Prenatal exposure to zinc oxide particles alters monoaminergic neurotransmitter levels in the brain of mouse offspring

Okada, Yoshinori; Tachibana, Kunihide; Yanagita, Shinya; Takeda, Ken

doi:10.2131/jts.38.363

Cited by 34 publications

(15 citation statements)

References 41 publications

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“…Many studies have confirmed that ZnO NPs can enter the central nervous system (CNS) by breaking through the blood-brain barrier or by neural transportation, leading to neurotoxic effects. In Okada et al's study, 7 the subcutaneous administration of ZnO NPs to pregnant ICR (Institute of Cancer Research) mice prenatally could disrupt the monoaminergic system of the offspring, suggesting the possibility that these particles have detrimental effects on mental health. Male Wistar rats were treated with a single intravenous injection of a suspension of ZnO-NPs in Amara et al's study.…”

Section: Introductionmentioning

confidence: 99%

Involvement of PINK1/parkin-mediated mitophagy in ZnO nanoparticle-induced toxicity in BV-2 cells

Wei

Wang

Chen

et al. 2017

IJN

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With the increasing application of zinc oxide nanoparticles (ZnO NPs) in biological materials, the neurotoxicity caused by these particles has raised serious concerns. However, the underlying molecular mechanisms of the toxic effect of ZnO NPs on brain cells remain unclear. Mitochondrial damage has been reported to be a factor in the toxicity of ZnO NPs. PINK1/parkin-mediated mitophagy is a newly emerging additional function of autophagy that selectively degrades impaired mitochondria. Here, a PINK1 gene knockdown BV-2 cell model was established to determine whether PINK1/parkin-mediated mitophagy was involved in ZnO NP-induced toxicity in BV-2 cells. The expression of total parkin, mito-parkin, cyto-parkin, and PINK1 both in wild type and PINK1 −/− BV-2 cells was evaluated using Western blot analysis after the cells were exposed to 10 μg/mL of 50 nm ZnO NPs for 2, 4, 8, 12, and 24 h. The findings suggested that the downregulation of PINK1 resulted in a significant reduction in the survival rate after ZnO NP exposure compared with that of control cells. ZnO NPs were found to induce the transportation of parkin from the cytoplasm to the mitochondria, implying the involvement of mitophagy in ZnO NP-induced toxicity. The deletion of the PINK1 gene inhibited the recruitment of parkin to the mitochondria, causing failure of the cell to trigger mitophagy. The present study demonstrated that apart from autophagy, PINK1/parkin-mediated mitophagy plays a protective role in ZnO NP-induced cytotoxicity.

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Section: Introductionmentioning

confidence: 99%

Involvement of PINK1/parkin-mediated mitophagy in ZnO nanoparticle-induced toxicity in BV-2 cells

Wei

Wang

Chen

et al. 2017

IJN

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“…These data indicate that dietary zinc deficiency may also affect central NE levels. Furthermore, prenatal exposure to zinc oxide nanoparticles was found to increase the level of normetanephrine, another NE metabolite, in the hippocampus of mouse offspring, as well as to decrease the MHPG level in the hypothalamus and cerebellum; however, it did not affect the NE level in any of the brain regions examined [103]. …”

Section: Norepinephrine (Ne)mentioning

confidence: 99%

“…An increased DA level in the hippocampus of mouse offspring following prenatal exposure to zinc oxide nanoparticles was observed [103]. This change was associated with increased levels of DA metabolites: homovanillic acid in the prefrontal cortex and in the hippocampus, as well as 3,4-dihydroxyphenylacetic acid (DOPAC) in the prefrontal cortex [103].…”

Section: Dopamine (Da)mentioning

confidence: 99%

“…This change was associated with increased levels of DA metabolites: homovanillic acid in the prefrontal cortex and in the hippocampus, as well as 3,4-dihydroxyphenylacetic acid (DOPAC) in the prefrontal cortex [103]. Prenatal exposure to zinc oxide nanoparticles also increased DA turnover in the prefrontal cortex, the neostriatum, the nucleus accumbens and the amygdala [103]. There were no changes in DA, DOPAC, or DOPAC-to-DA ratios in the PVN of rats subjected to administration of a zinc-deficient diet [102].…”

Section: Dopamine (Da)mentioning

confidence: 99%

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Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity

et al. 2017

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Preclinical and clinical studies have demonstrated that zinc possesses antidepressant properties and that it may augment the therapy with conventional, that is, monoamine-based, antidepressants. In this review we aim to discuss the role of zinc in the pathophysiology and treatment of depression with regard to the monoamine hypothesis of the disease. Particular attention will be paid to the recently described zinc-sensing GPR39 receptor as well as aspects of zinc deficiency. Furthermore, an attempt will be made to give a possible explanation of the mechanisms by which zinc interacts with the monoamine system in the context of depression and neural plasticity.

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“…Other toxicity studies have also shown that the nanomaterials could cross the placental barriers in pregnant mice and thereafter cause neurotoxicity effects in the offspring. 9,57 Thus, special attention must be given to the utilization of dental nanomaterials in pregnant patients, especially early on in their pregnancy.…”

mentioning

confidence: 99%

Application of dental nanomaterials: potential toxicity to the central nervous system

Feng¹,

Chen²,

Wang³

et al. 2015

IJN

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Nanomaterials are defined as materials with one or more external dimensions with a size of 1–100 nm. Such materials possess typical nanostructure-dependent properties (eg, chemical, biological, optical, mechanical, and magnetic), which may differ greatly from the properties of their bulk counterparts. In recent years, nanomaterials have been widely used in the production of dental materials, particularly in light polymerization composite resins and bonding systems, coating materials for dental implants, bioceramics, endodontic sealers, and mouthwashes. However, the dental applications of nanomaterials yield not only a significant improvement in clinical treatments but also growing concerns regarding their biosecurity. The brain is well protected by the blood–brain barrier (BBB), which separates the blood from the cerebral parenchyma. However, in recent years, many studies have found that nanoparticles (NPs), including nanocarriers, can transport through the BBB and locate in the central nervous system (CNS). Because the CNS may be a potential target organ of the nanomaterials, it is essential to determine the neurotoxic effects of NPs. In this review, possible dental nanomaterials and their pathways into the CNS are discussed, as well as related neurotoxicity effects underlying the in vitro and in vivo studies. Finally, we analyze the limitations of the current testing methods on the toxicological effects of nanomaterials. This review contributes to a better understanding of the nano-related risks to the CNS as well as the further development of safety assessment systems.

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Prenatal exposure to zinc oxide particles alters monoaminergic neurotransmitter levels in the brain of mouse offspring

Cited by 34 publications

References 41 publications

Involvement of PINK1/parkin-mediated mitophagy in ZnO nanoparticle-induced toxicity in BV-2 cells

Involvement of PINK1/parkin-mediated mitophagy in ZnO nanoparticle-induced toxicity in BV-2 cells

Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity

Application of dental nanomaterials: potential toxicity to the central nervous system

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