Exopolysaccharide from Marinobacter nauticus strain GH3 reduces oxidative stress and neurotoxicity caused by Nickel in Nile Tilapia (Oreochromis niloticus)
Abstract
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.
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BibTeX
@article{khalil2026exopolysaccharide,
title = {{Exopolysaccharide from Marinobacter nauticus strain GH3 reduces oxidative stress and neurotoxicity caused by Nickel in Nile Tilapia (Oreochromis niloticus)}},
author = {Wagdy K. B. Khalil and Noha M. Sabry and Marwa I. Abdel –Tawab and Samia A. El-Fiky and Samah M. Bassem and Ahmed A. Hamed and Mohamad Abdelrazik and Ghada Abdel-Razik and Ashraf Eltaher and Mohamed E. El Awady and Fagr Kh. Abdel-Gawad},
journal = {Scientific Reports},
year = {2026},
month = oct,
doi = {10.1038/s41598-026-71953-w},
url = {https://www.nature.com/articles/s41598-026-71953-w},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Exopolysaccharide from Marinobacter nauticus strain GH3 reduces oxidative stress and neurotoxicity caused by Nickel in Nile Tilapia (Oreochromis niloticus)
AU - Wagdy K. B. Khalil
AU - Noha M. Sabry
AU - Marwa I. Abdel –Tawab
AU - Samia A. El-Fiky
AU - Samah M. Bassem
AU - Ahmed A. Hamed
AU - Mohamad Abdelrazik
AU - Ghada Abdel-Razik
AU - Ashraf Eltaher
AU - Mohamed E. El Awady
AU - Fagr Kh. Abdel-Gawad
PY - 2026
DA - 2026/10/07
JO - Scientific Reports
DO - 10.1038/s41598-026-71953-w
UR - https://www.nature.com/articles/s41598-026-71953-w
AB - 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.
SN - 2045-2322
ER -