# Investigation of the Neurotoxic Effects and Mechanisms of Michler’s Ketone as Investigated by Network Toxicology and Transcriptomics

## TL;DR

This study investigates how Michler’s Ketone harms the nervous system in zebrafish, revealing mechanisms like oxidative stress and disrupted calcium signaling.

## Contribution

The study introduces a comprehensive approach combining network toxicology and transcriptomics to uncover MK’s neurotoxic mechanisms.

## Key findings

- MK exposure induces oxidative stress in zebrafish larvae.
- Disruption of calcium signaling and apoptosis leads to neurodevelopmental impairments.
- MK causes locomotor behavioral impairments in zebrafish.

## Abstract

Michler’s Ketone (MK), an aromatic ketone widely used in pigments, sunscreens, and packaging materials, has unclear developmental neurotoxicity and mechanisms. This study used zebrafish as a model and integrated techniques such as network toxicology, transcriptomics, qPCR, and behavioral analyses to systematically investigate the neurotoxic effects and molecular mechanisms of MK. The research established a comprehensive evidence chain for MK’s neurotoxicity, providing a scientific basis for its aquatic ecological risk assessment and the development of safety standards for related products.

Michler’s Ketone (MK) is widely utilized as an additive in pigments, dyes, and other colorants, and has become a non-negligible environmental presence. Currently, environmental monitoring data and toxicity data for MK are extremely limited, and its specific mechanisms of neurotoxicity remain poorly characterized. A zebrafish model was employed to systematically delineate the neurotoxic mechanisms of MK through the integration of network toxicology predictions, transcriptomic profiling, and RT-qPCR validation. The results demonstrated that MK exposure was found to induce oxidative stress in zebrafish larvae, which subsequently disrupted the calcium signaling pathway and triggered apoptosis, ultimately leading to neurodevelopmental and locomotor behavioral impairments. This study provides a fundamental basis for elucidating MK’s developmental neurotoxicity mechanisms, while also holding significant value for its ecological risk assessment.