Cadmium is a heavy metal that increasingly contaminates food and drink products. Once ingested, cadmium exerts toxic effects that pose a significant threat to human health. The nervous system is particularly vulnerable to prolonged, low-dose cadmium exposure. This review article provides an overview of cadmium’s primary mechanisms of neurotoxicity. Cadmium gains entry into the nervous system via zinc and calcium transporters, altering the homeostasis for these metal ions. Once within the nervous system, cadmium disrupts mitochondrial respiration by decreasing ATP synthesis and increasing the production of reactive oxygen species. Cadmium also impairs normal neurotransmission by increasing neurotransmitter release asynchronicity and disrupting neurotransmitter signaling proteins. Cadmium furthermore impairs the blood–brain barrier and alters the regulation of glycogen metabolism. Together, these mechanisms represent multiple sites of biochemical perturbation that result in cumulative nervous system damage which can increase the risk for neurological and neurodegenerative disorders. Understanding the way by which cadmium exerts its effects is critical for developing effective treatment and prevention strategies against cadmium-induced neurotoxic insult.

Mechanisms of Cadmium Neurotoxicity

Cadmium (Cd), a prevalent environmental contaminant, exerts widespread toxic effects on human health through various biochemical and molecular mechanisms. This review encapsulates the primary pathways through which Cd inflicts damage, including oxidative stress induction, disruption of Ca2+ signaling, interference with cellular signaling pathways, and epigenetic modifications. By detailing the absorption, distribution, metabolism, and excretion (ADME) of Cd, alongside its interactions with cellular components such as mitochondria and DNA, this paper highlights the extensive damage caused by Cd2+ at the cellular and tissue levels. The role of Cd in inducing oxidative stress—a pivotal mechanism behind its toxicity—is discussed with emphasis on how it disrupts the balance between oxidants and antioxidants, leading to cellular damage and apoptosis. Additionally, the review covers Cd’s impact on signaling pathways like Mitogen-Activated Protein Kinase (MAPK), Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB), and Tumor Protein 53 (p53) pathways, illustrating how its interference with these pathways contributes to pathological conditions and carcinogenesis. The epigenetic effects of Cd, including DNA methylation and histone modifications, are also explored to explain its long-term impact on gene expression and disease manifestation. This comprehensive analysis not only elucidates the mechanisms of Cd toxicity but also underscores the critical need for enhanced strategies to mitigate its public health implications. 

Cadmium Exposure: Mechanisms and Pathways of Toxicity and Implications for Human Health

Cadmium is a common environmental pollutant and used for industrial purposes all over the world. Cadmium exposure causes a variety of public health issues, mainly reproductive health. The present review discusses the information related to female reproductive health, including during and after pregnancy and its outcomes. Cadmium alters steroidogenesis, delays puberty, causes pregnancy loss of reproductive hormones, disturbs the menstrual cycle, causes premature births, and reduces birth weights in females. Besides that, their offspring are affected differently by prenatal mother exposure to cadmium, with more female offspring being distressed. During lactation period, nursing babies fed with milk containing cadmium causes disparity in brain physiology, reflex changes and physical immaturity. Together, these reviews highpoint the need for more studies into the consequences of cadmium exposure on reproductive health. 

Effect of cadmium exposure during and after pregnancy of female

Activation of NLRP3 signaling contributes to cadmium-induced bone defects, associated with autophagic flux obstruction.

Parkinson’s disease (PD) is characterized by motor symptoms based on a loss of nigrostriatal dopaminergic neurons and by non-motor symptoms which precede motor symptoms. Neurodegeneration accompanied by an accumulation of α-synuclein is thought to propagate from the enteric nervous system to the central nervous system. The pathogenesis in sporadic PD remains unknown. However, many reports indicate various etiological factors, such as oxidative stress, inflammation, α-synuclein toxicity and mitochondrial impairment, drive neurodegeneration. Exposure to heavy metals contributes to these etiopathogenesis and increases the risk of developing PD. Metallothioneins (MTs) are cysteine-rich metal-binding proteins; MTs chelate metals and inhibit metal-induced oxidative stress, inflammation and mitochondrial dysfunction. In addition, MTs possess antioxidative properties by scavenging free radicals and exert anti-inflammatory effects by suppression of microglial activation. Furthermore, MTs recently received attention as a potential target for attenuating metal-induced α-synuclein aggregation. In this article, we summarize MTs expression in the central and enteric nervous system, and review protective functions of MTs against etiopathogenesis in PD. We also discuss neuroprotective strategies for the prevention of central dopaminergic and enteric neurodegeneration by targeting MTs. This review highlights multifunctional MTs as a target for the development of disease-modifying drugs for PD.

/pdf/multifunctional-metallothioneins-as-a-target-for-v6b157n9.pdf

Multifunctional Metallothioneins as a Target for Neuroprotection in Parkinson’s Disease

Environmental and occupational exposure to cadmium has been shown to induce kidney damage, liver injury, neurodegenerative disease, and osteoporosis. However, the mechanism by which cadmium induces autophagy in these diseases remains unclear. Studies have shown that cadmium is an effective inducer of oxidative stress, DNA damage, ER stress, and autophagy, which are thought to be adaptive stress responses that allow cells exposed to cadmium to survive in an adverse environment. However, excessive stress will cause tissue damage by inducing apoptosis, pyroptosis, and ferroptosis. Evidently, oxidative stress-induced autophagy plays different roles in low- or high-dose cadmium exposure-induced cell damage, either causing apoptosis, pyroptosis, and ferroptosis or inducing cell survival. Meanwhile, different cell types have different sensitivities to cadmium, which ultimately determines the fate of the cell. In this review, we provided a detailed survey of the current literature on autophagy in cadmium-induced tissue damage. A better understanding of the complex regulation of cell death by autophagy might contribute to the development of novel preventive and therapeutic strategies to treat acute and chronic cadmium toxicity.

/pdf/the-effect-of-oxidative-stress-induced-autophagy-by-cadmium-1f9spcm4.pdf

The Effect of Oxidative Stress-Induced Autophagy by Cadmium Exposure in Kidney, Liver, and Bone Damage, and Neurotoxicity

The dispersion and orientation arrangement of functional polymers with fillers are critical to their performance. However, there are rare detailed researches on the visualization of the orientation process about functional fillers in composite melts and the mechanistic effects on performance. In this work, it explored the change process of the orientation morphology for polyacrylate/silica (PAcr/SiO2) composite microspheres in polymethyl methacrylate (PMMA) at different melting temperatures. Afterwards, the morphology and distribution of oriented microfibers in composite fibers melted at different temperatures were observed by transmission electron microscope (TEM). The results showed that composite microfibers could be formed in tight arrangement and obtained average orientation of 50.88 in the composite fibers at 250°C. Under this circumstance, the addition of nano SiO2 particles had no effect on the rheological type. Meanwhile, the shear stress was 99.29% higher than that of pure PMMA system under the same conditions. As for the elongation at break, it was found that the elongation at break of the composite fiber prepared at 250°C was 169.43% higher than that of pure PMMA. Therefore, it provided a new method to achieve well dispersion of functional fillers in molten systems. Furthermore, it was beneficial to enhance the elongation at break of functional composites. 

Effect of melting temperatures on the orientation and rheology of polyacrylate/silica (
 PAcr
 /
 
 SiO
 2
 
 ) composite microspheres in twin‐screw extruder

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The Effect of Oxidative Stress-Induced Autophagy by Cadmium Exposure in Kidney, Liver, and Bone Damage, and Neurotoxicity

Effect of melting temperatures on the orientation and rheology of polyacrylate/silica ( PAcr / SiO 2 ) composite microspheres in twin‐screw extruder