ArticleVeterinary research communications2026
Dietary banana peels modulate waterborne oxyfluorfen-induced hepatotoxicity in Nile tilapia (Oreochromis niloticus) via regulation of redox homeostasis and ER stress signaling.
Article in Veterinary research communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aquatic habitats are increasingly endangered by oxyfluorfen (OXY), a diphenyl ether herbicide that induces hepatotoxicity and oxidative stress in aquatic organisms. Banana (Musa acuminata) peel, a valuable byproduct, is known for its antioxidant properties; however, its potential to counteract OXY-induced liver toxicity in Oreochromis niloticus remains unexplored. Therefore, this study investigated the hepatoprotective effects of banana peel powder (BPP) against OXY-induced liver damage and the underlying pathways. A hepatotoxicity model was implemented by subjecting O. niloticus to OXY (0.33 mg/L) for 9 weeks, with or without dietary BPP supplementation (20 g/kg). To assess hepatic injury, oxidative stress, lipid metabolism, and biochemical alterations, hepatic histopathological examination, and real-time quantitative PCR analyses were conducted. Outcomes revealed that OXY exposure disrupted lipid and protein profiles, as evidenced by increased blood cholesterol and triglycerides and reduced serum protein levels. In addition, an elevation in bilirubin content, liver functional enzymes, and lipid peroxides (malondialdehyde), with a lowering of antioxidant enzymes, was observed in the OXY-exposed fish. Moreover, OXY induced upregulation of endoplasmic reticulum stress and apoptotic-related genes (ire-1α, xbp-1, atf-6, eif-2α, chop, and jnk). In addition to that, histopathological investigation of hepatic tissues demonstrated severe hepatic degeneration, peripancreatic hemorrhage, necrosis, and congestion. Notably, dietary BPP improves antioxidant response, lipid metabolism, and liver structure, while alleviating hepatocyte damage and disrupted gene expression. Overall, BPP (20 g/kg) may protect O. niloticus against OXY-induced liver damage through its antioxidant potential, supporting its application as a functional additive in aquaculture.
Indexed as
Identifiers
42658325What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.