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von Mikecz, A.

Publications and source records attributed to von Mikecz, A..

2 recordsLinked to original sources

Differential neurobehavioral responses to silica nanoparticles and temperature in a wild rhabditid nematode and C. elegans: toward an exposome map of phenotypes

Environmental factors shape organismal health through complex interactions known as the exposome. However, the interactions between chemical and non-chemical exposome factors remain largely unclear. Here, a dopaminergic reporter strain of Caenorhabditis elegans and a field isolated rhabditid nematode were used in a behavioral arena to assess natural variation in locomotory behavior in response to silica nanoparticles as a chemical exposome factor, and ambient temperature conditions (15 {degrees}C, 20 {degrees}C, and 25 {degrees}C) as non-chemical factors. Our results reveal that in the C. elegans strain lower temperature (15 {degrees}C) mitigates silica-induced locomotion deficits, while higher temperature (25 {degrees}C) exacerbates neurotoxicity, suggesting a temperature-dependent response. Notably, the wild rhabditid isolate showed distinct behavioral responses compared to the laboratory strain, highlighting the importance of species-specific ecological backgrounds in toxicological studies. This study provides a conceptual basis for integrating environmental factors and natural diversity into exposome research: Phenotype exposome maps, as presented here, broaden the identification of ecotoxicological hazards of nanomaterials across species. Author summaryIncorporating wild rhabditid species with unknown genotypes into neurotoxicology research broadens the traditional model-organism framework by extending beyond C. elegans to encompass a wider range of naturally occurring neuronal and behavioral variation. This phenotype-driven approach enables the detection of both conserved and species-specific responses to neurotoxicants, independent of prior genomic knowledge. Observed differences in locomotor behavior across nematode species may reflect underlying diversity in neural architecture or compensatory mechanisms, offering insights into the functional plasticity of nervous systems. By adopting a comparative perspective grounded in the ecological context, this strategy enhances the environmental relevance of neurotoxicity studies and promotes more inclusive ecological risk assessment through the use of field isolated nematodes in controlled laboratory settings. SynopsisWild nematodes and C. elegans differ in pollutant responses, highlighting the need for broader toxicology models. HighlightsO_LIWe report comparative testing of Caenorhabditis elegans and a wild rhabditid isolate in a behavioral arena. C_LIO_LIC. elegans and the wild isolate were assessed under multiple exposome conditions: silica nanoparticles and ambient temperatures (15-25 {degrees}C). C_LIO_LIField isolated rhabditid nematodes showed distinct behavioral responses to chemical and temperature exposures compared to C. elegans. C_LIO_LIThis study highlights the importance of including wild nematode isolates alongside C. elegans for ecological hazard identification of emerging pollutants like silica nanoparticles. C_LIO_LIWe culture wild nematode isolates under standardized laboratory conditions to probe the limits of C. elegans as a toxicology model and enhance its real-world relevance. C_LI

pharmacology and toxicology↗

Pollutants corrupt resilience pathways of aging in the nematode C. elegans

Delaying aging while prolonging health and lifespan is a major goal in aging research. While many resources have been allocated to find positive interventions with promising results, negative interventions such as pollution and their accelerating effect on age-related degeneration and disease have been mostly neglected. Here, we used the short-lived model organism C. elegans to analyze whether two candidate pollutants interfere with positive interventions by corrupting general aging pathways. We took advantage of the immense data sets describing the age-related remodeling of the proteome including increased protein insolubilities to complement our analysis. We show that the emergent pollutant silica nanoparticles (NP) and the classic xenobiotic inorganic mercury reduce lifespan and cause a premature protein aggregation phenotype. Silica NPs rescaled the longevity effect of genetic interventions targeting the IGF-1/insulin-like signaling pathway. Comparative mass spectrometry revealed that increased insolubility of proteins with important functions in proteostasis is a shared phenotype of intrinsic- and pollution-induced aging supporting the hypothesis that proteostasis is a central resilience pathway controlling lifespan and aging. The presented data demonstrate that pollutants corrupt intrinsic aging pathways, which results in premature aging phenotypes. Reducing pollution is therefore an important step to increase healthy aging and prolong life expectancies on a population level in humans and animals.

developmental biology↗