Biology · 5 authors, 3 centres
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This study investigated how zinc deficiency and supplementation affect gene expression in Asian sea bass cells. Zinc deficiency upregulated certain zinc transporters (ZIP14, ZIP10, ZIP6, ZIP4, ZnT4, ZnT9), SOD1, and insulin-like growth factors (IGF I and IGF II), while downregulating ZnT1 and metallothionein. The findings suggest that adequate zinc supplementation in aquaculture may help prevent stress responses and support growth in Asian sea bass.
**Background:** Asian sea bass (Lates calcarifer) is an economically important aquaculture species. Zinc is an essential trace element that promotes growth, immune function, and redox balance in fish. However, knowledge about zinc homeostasis at the molecular level in Asian sea bass was limited. This study aimed to characterize the effects of zinc deficiency and supplementation on the expression of zinc transporters, zinc-binding proteins, redox-related enzymes, and growth factors in Asian sea bass cells, and to compare the effects of organic (ZnAA) versus inorganic (ZnSO4) zinc sources.
**Methods:** Asian sea bass fry (SF) epithelial cells were cultured under three conditions: zinc-adequate (ZA, regular medium), zinc-supplemented (ZS, 50 µM ZnSO4 or ZnAA), and zinc-deficient (ZD, CHELEX-treated medium). Intracellular free zinc was measured using FluoZin-3AM fluorescence. Total cellular zinc was quantified by flame atomic absorption spectrophotometry (AAS). Gene expression of 11 zinc transporters (ZIP and ZnT families), metallothionein (MT), superoxide dismutase 1 (SOD1), catalase (CAT), and insulin-like growth factors (IGF I and IGF II) was analyzed by quantitative real-time PCR. Metabolic activity was assessed using the MTT assay. Statistical analysis used paired t-tests or one-way ANOVA with Tukey's post hoc test (p < 0.05).
**Key Results:** Both ZnSO4 and ZnAA were taken up by cells, with ZnAA showing significantly higher intracellular free zinc within the first 30 minutes (p < 0.05). However, after 7 days, total cellular zinc and MT expression showed no significant differences between the two zinc sources. Zinc deficiency significantly decreased total cellular zinc and MT expression compared to ZA controls. Zinc deficiency upregulated the expression of ZIP14, ZIP10, ZIP6, ZIP4, ZnT4, and ZnT9, while downregulating ZnT1 and MT. Zinc supplementation decreased ZIP10 expression and increased ZnT1 and MT expression. No significant differences were observed between ZnSO4 and ZnAA effects on any transporter. Zinc deficiency significantly increased SOD1 expression compared to ZA and ZS cells (p < 0.05), while catalase showed similar trends but was not statistically significant. Both IGF I and IGF II expression were significantly increased under zinc deficiency compared to ZA controls (p < 0.05). The MTT assay showed that zinc supplementation significantly increased metabolic activity compared to ZA cells, while zinc deficiency showed a non-significant trend toward reduced metabolic activity.
**Clinical Implications:** This study provides foundational molecular evidence that zinc status regulates zinc transporter expression, redox metabolism, and growth factor expression in Asian sea bass cells. The finding that zinc deficiency induces a stress response (upregulation of SOD1, IGF I, IGF II) suggests that inadequate zinc in aquaculture diets may compromise fish health and growth. The comparable efficacy of ZnSO4 and ZnAA after 7 days indicates that either form can be used for supplementation, offering flexibility in feed formulation. The parallels between zinc homeostasis mechanisms in Asian sea bass and mammals suggest that SF cells could serve as a model for broader zinc biology research in fish. These data support recommendations for adequate zinc supplementation in Asian sea bass aquaculture to prevent the detrimental effects of zinc deficiency.