High throughput fluorimetric assessment of iron traffic and chelation in iron-overloaded Caenorhabditis elegans

Espósito, Breno Pannia; Martins, Airton C.; Carvalho, Rodrigo Rodrigues Victor de; Aschner, Michael

doi:10.1007/s10534-020-00250-4

Cited by 5 publications

(3 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, disruptions in the balance of Fe within the mitochondria result in diminished ATP production, the release of cytochrome c, and the fracturing of mitochondrial structures, thereby causing changes in morphology [125,126]. In this regard, our group recently addressed the involvement of Fe in the C. elegans model to investigate molecular mechanisms such as oxidative stress, mitochondrial dysfunction, disrupted homeostasis, and how these factors contribute to neurodegenerative diseases triggered by Fe [127,128].…”

Section: Iron and Cuppermentioning

confidence: 99%

Mitochondria in the Spotlight: C. elegans as a Model Organism to Evaluate Xenobiotic-Induced Dysfunction

Martins,

Virgolini,

Ávila

et al. 2023

Cells

Self Cite

View full text Add to dashboard Cite

Mitochondria play a crucial role in cellular respiration, ATP production, and the regulation of various cellular processes. Mitochondrial dysfunctions have been directly linked to pathophysiological conditions, making them a significant target of interest in toxicological research. In recent years, there has been a growing need to understand the intricate effects of xenobiotics on human health, necessitating the use of effective scientific research tools. Caenorhabditis elegans (C. elegans), a nonpathogenic nematode, has emerged as a powerful tool for investigating toxic mechanisms and mitochondrial dysfunction. With remarkable genetic homology to mammals, C. elegans has been used in studies to elucidate the impact of contaminants and drugs on mitochondrial function. This review focuses on the effects of several toxic metals and metalloids, drugs of abuse and pesticides on mitochondria, highlighting the utility of C. elegans as a model organism to investigate mitochondrial dysfunction induced by xenobiotics. Mitochondrial structure, function, and dynamics are discussed, emphasizing their essential role in cellular viability and the regulation of processes such as autophagy, apoptosis, and calcium homeostasis. Additionally, specific toxins and toxicants, such as arsenic, cadmium, and manganese are examined in the context of their impact on mitochondrial function and the utility of C. elegans in elucidating the underlying mechanisms. Furthermore, we demonstrate the utilization of C. elegans as an experimental model providing a promising platform for investigating the intricate relationships between xenobiotics and mitochondrial dysfunction. This knowledge could contribute to the development of strategies to mitigate the adverse effects of contaminants and drugs of abuse, ultimately enhancing our understanding of these complex processes and promoting human health.

show abstract

Section: Iron and Cuppermentioning

confidence: 99%

Mitochondria in the Spotlight: C. elegans as a Model Organism to Evaluate Xenobiotic-Induced Dysfunction

Martins,

Virgolini,

Ávila

et al. 2023

Cells

Self Cite

View full text Add to dashboard Cite

show abstract

“…A relatively short incubation or treatment period is needed to examine the mortality or behavioral trials, ranging from a few minutes [ 26 ] to hours [ 5 , 7 , 8 , 34 ]. In this regard, neurodegeneration, reduction in growth, reproduction, feeding, locomotion, and worm lifespan have been evaluated under metal exposure, including with lead (Pb) [ 35 ], manganese (Mn) [ 36 ], titanium (Ti) [ 37 ], copper (Cu) [ 38 ], zinc (Zn) [ 39 ], gold (Au) [ 40 ], mercury (Hg) [ 41 ], iron (Fe) [ 42 ], and chrome (Cr) [ 43 ].…”

Section: C Elegans As An Alternative Model To Study Neurotox...mentioning

confidence: 99%

Caenorhabditis elegans as a Model to Study Manganese-Induced Neurotoxicity

Martins

Gubert

et al. 2022

Biomolecules

View full text Add to dashboard Cite

Caenorhabditis elegans (C. elegans) is a nematode present worldwide. The worm shows homology to mammalian systems and expresses approximately 40% of human disease-related genes. Since Dr. Sydney Brenner first proposed C. elegans as an advantageous experimental worm-model system for genetic approaches, increasing numbers of studies using C. elegans as a tool to investigate topics in several fields of biochemistry, neuroscience, pharmacology, and toxicology have been performed. In this regard, C. elegans has been used to characterize the molecular mechanisms and affected pathways caused by metals that lead to neurotoxicity, as well as the pathophysiological interrelationship between metal exposure and ongoing neurodegenerative disorders. Several toxic metals, such as lead, cadmium, and mercury, are recognized as important environmental contaminants, and their exposure is associated with toxic effects on the human body. Essential elements that are required to maintain cellular homeostasis and normal physiological functions may also be toxic when accumulated at higher concentrations. For instance, manganese (Mn) is a trace essential element that participates in numerous biological processes, such as enzymatic activities, energy metabolism, and maintenance of cell functions. However, Mn overexposure is associated with behavioral changes in C. elegans, which are consistent with the dopaminergic system being the primary target of Mn neurotoxicity. Caenorhabditis elegans has been shown to be an important tool that allows for studies on neuron morphology using fluorescent transgenic worms. Moreover, behavioral tests may be conducted using worms, and neurotransmitter determination and related gene expression are likely to change after Mn exposure. Likewise, mutant worms may be used to study molecular mechanisms in Mn toxicity, as well as the expression of proteins responsible for the biosynthesis, transport, storage, and uptake of dopamine. Furthermore, this review highlights some advantages and limitations of using the experimental model of C. elegans and provides guidance for potential future applications of this model in studies directed toward assessing for Mn neurotoxicity and related mechanisms.

show abstract

“…[19][20][21][22] Recent studies have shown in C. elegans model have addressed the mechanism by which Fe may enter in the brain, its role in neurodegenerative diseases caused by metal overload and potential treatment or chelator therapy. 13,23 Indeed, C. elegans has orthologs proteins of humans that are highly conserved and participate in Fe metabolism, such as the divalent metal transporter 1 (DMT-1), ferritin (FTN-1, FTN-2), and ferroportin (FPN-1.1, FPN-1.2, FPN-1.3). 24 Moreover, the nematode has been used to evaluate dyshomeostasis and toxicity induced by Fe addressing several important parameters such as lifespan, brood size, body bend frequency, oxidative stress, ATP levels, chemotaxis plasticity, neuronal viability, to name a few.…”

Section: Introductionmentioning

confidence: 99%

Iron overload and neurodegenerative diseases: What can we learn from Caenorhabditis elegans?

Martins

Virgolini

Tinkov

et al. 2022

Toxicology Research and Application

View full text Add to dashboard Cite

Iron (Fe) is an essential trace element required for several physiological processes. It plays important roles in mitochondrial function, synthesis, and metabolism of the neurotransmitter, as well as oxygen transport. However, excess Fe can cause toxicity. Particularly, Fe overload may result in neurotoxicity, contributing to the development and progression of neurodegenerative diseases, although the molecular mechanisms underlying Fe-induced neurodegeneration have yet to be entirely understood. Alternative (non-rodent) experimental models have been pointed as important approaches to elucidate molecular and physiological events mediating Fe-induced pathology. Among such alternative strategies, an advantageous experimental worm-model system, Caenorhabditis elegans ( C. elegans), has been used to investigate Fe-induced neurotoxicity and neurodegenerative disorders. Its genome has been fully sequenced, corroborating that it shares significant homology with mammalians, and has approximately 40% of human disease-related genes. As part of this review, we discuss studies using the C. elegans model to study molecular mechanisms such as oxidative stress, mitochondrial dysfunction, disturbed homeostasis, and its potential contribution to the study of metal-induced neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s disease (AD).

show abstract

High throughput fluorimetric assessment of iron traffic and chelation in iron-overloaded Caenorhabditis elegans

Cited by 5 publications

References 49 publications

Mitochondria in the Spotlight: C. elegans as a Model Organism to Evaluate Xenobiotic-Induced Dysfunction

Mitochondria in the Spotlight: C. elegans as a Model Organism to Evaluate Xenobiotic-Induced Dysfunction

Caenorhabditis elegans as a Model to Study Manganese-Induced Neurotoxicity

Iron overload and neurodegenerative diseases: What can we learn from Caenorhabditis elegans?

Contact Info

Product

Resources

About