Mitigation of benzo(a)pyrene-induced hepatotoxicity and oxidative damage in Nile tilapia (Oreochromis niloticus) using N-acetylcysteine-loaded starch nanoparticles in porous alginate beads through the CYP1A/Nrf2/HO-1 pathway

Benzo(a)pyrene (BaP), a widespread polycyclic aromatic hydrocarbon, poses severe risks to terrestrial and aquatic organisms through oxidative damage and necroptosis in vital organs. This study explored the hepatotoxic effects of BaP in Nile tilapia (Oreochromis niloticus) and evaluated the protective potential of N-acetylcysteine-loaded starch nanoparticles encapsulated in porous alginate beads (NAC-SNPs/pALG). NAC-SNPs/pALG were characterized, and drug entrapment efficiency was measured. Six experimental groups (n = 24 each) were established: control, solvent control, vehicle (blank SNPs/pALG), BaP-exposed (50 μg/L), NAC-treated, and NAC-SNPs/pALG-treated groups, with NAC administered at 200 mg/kg fish diet for 4 weeks. BaP exposure significantly impaired growth performance; increased liver transaminases, oxidative stress biomarkers, cortisol, and proinflammatory cytokines; and elevated mRNA expression of CYP1A, caspase3, and BAX. Histopathological analysis revealed severe damage in hepatic, branchial, and intestinal tissues. NAC-SNPs/pALG co-treatment effectively mitigated these effects by improving growth indices, enhancing antioxidant enzyme activities, suppressing cortisol and inflammatory markers, and upregulating the Nrf2/HO-1 pathway. These findings underscore the enhanced bioavailability and therapeutic potential of NAC-SNPs/pALG as a protective strategy against BaP-induced oxidative stress and hepatotoxicity in aquatic organisms.