Exploring the impact of environmental factors on male reproductive health through epigenetics

Reproductive Toxicology, Journal Year: 2025, Volume and Issue: 132, P. 108832 - 108832

Published: Jan. 6, 2025

Language: Английский

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The Role of Nutrition, Oxidative Stress, and Trace Elements in the Pathophysiology of Autism Spectrum Disorders

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(2), P. 808 - 808

Published: Jan. 18, 2025

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by deficits in social communication and interaction, alongside repetitive behaviors, atypical sensory-motor patterns. The growing prevalence of ASD has driven substantial advancements research aimed at understanding its etiology, preventing onset, mitigating impact. This ongoing effort necessitates continuous updates to the body knowledge identification previously unexplored factors. present study addresses this need examining roles nutrition, oxidative stress, trace elements pathophysiology ASD. In review, an overview provided key dietary recommendations for individuals with ASD, including gluten-free casein-free (GFCF) diets, ketogenic diets (KDs), other nutritional interventions. Furthermore, it explores involvement stress highlights significance maintaining neuropsychiatric health. impact these factors on molecular cellular mechanisms was discussed, therapeutic strategies their efficacy managing

Language: Английский

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Metal Profiles in Autism Spectrum Disorders: A Crosstalk between Toxic and Essential Metals

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 24(1), P. 308 - 308

Published: Dec. 24, 2022

Since hundreds of years ago, metals have been recognized as impacting our body's physiology. As a result, they studied potential cure for many ailments well cause acute or chronic poisoning. However, the link between aberrant metal levels and neuropsychiatric illnesses such schizophrenia neurodevelopmental disorders, autism spectrum disorders (ASDs), is relatively new finding, despite some evident ASD-related consequences shortage excess specific metals. In this review, we will summarize past current results explaining pathomechanisms toxic at cellular molecular that are still not fully understood. While may interfere with dozens physiological processes concurrently, focus on ASD-relevant activity inflammation/immune activation, mitochondrial malfunction, increased oxidative stress, impairment axonal myelination, synapse formation function. particular, highlight competition essential explain why both presence certain absence emerged risk factors ASD. Although often investigated separately, through agonistic antagonistic effects metals, common imbalance result in relation to

Language: Английский

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Plasma zinc, copper and serum ceruloplasmin levels of autism spectrum disorder children in Bangladesh

Heliyon, Journal Year: 2023, Volume and Issue: 9(8), P. e18624 - e18624

Published: Aug. 1, 2023

Neural and cognitive processes require zinc copper homeostasis a normal zinc/copper ratio. Ceruloplasmin, an intrinsic antioxidant protein, maintains homeostasis, which might also influence autism spectrum disorder (ASD). ASD children are frequently reported with altered levels of these elements wide geographical variations. This study evaluated any alteration in plasma zinc, copper, ratio serum ceruloplasmin Bangladeshi respect to healthy controls. A cross-sectional was conducted on 67 aged 2 9 years both sexes. Among them, 35 had ASD, while 32 were age, sex body mass index (BMI) matched apparently children. Plasma estimated by the flame atomic absorption spectrophotometry method. Serum immunoturbidimetric Zinc 2-9 old group significantly lower (p=0.032 p=0.002 respectively). On other hand, (p=0.020) (p = 0.045) higher than those associated deficiency (p=0.000) toxicity (p=0.05). All again divided into 2-5 6-9 age groups according laboratory reference values for copper. Copper (p=0.011), significant difference (p=0.009) (p=0.001) but not (p=0.110) compared positively all groups. shows that Bangladesh can be low high levels.

Language: Английский

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Characterization of Mice Carrying a Neurodevelopmental Disease-Associated GluN2B(L825V) Variant

Journal of Neuroscience, Journal Year: 2024, Volume and Issue: 44(31), P. e2291232024 - e2291232024

Published: June 26, 2024

N -Methyl- d -aspartate receptors (NMDARs), encoded by GRIN genes, are ionotropic glutamate playing a critical role in synaptic transmission, plasticity, and synapse development. Genome sequence analyses have identified variants genes patients with neurodevelopmental disorders, but the underlying disease mechanisms not well understood. Here, we created evaluated transgenic mouse line carrying missense variant Grin2b L825V , corresponding to de novo GRIN2B encoding GluN2B(L825V) found patient intellectual disability (ID) autism spectrum disorder (ASD). We used HEK293T cells expressing recombinant primary hippocampal neurons prepared from heterozygous L825V/+ (L825V/+) wild-type (WT) +/+ (+/+) male female mice assess functional impact of variant. Whole-cell NMDAR currents were reduced compared mice. The peak amplitude NMDAR-mediated evoked excitatory postsynaptic (NMDAR-eEPSCs) was unchanged, NMDAR-eEPSCs had faster deactivation less sensitive GluN2B-selective antagonist ifenprodil. Together, these results suggest decreased contribution GluN2B subunits analysis subunit surface expression localization revealed no differences WT GluN2B. Behavioral testing both sexes demonstrated hypoactivity, anxiety, impaired sensorimotor gating strain, particularly affecting males, as cognitive symptoms. offers clinically relevant model -related ID/ASD, our synaptic-level changes that may contribute pathology.

Language: Английский

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Metal Dyshomeostasis as a Driver of Gut Pathology in Autism Spectrum Disorders

Journal of Neurochemistry, Journal Year: 2025, Volume and Issue: 169(3)

Published: March 1, 2025

ABSTRACT Despite being classified as neurodevelopmental disorders, in recent years, there has been a growing interest the association between autism spectrum disorders (ASDs) and gut pathology. This comprehensive systematic review explores potential mechanism underlying pathology ASDs, including alterations microbiota, intestinal permeability, immune dysregulation, gastrointestinal (GI) symptoms. Specifically, it delves into role of toxic essential metals their interplay, affecting development function GI tract. The also discusses implications this management ASDs. Studies have shown that heavy metal exposure, whether through environmental sources or dietary intake, can disrupt delicate balance trace elements gut. disruption adversely affect zinc homeostasis, potentially exacerbating individuals with impaired absorption resulting from exposure may contribute to oxidative stress, inflammation observed By shedding light on multifaceted nature pathology, impact dyshomeostasis non‐genetic factor ASD, underscores significance gut‐brain axis etiology image

Language: Английский

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The role of zinc dysregulation in Autism Spectrum Disorder: A systematic review of genetic and environmental influences and therapeutic potential

Published: April 6, 2025

Language: Английский

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The Role of Zinc and NMDA Receptors in Autism Spectrum Disorders

Pharmaceuticals, Journal Year: 2022, Volume and Issue: 16(1), P. 1 - 1

Published: Dec. 20, 2022

NMDA-type glutamate receptors are critical for synaptic plasticity in the central nervous system. Their unique properties and age-dependent arrangement of subunit types underpin their role as a coincidence detector pre- postsynaptic activity during brain development maturation. NMDAR function is highly modulated by zinc, which co-released with concentrates spines. Both NMDARs zinc have been strongly linked to autism spectrum disorders (ASDs), suggesting that an important player beneficial effects observed both animal models children ASDs. Significant evidence emerging these occur via zinc-dependent regulation SHANK proteins, form backbone density. For example, dietary supplementation enhances SHANK2 or SHANK3 recruitment rescues deficits hypofunction Shank3ex13–16−/− Tbr1+/− ASD mice. Across multiple studies, changes parallel reversal ASD-associated behaviours, highlighting glutamatergic synapses therapeutic targets severe forms ASDs, either postnatally. The data from rodent set strong foundation future translational studies human cells people affected

Language: Английский

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Zinc Water Prevents Autism-Like Behaviors in the BTBR Mice

Biological Trace Element Research, Journal Year: 2023, Volume and Issue: 201(10), P. 4779 - 4792

Published: Jan. 5, 2023

Abstract This study aims to explore the effects of zinc water on autism-like behavior, convulsion threshold, and neurogenesis in ASD model animals. used young BTBR mouse effect a 6-week supplementation ASD-like behaviors such as repetitive behavior social communication disorder, seizure correlation with excitability regulation. The mice were divided into four groups normal controls (B6) models (BTBR) who did not receive (B6, B6 + zinc, BTBR, zinc). For morphological changes hippocampus, we selected two indicators: hippocampal mossy fiber sprouting neurogenesis. testing, threshold determination, Timm staining, neurogenesis-related assays—represented by Ki67 DCX—were performed after 6 weeks supplementation. Our results show that can prevent reduce susceptibility convulsions, increase proliferation progenitor cells but has less neural cell differentiation. Zinc reduces partially inherited autism mice—BTBR—which may be associated precursor reversed hyperexcitability.

Language: Английский

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Gestational hypothyroxinemia induces ASD-like phenotypes in behavior, proinflammatory markers, and glutamatergic protein expression in mouse offspring of both sexes

Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15

Published: May 1, 2024

Background The prevalence of autism spectrum disorder (ASD) has significantly risen in the past three decades, prompting researchers to explore potential contributions environmental factors during pregnancy ASD development. One such factor interest is gestational hypothyroxinemia (HTX), a frequent condition associated with cognitive impairments offspring. While retrospective human studies have linked HTX autistic traits, cellular and molecular mechanisms underlying development ASD-like phenotypes remain poorly understood. This study used mouse model evaluate Methods To induce HTX, pregnant mice were treated 2-mercapto-1-methylimidazole (MMI), thyroid hormones synthesis inhibitor, tap-drinking water from embryonic days (E) 10 E14. A separate group received MMI along daily subcutaneous injection T 4 , while control regular tap entire pregnancy. Female male offspring underwent assessments for repetitive, anxious, social behaviors postnatal day (P) 55 P64. On P65, euthanized evaluation ASD-related inflammatory markers blood, spleen, specific brain regions. Additionally, expression glutamatergic proteins (NLGN3 HOMER1) was analyzed prefrontal cortex hippocampus. Results HTX-offspring exhibited anxious-like behavior, subordinate state, impaired interactions. Subsequently, both female displayed elevated proinflammatory cytokines including IL-1β, IL-6, IL-17A, TNF-α, only males showed reduced levels IL-10. spleen sexes increased Th17/Treg ratio M1-like macrophages. In hippocampus HTX-offspring, IL-17A IL-10 observed, accompanied by hippocampal NLGN3 HOMER1. All these observations compared those observed Control-offspring. Notably, supplementation treatment prevents phenotypes. Correlation analysis revealed an association between maternal outcomes. Discussion validates observations, demonstrating first time that induces offspring, highlighting need monitoring function

Language: Английский

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