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A Microplate Assay to Assess Chemical Effects on RBL-2H3 Mast Cell Degranulation: Effects of Triclosan without Use of an Organic Solvent
Published on: November 1, 2013
Mechanistic insights into novel triclosan target pathways in Neocaridina denticulata revealed by multi-omics
Sang-Eun Nam1, Seongmin Cheon2, Somyeong Lee1
1Department of Marine Science, College of Natural Sciences, Incheon National University, Incheon 22012, Republic of Korea.
Abstract:
Crustaceans have received comparatively limited attention in the identification of novel target pathways of triclosan (TCS) toxicity relative to vertebrates and common model species. In this study, we employed an integrated multi-omics approach, including transcriptomics, proteomics, and metabolomics, to elucidate the molecular mechanisms underlying TCS toxicity in the freshwater shrimp Neocaridina denticulata. Individuals were exposed to three TCS concentrations (1, 5, and 10 μg L-1), including an environmentally relevant level, for 24 h. TCS body accumulation, along with molecular and biochemical alterations in whole-body tissues, was assessed through omics integration and in silico analyses. Results showed that TCS induced reactive oxygen species generation through disruption of the mitochondrial electron transport chain, accompanied by an atypical antioxidant response characterized by downregulation of the first-line antioxidant enzymes. Although endoplasmic reticulum stress markers were not significantly activated, the expression of mitochondrial chaperone-related molecules increased, likely reflecting mitochondrial oxidative stress. A compensatory metabolic response was also evident, in which amino acid metabolism appeared to supplement reduced glucose utilization. Impaired Complex I activity decreased NAD⁺ levels, driving increased LDHC expression as a compensatory mechanism to maintain TCA cycle flux. Additionally, alterations in Ca2+-dependent, muscle contraction-related genes were detected in the sarcomere. Collectively, these findings reveal distinct TCS-induced toxicological pathways in N. denticulata, underscoring mechanistic differences between crustaceans and vertebrate models. SYNOPSYS: Integrated multi-omics analyses reveal triclosan-induced mitochondrial dysfunction, atypical antioxidant responses, and distinct mechanistic toxicity pathways in the crustacean Neocaridina denticulata.
Insights
Triclosan (TCS) causes mitochondrial dysfunction and atypical antioxidant responses in freshwater shrimp. This study reveals distinct toxicity pathways in crustaceans, differing from vertebrate models.
Area of Science:
- Environmental toxicology
- Crustacean biology
- Multi-omics research
Background:
- Crustaceans are understudied models for triclosan (TCS) toxicity.
- Understanding TCS effects in aquatic invertebrates is crucial for environmental risk assessment.
Purpose of the Study:
- To elucidate molecular mechanisms of TCS toxicity in Neocaridina denticulata using integrated multi-omics.
- To identify novel toxicological pathways and compare crustacean responses to vertebrates.
Main Methods:
- Exposure of N. denticulata to environmentally relevant TCS concentrations (1, 5, 10 μg/L) for 24 hours.
- Integrated transcriptomics, proteomics, and metabolomics analyses.
- In silico analysis of omics data and assessment of TCS body accumulation.
Main Results:
- TCS induced reactive oxygen species (ROS) via mitochondrial electron transport chain disruption.
- An atypical antioxidant response was observed, with downregulation of primary antioxidant enzymes.
- Mitochondrial dysfunction, compensatory amino acid metabolism, and altered muscle contraction genes were identified.
Conclusions:
- TCS elicits unique toxicological pathways in N. denticulata, primarily involving mitochondrial dysfunction and oxidative stress.
- Crustacean responses to TCS show mechanistic divergence from vertebrate models.
- Integrated multi-omics is effective for uncovering complex toxicological mechanisms in non-model organisms.
