2. Academic Validation
  3. Theasaponin E1 Induce Ferroptotic Cell Death in Pomacea canaliculata through Coordinated Disruption of Cholesterol Homeostasis and Sphingolipid Metabolism

Theasaponin E1 Induce Ferroptotic Cell Death in Pomacea canaliculata through Coordinated Disruption of Cholesterol Homeostasis and Sphingolipid Metabolism

  • J Agric Food Chem. 2025 Nov 19;73(46):29581-29592. doi: 10.1021/acs.jafc.5c06159.
Cheng-Jun Ma 1 2 3,  Gui-Ming Liao 1 3,  Yan-Wei Han 1 3,  Pei Chen 1 3,  Xin-Ao Wang 1 3,  Jia-Wei Li 1 3,  Youming Hou 1 3,  Baozhen Tang 1 3
Affiliations

Affiliations

  • 1 State Key Laboratory of Agricultural and Forestry Biosecurity, Department of Plant Protection, Fujian Agriculture and Forestry University, Fuzhou 350002 Fujian, China.
  • 2 School of Life Science and Engineering, Jining University, Qufu 273155 Shandong, China.
  • 3 Fujian Provincial Key Laboratory of Insect Ecology, Department of Plant Protection, Fujian Agriculture and Forestry University, Fuzhou 350002 Fujian, China.
PMID: 41194770 DOI: 10.1021/acs.jafc.5c06159
Abstract

The invasive golden apple snail, Pomacea canaliculate, threatens agriculture and public health globally. This study systematically investigates the molluscicidal mechanism of theasaponin E1 (TSE1), a tea saponin monomer. TSE1 exhibited concentration- and time-dependent toxicity. Transcriptomics revealed dysregulation of Cholesterol homeostasis, including marked upregulation of squalene monooxygenase, lanosterol synthase, and Cholesterol catabolic Enzymes (CYP3A24, CYP2U1). Concurrently, sphingolipid metabolism exhibited dual perturbation, with both sphingomyelin accumulation and ceramide elevation mediated by differential expression of DEGS2 and MOXD1. Ultrastructural analysis showed mitochondrial cristae dissolution and membrane rupture, with Ferroptosis activation through voltage-dependent anion channel 2 upregulation and oxidative stress. Notably, granulocytes displayed distinct resistance to TSE1-induced cytotoxicity, suggesting cell-type specific protective mechanisms. These findings establish that TSE1 exerts its molluscicidal effect through coordinated disruption of lipid homeostasis, culminating in iron-dependent cell death. The conserved ferroptotic pathway and cell-selective vulnerabilities identified in this study provide critical insights for developing targeted, environmentally sustainable molluscicides.

Keywords

Pomacea canaliculata; cholesterol metabolism; ferroptosis; hemocyte; sphingolipid metabolism; tea saponin.

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