Aquatic Toxicology and Ecotoxicology Lipidomics Services

The zebrafish is a premier aquatic model, but characterizing the minute metabolic environment of the dissected larval intestinal tract poses severe sensitivity challenges. The client needed to prove that specific pathogen secretion systems disrupt the microbial ecosystem, which in turn feeds back into the host's metabolic status.

We deployed a micro-volume Untargeted Metabolomics and Lipidomics workflow. By leveraging the extreme sensitivity of the Orbitrap mass spectrometry platform, we successfully captured the metabolic signals from dissected zebrafish larval intestines. This was integrated with microbial structural analysis to correlate diversity shifts with metabolic disruption.

The analysis demonstrated clear shifts in the β-diversity of the zebrafish intestinal microbiome following infection using PCoA plots. These plots provided the essential structural evidence that the pathogen significantly alters the microbial community. This framework empowers researchers to link microbiome structural failure to the subsequent collapse of the host’s gut lipid barrier.

Assessing the ecological fitness of marine fish larvae during metamorphosis is vital for predicting population survival against stressors. Traditional bulk fat measurements are too blunt; researchers needed class-specific characterization to differentiate between lipids used for energy (TAGs) and lipids used for tissue development (phospholipids).

We utilized a customized Targeted Glycerolipid and Phospholipid Analysis workflow. By using optimized biphasic solvent extractions fortified with antioxidant shields, we accurately mapped the larvae's metabolic status while preserving delicate marine PUFAs.

The quantitative lipidomic data successfully mapped the larvae’s key lipid reserves and class-specific compositional balance. This molecular baseline allows ecotoxicologists to evaluate how environmental toxicants or thermal stressors deplete energy-storage lipids and disrupt membrane-building lipid pools, ultimately reducing oceanic survival potential.

Aquatic ecosystems are frequently contaminated with metal mixtures. Co-exposure to Nickel (Ni) and Copper (Cu) often causes profound synergistic lethality. While transcriptomic assays indicate general stress, researchers required metabolic validation to locate the actual "choke points" causing sudden cellular death.

We deployed an Untargeted Metabolomics Profiling workflow to contrast single-exposure and synergistic groups. High-resolution mass spectrometry was used to isolate the specific metabolite species uniquely destroyed by the metal combination.

The data in Figure 4 revealed that Ni and Cu synergistically obstruct specific synthesis hubs, obliterating cellular integrity. This precise validation provided the evidence chain required for establishing new, multi-metal exposure regulatory limits in aquatic environments.