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1.
Toxics ; 12(5)2024 Apr 26.
Artículo en Inglés | MEDLINE | ID: mdl-38787095

RESUMEN

Objective: We aimed to investigate the relationship between metal exposure and novel immunoinflammatory indicators. Methods: Data on adults participating in the National Health and Nutrition Examination Survey (NHANES) from 2009 to 2018 were analyzed. Various statistical models were employed to assess the association between metal exposure and novel immune-inflammation-related indicators. Additionally, the impact of metal exposure on inflammation in different gender populations was explored. Results: This study included 4482 participants, of whom 51.1% were male. Significant correlations were observed among various metals. Both elastic net (ENET) and linear regression models revealed robust associations between cadmium (Cd), cobalt (Co), arsenic (As), mercury (Hg), and immunoinflammatory indicators. Weighted quantile sum (WQS) and Quantile g-computation (Q-gcomp) models demonstrated strong associations between barium (Ba), Co, and Hg and immunoinflammatory indicators. Bayesian kernel machine regression (BKMR) analysis indicated an overall positive correlation between in vivo urinary metal levels and systemic inflammation response index (SIRI) and aggregate index of systemic inflammation (AISI). Furthermore, Co, As, and Hg emerged as key metals contributing to changes in novel immunoinflammatory indicators. Conclusions: Metals exhibit associations with emerging immunoinflammatory indicators, and concurrent exposure to mixed metals may exacerbate the inflammatory response. Furthermore, this relationship varies across gender populations.

2.
Int J Nanomedicine ; 18: 1899-1914, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37057188

RESUMEN

Purpose: The widespread use of zinc oxide nanoparticles (ZnONPs) has raised concerns about its potential toxicity. Melatonin is a neurohormone with tremendous anti-toxic effects. The enterochromaffin cells are an essential source of melatonin in vivo. However, studies on the effects of ZnONPs on endogenous melatonin are minimal. In the present study, we aimed to investigate the effects of ZnONPs exposure on gut-derived melatonin. Methods: In the present study, 64 adult male mice were randomly and equally divided into four groups, and each group was exposed to ZnONPs (0, 6.5, 13, 26 mg/kg/day) for 30 days. Subsequently, the neurobehavioral changes were observed. The effects of ZnONPs on the expression of melatonin-related genes arylalkylamine N-acetyltransferase (Aanat), melatonin receptor1A (Mt1/Mtnr1a), melatonin receptor1B (Mt2/Mtnr1b), and neuropeptide Y (Npy) on melatonin synthesis and secretion in duodenum, jejunum, ileum and colon during day and night were also assessed. Results: The results revealed that oral exposure to ZnONPs induced impairments of locomotor activity and anxiety-like behavior in adult mice during the day. The transcriptional analysis of brain tissues revealed that exposure to ZnONPs caused profound effects on genes and transcriptional signaling pathways associated with melatonin synthesis and metabolic processes during the day and night. We also observed that, in the duodenum, jejunum, ileum and colon sites, ZnONPs resulted in a significant reduction in the expression of the gut-derived melatonin rate-limiting enzyme Aanat, the membrane receptors Mt1 and Mt2 and Npy during the day and night. Conclusion: Taken together, this is the first study shows that oral exposure to ZnONPs interferes with melatonin synthesis and secretion in different intestinal segments of adult mice. These findings will provide novelty insights into the neurotoxic mechanisms of ZnONPs and suggest an alternative strategy for the prevention of ZnONP neurotoxicity.


Asunto(s)
Melatonina , Nanopartículas , Óxido de Zinc , Masculino , Ratones , Animales , Óxido de Zinc/farmacología , Melatonina/farmacología , Nanopartículas/toxicidad
3.
Neurosci Lett ; 791: 136907, 2022 11 20.
Artículo en Inglés | MEDLINE | ID: mdl-36209975

RESUMEN

Parkinson's disease (PD) is one of the most common neurodegenerative disorders of aging that impairs predominately dopaminergic neurons. N6-methyladenosine (m6A) is the most prevalent form of internal RNA modification in eukaryotes and it plays an essential role in normal brain development and neurodegenerative diseases. The m6A status is dynamically modulated by diverse types of genes called "writers", "erasers" and "readers". However, whether these m6A regulators are perturbed in PD remains poorly understood. To clarify this point, we established a PD mouse model using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The motor as well as learning and memory ability of mice were evaluated through and rotarod and Y maze spontaneous alternation tests. Morphological characteristics of tyrosine hydroxylase (TH)-positive cells were visualized using immunohistochemistry, while expressions of alpha-synuclein (α-syn) and TH were determined by using western blot. Furthermore, the expressions of the m6A regulators in the substantia nigra and striatum were evaluated by using qRT-PCR and western blot. As a result, the MPTP-induced PD mice suffered from learning and memory as well as motor defects. Additionally, there were significant TH+ neuron losses in the substantia nigra and striatum of MPTP-injected mice. In the PD mice, proteins including ALKBH5, IGF2BP2 were up-regulated in the substantia nigra, while YTHDF1 and FMR1 was down-regulated. For the striatum, FMR1 and CBLL1 were up-regulated, while IGF2BP3, METTL3 and RBM15 were down-regulated. The expression of genes at the mRNA level were partially in accordance with the protein changes. These findings indicate the m6A regulators may participate in PD pathogenesis.


Asunto(s)
Enfermedad de Parkinson , Ratones , Animales , Enfermedad de Parkinson/metabolismo , 1-Metil-4-fenil-1,2,3,6-Tetrahidropiridina/farmacología , Ratones Endogámicos C57BL , Sustancia Negra/metabolismo , Cuerpo Estriado/metabolismo , Neuronas Dopaminérgicas/metabolismo , Tirosina 3-Monooxigenasa/metabolismo , Modelos Animales de Enfermedad , Proteína de la Discapacidad Intelectual del Síndrome del Cromosoma X Frágil/metabolismo
4.
Food Chem Toxicol ; 169: 113402, 2022 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-36108982

RESUMEN

Gestational exposure to titanium dioxide nanoparticles (TiO2NPs) has been widely reported to have deleterious effects on the brain functions of offspring. However, little attention has been paid to the neurotoxic effects of TiO2NPs on maternal body after parturition. The pregnant mice were orally administrated with TiO2NPs at 150 mg/kg from gestational day 8-21. The potential effects of TiO2NPs on the neurobehaviors were evaluated at postnatal day 60. The gut microbiota, morphological alterations of intestine and brain, and other indicators that involved in gut-brain axis were all assessed to investigate the underlying mechanisms. The results demonstrated that exposure to TiO2NPs during pregnancy caused the persistent neurobehavioral impairments of maternal mice after delivery for 60 days, mainly including behavioural changes, pathological changes in hippocampus, cortex and intestine. Our data also showed that persistent dysfunction and tissue injuries were probably associated with the disruption of gut-brain axis, manifested by the shift in the composition of gut microbial community, alteration of Sstr1, inhibition of enteric neurons and reduction of diamine oxidase contents in maternal mice. These findings provide a novel insight that regulation of gut microecology may be an alternative strategy for the protection against the neurotoxicity of TiO2NPs in pregnant women.


Asunto(s)
Eje Cerebro-Intestino , Exposición Materna , Nanopartículas , Síndromes de Neurotoxicidad , Lesiones Preconceptivas , Titanio , Animales , Femenino , Humanos , Ratones , Embarazo , Amina Oxidasa (conteniendo Cobre)/metabolismo , Eje Cerebro-Intestino/efectos de los fármacos , Microbioma Gastrointestinal , Nanopartículas/toxicidad , Síndromes de Neurotoxicidad/etiología , Titanio/toxicidad , Lesiones Preconceptivas/inducido químicamente
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