ArticleFish physiology and biochemistry2025
The ability of dietary essential oils to mitigate nickel-induced growth retardation, immune-antioxidant suppression, and endoplasmic reticulum stress activation in Nile tilapia.
Article in Fish physiology and biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Dietary watermelon (Citrullus lanatus) rind mitigates nickel- and copper-induced hepatic, metabolic, and nrf2/keap1 signaling disruptions in Nile tilapia (Oreochromis niloticus).Veterinary research communications · 2026Article
- Immune-antioxidant potential, splenic cytokines regulation, and tissue architecture restoration by grape seed oil nanoemulsion in Nile tilapia subjected to acrylamide toxicity.Fish physiology and biochemistry · 2026Article
- Thyme-synthesized silver nanoparticles mitigate immunosuppression, oxidative damage, and histopathological alterations induced by multidrug-resistant Enterococcus faecalis in Oreochromis niloticus: in vitro and in vivo assays.Fish physiology and biochemistry · 2025Article
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9 authors.
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Abstract
Fish immunity is significantly impacted by waterborne metal intoxication. Nickel is a ubiquitous metal in aquatic bodies which badly impacts fish immune responses and survival. In the current research, we looked into the possible protective effects of essential oils of tea tree (TTO) and basil (BEO) against nickel exposure in Nile tilapia, or Oreochromis niloticus. To achieve this, 240 Nile tilapia (27.92 ± 0.22 g) were categorized into six groups for 45 days; three groups were fed on basal control, TTO, and BEO diets without Ni exposure. The other three groups were subjected to Ni at a level of 3.6 mg/L and fed on basal, TTO, and BEO diets. The outcomes showed a substantial decrease in the growth measures and survival % in the Ni-exposed fish. Oxidative stress (higher splenic malondialdehyde and lower splenic catalase, reduced glutathione, and superoxide dismutase), immune suppression (lower serum lysozyme, myeloperoxidase, and nitric oxide), and elevated serum cortisol levels were observed in the Ni-intoxicated group. The Ni-intoxicated group exhibited various pathological alterations detected in the intestinal tissue mainly inflammatory and necrotic changes, moreover, moderate depletion of lymphoid elements represented by necrotic lymphocytes in the splenic tissue. Ni-exposure induced endoplasmic reticulum stress through up-regulation of the splenic expression of protein kinase R-like endoplasmic reticulum kinase, activating transcription factor 6, CCAAT/enhancer-binding protein homologous protein, X-box binding protein 1, α-subunit of eukaryotic initiation factor 2, inositol-requiring kinase 1a, mitogen-activated protein kinase, c-JunN-terminal kinase, and binding protein for immunoglobulins. Feeding on the TTO and BEO diets improved the growth measures, survival, and antioxidant capacity. Immunomodulation, enhancement of the intestinal and splenic architecture, and relief of the endoplasmic reticulum stress condition were noticed when the Ni-intoxicant groups were fed on TTO and BEO diets. Overall, the effect of the TTO diet was more pronounced than the BEO diet in mitigating the negative consequences of Ni-intoxication in Nile tilapia. Dietary fortification of 0.1% TTO and/or 0.1% BEO is recommended during Ni exposure in aquaculture practices.
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