Co-exposure of melamine and cyanuric acid as a risk factor for oxidative stress and energy metabolism: Adverse effects on hippocampal neuronal and synaptic function induced by excessive ROS production

Sun, Wei; Chen, Xiao; Mei, Yazi; Li, Xiaoliang; Yang, Yang; Liu, An

doi:10.1016/j.ecoenv.2022.114230

Cited by 11 publications

(6 citation statements)

References 80 publications

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“…12 Therefore, it is possible that several mechanisms are acting in parallel to disrupt CA3-CA1 synaptic function across learning while the dysfunction of CA1 but not CA3 is associated with the behavioral impairments. Furthermore, consistent with our previous findings, 12,17,75 the similar moving velocity for CA control and other groups indicates that these behavioral findings are not caused by decreased locomotor activity.…”

Section: Discussionsupporting

confidence: 92%

Prenatal cyanuric acid exposure induced spatial learning impairments associated with alteration of acetylcholine-mediated neural information flow at the hippocampal CA3-CA1 synapses of male rats

et al. 2023

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Cyanuric acid (CA) is reported to induce nephrotoxicity but its toxic effect is not fully known. Prenatal CA exposure causes neurodevelopmental deficits and abnormal behavior in spatial learning ability. Dysfunction of the acetyl-cholinergic system in neural information processing is correlated with spatial learning impairment and was found in the previous reports of CA structural analogue melamine. To further investigate the neurotoxic effects and the potential mechanism, the acetylcholine (ACh) level was detected in the rats which were exposed to CA during the whole of gestation. Local field potentials (LFPs) were recorded when rats infused with ACh or cholinergic receptor agonist into hippocampal CA3 or CA1 region were trained in the Y-maze task. We found the expression of ACh in the hippocampus was significantly reduced in dose-dependent manners. Intra-hippocampal infusion of ACh into the CA1 but not the CA3 region could effectively mitigate learning deficits induced by CA exposure. However, activation of cholinergic receptors did not rescue the learning impairments. In the LFP recording, we found that the hippocampal ACh infusions could enhance the values of phase synchronization between CA3 and CA1 regions in theta and alpha oscillations. Meanwhile, the reduction in the coupling directional index and the strength of CA3 driving CA1 in the CA-treated groups was also reversed by the ACh infusions. Our findings are consistent with the hypothesis and provide the first evidence that prenatal CA exposure induced spatial learning defect is attributed to the weakened ACh-mediated neuronal coupling and NIF in the CA3-CA1 pathway.

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Section: Discussionsupporting

confidence: 92%

Prenatal cyanuric acid exposure induced spatial learning impairments associated with alteration of acetylcholine-mediated neural information flow at the hippocampal CA3-CA1 synapses of male rats

et al. 2023

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“…According to our findings and those of others [ 11 , 13 ], hepatic oxidative damage following ML exposure is triggered by increased ROS generation and liver antioxidant enzyme exhaustion. These findings were further supported by immunohistochemistry results that revealed the downregulation of Nrf2 expression in hepatic tissues after ML exposure.…”

Section: Discussionsupporting

confidence: 88%

“…Many compelling publications have supported the presence of oxidative stress following ML exposure, primarily due to the depletion of the intracellular antioxidant defense systems and the uncontrolled formation of reactive oxygen species (ROS) such as superoxide anion, O 2 •– ; hydrogen peroxide, H 2 O 2 ; and hydroxyl radical, OH • ; as well as reactive nitrogen species such as nitric oxide (NO) [ 11 , 13 ]. These events cause tissue damage, lipid peroxidation (LPO), protein cross-linking, and DNA oxidation [ 12 , 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

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Nootkatone Mitigated Melamine-Evoked Hepatotoxicity by Featuring Oxidative Stress and Inflammation Interconnected Mechanisms: In Vivo and In Silico Approaches

Habotta,

Abdeen,

Roomi

et al. 2023

Toxics

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Melamine (ML) is a common environmental contaminant, commonly used in food fraud, representing a serious health hazard and jeopardizing human and animal health. Recently, nootkatone (NK), a naturally occurring sesquiterpenoid, has garnered considerable attention due to its potential therapeutic advantages. We investigated the potential mechanisms underlying the protective effects of NK against ML-induced liver injury in rats. Five groups were utilized: control, ML, NK10, ML-NK5, and ML-NK10. ML induced substantial hepatotoxicity, including considerable alterations in biochemical parameters and histology. The oxidative distress triggered by ML increased the generation of malondialdehyde (MDA) and nitric oxide (NO) and decreased levels of reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities. In addition, decreased expression of nuclear factor-erythroid 2-related factor 2 (Nrf2) and increased nuclear factor kappa beta (NF-κB) expression levels were observed in hepatocytes, which indicated the occurrence of inflammatory changes following ML exposure. These alterations were alleviated by NK supplementation in a dose-dependent manner. The data revealed that the favorable effects of NK were attributed, at least in part, to its antioxidant and anti-inflammatory properties. Moreover, our results were supported by molecular docking studies that revealed a good fit and interactions between NK and antioxidant enzymes. Thus, the current study demonstrated that NK is a potential new food additive for the prevention or treatment of ML-induced toxicity.

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“…Also, co-exposure leads to significant oxidative stress and damage to placental development, resulting in increased apoptosis and decreased fetal cell proliferation ( 30 ). The co-exposure severely impairs neuronal and synaptic functions, reducing the amplitude, decay time, and frequency of miniature excitatory postsynaptic currents (mEPSCs) without affecting miniature inhibitory postsynaptic currents (mIPSCs) ( 31 ). Prenatal exposure to cyanuric acid elevates alkaline phosphatase levels in the maternal placenta and fetal brains ( 32 ).…”

Section: Study On Health Risk and Control Standard Of Cyanuric Acid I...mentioning

confidence: 99%

Study on the health risk of cyanuric acid in swimming pool water and its prevention and control measures

Chen,

Su,

Chen

et al. 2024

Front. Public Health

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Cyanuric acid is a widely used fine chemical intermediate that acts as a free chlorine buffer in swimming pool water, wherein it is often used as a stabilizer to maintain the germicidal efficacy of chlorinated disinfectants. However, it has also been associated with health risks. Herein, we introduced the sources and functions of cyanuric acid in swimming pool water, focusing on potential health risks associated with excessive concentration of the component and the current control standards worldwide. Also, the prevention and control measures were summarized in terms of physical chemistry, biodegradation, and ultraviolet radiation to provide a basis for the development of public health policies for swimming pool management.

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Co-exposure of melamine and cyanuric acid as a risk factor for oxidative stress and energy metabolism: Adverse effects on hippocampal neuronal and synaptic function induced by excessive ROS production

Cited by 11 publications

References 80 publications

Prenatal cyanuric acid exposure induced spatial learning impairments associated with alteration of acetylcholine-mediated neural information flow at the hippocampal CA3-CA1 synapses of male rats

Prenatal cyanuric acid exposure induced spatial learning impairments associated with alteration of acetylcholine-mediated neural information flow at the hippocampal CA3-CA1 synapses of male rats

Nootkatone Mitigated Melamine-Evoked Hepatotoxicity by Featuring Oxidative Stress and Inflammation Interconnected Mechanisms: In Vivo and In Silico Approaches

Study on the health risk of cyanuric acid in swimming pool water and its prevention and control measures

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