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P. Álvarez-Ruíz

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Open access Sep 2026

Dietary Folic Acid Modulates Growth Performance, Expression of Antioxidant- and Immune-Related Genes, and Response to Acute Hepatopancreatic Necrosis Disease in Pacific White Shrimp (Penaeus vannamei)

This study evaluated the effects of dietary folic acid supplementation on growth performance, antioxidant- and immune-related gene expression, and the response to acute hepatopancreatic necrosis disease (AHPND) in Pacific white shrimp (Penaeus vannamei). Juveniles (12 shrimp per tank; four replicate tanks per treatment) were fed diets containing nominal supplemental folic acid levels of 0, 2, 5, or 10 mg kg−1 for 35 days, and 30 shrimp per dietary treatment (three replicate aquaria; 10 shrimp per aquarium) were subsequently challenged with an AHPND-causing strain of Vibrio parahaemolyticus. Among the supplementation levels evaluated, the 5 mg kg−1 diet produced the highest final weight (14.8 ± 0.5 g), weight gain (7.9 ± 0.3 g), a specific growth rate (2.14 ± 0.1% day−1), and the lowest apparent feed conversion ratio (1.3 ± 0.1), whereas the Control showed values of 12.3 ± 0.7 g, 5.4 ± 0.3 g, 1.6 ± 0.1% day−1, and 1.6 ± 0.1, respectively (p ≤ 0.05). Dietary folic acid modulated the relative expression of antioxidant-related genes (SOD, CAT, and GPX) in the gills and hepatopancreas and altered basal and post-challenge expression of the immune-related genes ALFP, CTL3, GILT, MNK, and SR in the gills. At 72 h post-challenge, final cumulative mortality differed among treatments (F3,8 = 5.405, p = 0.025), with lower mortality in T5 (36.7 ± 7.6%) than in the Control (53.3 ± 2.9%; Tukey, p = 0.022). These findings indicate that dietary folic acid supplementation influenced growth performance, challenge outcomes, and transcriptional responses in juvenile Penaeus vannamei. Among the supplementation levels evaluated, the 5 mg kg−1 diet consistently produced the most favorable combination of growth performance, lower final challenge mortality, and modulation of antioxidant- and immune-related gene expression.

German León-Valdez, J. A. Estrada-Godínez, Gabriela López-Cervantes et al. · 0 citations

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