Transcriptomics-Based Toxicological Study of Nickel on Caenorhabditis elegans

Area of Science:

• Environmental Toxicology
• Invertebrate Biology
• Molecular Toxicology

Background:

• Nickel (Ni) is a persistent heavy metal with industrial uses, posing ecological and health risks.
• Mammalian and plant toxicity data for Ni are established, but invertebrate responses, especially at environmental concentrations, are less understood.
• Caenorhabditis elegans is a valuable model organism for studying heavy metal toxicity.

Purpose of the Study:

• To systematically evaluate the toxicity of Ni²⁺ on the nematode Caenorhabditis elegans.
• To integrate phenotypic assays and transcriptomic profiling to assess Ni impacts on growth, reproduction, neuromuscular function, lifespan, and aging.
• To understand the molecular mechanisms underlying Ni toxicity in invertebrates at environmentally relevant concentrations.

Main Methods:

• Phenotypic assays were used to assess developmental delays, reproductive capacity, and aging indicators (lipofuscin accumulation).
• Transcriptomic profiling identified differentially expressed genes (DEGs) in response to Ni²⁺ exposure.
• Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed on DEGs.

Main Results:

• Nickel exposure induced dose-dependent developmental delays in C. elegans, with significant increases in L1-stage larvae at 80 μg/L.
• Reproductive capacity was reduced by 88.5% at 80 µg/L Ni²⁺.
• Transcriptomic analysis revealed significant changes in gene expression, with 2235 DEGs at 8 μg/L and 249 DEGs at 0.8 μg/L.
• Affected pathways included collagen metabolism, fatty acid metabolism, amino acid biosynthesis, and lysosomal function, leading to cuticle defects, altered energy metabolism, and feeding behavior changes.
• Ni exposure accelerated aging, indicated by increased lipofuscin accumulation.

Conclusions:

• Nickel toxicity in C. elegans manifests as developmental delays, reduced reproduction, and accelerated aging.
• Molecular disruptions involve collagen, lipid, amino acid, and lysosomal pathways, impacting cellular integrity and function.
• This study highlights the ecological risks of Ni pollution and its potential to accelerate aging in invertebrates.