Vitamin E Ameliorates Impaired Ovarian Development, Oxidative Stress, and Disrupted Lipid Metabolism in Oreochromis niloticus Fed with a Diet Containing Olive Oil Instead of Fish Oil

Aquaculture feed containing olive oil (OO) instead of fish oil (FO) can cause oxidative stress and impair gonad development in fish. We determined the effect of dietary OO-induced oxidative stress on ovarian development, and explored whether vitamin E (VE) could mitigate negative effects. Female Nile tilapia (Oreochromis niloticus) were fed for 10 weeks with four diets: 5% OO + 70 mg/kg VE, 5% OO + 200 mg/kg VE, 5% FO + 70 mg/kg VE, or 5% FO + 200 mg/kg VE. Dietary OO reduced the specific growth rate and gonadosomatic index, inhibited superoxide dismutase and catalase, delayed ovarian development, decreased serum sex hormone levels, and reduced ovarian triglyceride and n-3 highly unsaturated fatty acid contents. The transcript levels of genes encoding sex hormone receptors (er a, fshr, lhr) and components of the lipid metabolism pathway (ppar a, ppar g, hsl, acc a, elovl6), the nrf2 signaling pathway (nrf2, keap1), and the nf- kb signaling pathway (nf- kb, tnf a, inf g, il1b) differed between the 70VE/OO and 70VE/FO groups. Supplementation with 200 mg/kg VE mitigated the adverse effects of OO by improving antioxidant capacity and alleviating inflammation and abnormal lipid metabolism. This may be because VE is an antioxidant and it can regulate the nrf2-nf-kb signaling pathway.

Automated summary

Aquaculture feed containing olive oil (OO) instead of fish oil (FO) can cause oxidative stress and impair gonad development in fish. This study investigated the effect of dietary OO-induced oxidative stress on ovarian development and found that supplementation with vitamin E (VE) could mitigate the negative effects. OO reduced growth rate, inhibited antioxidant enzymes, delayed ovarian development, decreased sex hormone levels, and affected lipid metabolism in fish. However, supplementation with VE improved antioxidant capacity, alleviated inflammation and abnormal lipid metabolism, possibly through regulating the nrf2-nf-kb signaling pathway.