nuclear factor κB (NF‐κB) gene expressions while decreasing NR4A2. CRV co‐administration mitigated gait abnormalities, elevated GSH levels and lowered MDA levels in both tissues. CRV also modulated gene expression, reducing Nrf2 and NF‐κB while increasing NR4A2. Histopathological signs of AA‐induced neurodegeneration and elevated glial fibrillary acidic protein levels observed in brain and sciatic nerve tissues were rectified with simultaneous administration of CRV, thereby demonstrating neuroprotective efficacy in both regions. This study is pioneering in demonstrating CRV's neuroprotective potential against AA‐induced neurotoxicity in both central and peripheral nervous systems, effectively addressing limitations in the literature. In conclusion, the study revealed AA‐induced neurodegeneration in the brain and sciatic nerve, with CRV significantly mitigating this neurotoxicity. This novel research underscores CRV's promise as a neuroprotective agent against AA‐induced adverse effects in both the central and peripheral nervous systems.

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