Perfluorinated compounds (PFCs) are environmental pollutants, and dietary intake is a major route of human exposure to them. We aimed to see the effects of washing, soaking, and cooking (grilling, braising, frying, and steaming) on the change of PFCs in mackerel fillets and PFCs before and after each treatment were analyzed using LC-MS/MS. Washing resulted in a decrease in the PFC content of mackerel (average 74%) comparing to control. Among the 19 PFCs detected, perfluorobutanoic acid and perfluorotridecanoic acid (PFTrDA) were found to be abundant after washing. Soaking mackerel in sake reduced its PFC content by 51%, whereas soaking in rice-washed solution reduced by 80% comparing to control. All the four cooking methods were effective in reducing the PFC content of mackerel. The degree by which the PFC content decreased varied with the cooking method: grilling (91%), steaming (75%), frying (58%), and braising (47%) comparing to uncooked sample. In addition, when mackerel was braised with potato, PFCs decreased more in fillet than the ones without potato. PFCs in potato increased after cooking with mackerel. The excessive consumption through the mackerel was 0.1997 ng/kg bw/day and 0.7987 ng/kg bw/day, respectively. These exposure levels were well below the tolerable daily intake values of both compounds (PFOS, 150 ng/kg bw/day; PFOA, 1,500 ng/kg bw/day). The results of this study indicated that employing appropriate pretreatment and cooking methods could be an effective way to reduce the dietary exposure to PFCs in mackerel.
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http://dx.doi.org/10.1002/fsn3.1737 | DOI Listing |
Int J Mol Sci
November 2024
Department of Psychology, Binghampton University-State University of New York, Binghampton, NY 13902, USA.
Elevated risk for schizophrenia is associated with a variation in the gene encoding dysbindin-1, which may underpin cognitive impairments in this prevalent neuropsychiatric disorder. The cognitive symptoms of schizophrenia involve anomalies in glutamate and dopamine signaling, particularly within the prefrontal cortex (PFC). Indeed, mice with mutations exhibit spatial and working memory deficits that are associated with deficits in glutamate release and NMDA receptor function as determined by slice electrophysiology.
View Article and Find Full Text PDFPharmacol Res
December 2024
Department of Biomedicine, Aarhus University, Denmark; Translational Neuropsychiatry Unit, Aarhus University, Denmark. Electronic address:
Ketamine (KET) is recognized as rapid-acting antidepressant, but its mechanisms of action remain elusive. Considering the role of endocannabinoids (eCB) in stress and depression, we investigated if S-KET antidepressant effects involve the regulation of the eCB system using an established rat model of depression based on selective breeding: the Flinders Sensitive Line (FSL) and their controls, the Flinders Resistant Line (FRL). S-KET (15 mg/kg) effects were assessed in rats exposed to the open field and forced swimming test (FST), followed by analysis of the eCB signaling in the rat prefrontal cortex (PFC), a brain region involved in depression neurobiology.
View Article and Find Full Text PDFJ Neurosci
December 2024
MRC Cognition and Brain Sciences Unit, University of Cambridge, UK.
Implementing cognitive control relies on neural representations that are inherently high-dimensional and distributed across multiple subregions in the prefrontal cortex (PFC). Traditional approaches tackle prefrontal representation by reducing it into a unidimensional measure (univariate amplitude) or using them to distinguish a limited number of alternatives (pattern classification). By contrast, representational similarity analysis (RSA) enables flexibly formulating various hypotheses about informational contents underlying the neural codes, explicitly comparing hypotheses, and examining the representational alignment between brain regions.
View Article and Find Full Text PDFCNS Neurosci Ther
November 2024
Sean M. Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA.
Aims: Although the genetic locus of X-linked dystonia parkinsonism (XDP), a neurodegenerative disease endemic in the Philippines, is well-characterized, the exact mechanisms leading to neuronal loss are not yet fully understood. Recently, we demonstrated an increase in myeloperoxidase (MPO) levels in XDP postmortem prefrontal cortex (PFC), suggesting a role for inflammation in XDP pathogenesis. Therefore, we hypothesized that inhibiting MPO could provide a therapeutic strategy for XDP.
View Article and Find Full Text PDFCureus
October 2024
Department of Anesthesiology, Uniformed Services University of the Health Sciences, Bethesda, USA.
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