Exopolysaccharide from Marinobacter nauticus strain GH3 reduces oxidative stress and neurotoxicity caused by Nickel in Nile Tilapia (Oreochromis niloticus)

Nickel (Ni) is a ubiquitous environmental contaminant that poses significant risks to the nervous systems of diverse organisms. This study investigated the neurotoxic effects of nickel chloride (NiCl 2 ) on Nile tilapia and the potential protective role of extracellular polymeric substances (EPS) derived from Marinobacter nauticus strain GH3 (GH3-EPS). Nile tilapia were divided into eight groups and fed for 8 weeks either a standard diet, diets supplemented with graded doses of GH3-EPS (0.075–0.3 g), GH3-EPS combined with sublethal Nickel (II) chloride exposure (1/10 LC50 ≈ 113.4 mg/L), or NiCl2 alone. At the experiment end, fish were euthanized, and brain, liver, and gill tissues were rapidly collected for accurate biochemical, molecular, and histological analyses. The expression of neurodegeneration-related genes (ApoE, Clu, and CR1) in brain tissues, antioxidant enzyme activities (GPx and GR) in liver tissues, and histopathological changes in gills and liver tissue were evaluated. NiCl 2 exposure significantly increased the expression of ApoE, Clu, and CR1 genes and decreased GPx and GR enzyme activities compared to the control group. Treatment with medium- and high-dose GH3-EPS significantly reduced the expression of these genes and increased GPx and GR activities in NiCl 2 -exposed fish. Additionally, GH3-EPS treatment significantly reduced reactive oxygen species (ROS) formation in the liver of NiCl 2 -exposed fish, with medium and high doses exhibiting inhibition rates of 32.9% and 36.6%, respectively. These findings suggest that GH3-EPS may have protective effects against NiCl 2 -induced neurotoxicity in Nile tilapia by normalizing gene expression, improving antioxidant levels, and reducing oxidative stress. This study highlights the potential of EPS as a mitigation strategy for metal-induced neurotoxicity in aquatic organisms.