Heavy Metal Exposure and Toxicity

This study shows that S-equol, a microbial metabolite, reduces cadmium-induced neurotoxicity in mice by restoring neural gene expression and is associated with lower levels in humans carrying the apolipoprotein E4 allele.

This study shows that Akkermansia muciniphila prevents cadmium-induced cognitive impairment in mice through gut microbiome and metabolite mechanisms, not by reducing brain cadmium levels.

This study shows that lead exposure during human iPSC-derived cardiomyocyte differentiation alters gene expression and pathway dysregulation, with persistent transcriptional changes even after exposure stops.

This study shows perinatal exposure to heavy metals and their mixtures alters cardiac gene expression, cellular composition, and immune signaling in a sex-specific manner in mice.

This study shows that ATP7B and lysosomal exocytosis work together to detoxify cadmium by sequestering it in lysosomes, with ATP7B playing a key role in this process.

This study shows that type 2 diabetes increases susceptibility to lead toxicity, leading to organ damage and intergenerational health risks.

The paper investigates whether manganese exposure contributes to mental disorders by analyzing its effects on airborne and gut microbiomes.

The paper examines strain and sex effects on blood levels of lead, chromium, and cadmium in Collaborative Cross mice after acute exposure, finding strain-dependent trends for lead but different patterns for chromium and cadmium.

This study predicts metal speciation in blood plasma, incorporating proteins, peptides, and small molecules, and shows its dependence on pH and chelator concentration.

This study shows that perinatal lead exposure increases mouse embryonic weight and alters gene expression in neuronal and sexually dimorphic pathways.

The paper investigates how manganese affects tumor cell migration and proliferation in vitro by modulating the metallome and analyzing metal interactions with the glycocalyx.

This study shows chronic cadmium exposure combined with hyperglycemia worsens mitochondrial dysfunction in liver cells, suggesting a role in MASLD development.

This study shows that prenatal lead exposure biases neural cell fate in human brain development by increasing neurons and reducing astrocytes through epigenetic changes.

This study shows ZIP14 facilitates manganese efflux from the brain by relocalizing to the basolateral membrane in BBB endothelial cells, and its deletion causes Mn accumulation.

This study shows heavy metals disrupt electrotactic behavior in C. elegans, with varying toxicity levels, and highlights electrotaxis as a tool for assessing neurobehavioral toxicity.

This study uses network toxicology, AlphaFold 3, and molecular docking to analyze the toxicity of Co(II) and BPCo(II), revealing their impact on signaling pathways and neurodegenerative diseases.

This study examines how different levels of lead exposure affect neural differentiation in SH-SY5Y cells, showing significant changes in protein expression and cell morphology.

This study shows that Brideliaferruginea extract reduces cadmium chloride toxicity in rats by improving reproductive hormones, oxidative stress, liver and kidney damage, and hematological parameters.

The paper establishes a humanized neuronal model to investigate the effects of manganese dysregulation on neuronal function and disease mechanisms.

This study examines the toxic effects of lead nitrate on human keratinocytes, finding cytotoxicity, genotoxicity, oxidative stress, and mitochondrial dysfunction at varying concentrations.

This study shows cadmium exposure disrupts blood-testis barrier function in prepubertal rats via oxidative stress-induced autophagy and mTOR2 signaling impairment.

This study identifies circRNA, lncRNA, miRNA, and mRNA regulatory networks affected by cadmium exposure in C. elegans, revealing potential molecular mechanisms of Cd toxicity.

This study shows that SLC30A10 in dopaminergic neurons protects against manganese-induced neurotoxicity, while its absence in GABAergic neurons does not cause similar deficits.

This study investigates the effects of chronic lead exposure on hippocampal network dynamics and behavior in rats, finding altered rhythms and impaired cognitive functions.

This study identifies persistent transcriptional and epigenetic changes in human lung epithelial cells after nickel exposure, revealing mechanisms behind long-term health effects.

This study shows that cadmium exposure disrupts otolith formation in zebrafish, leading to balance disorders and hyperactivity, with calcium rescue for otolith defects but not hyperactivity.