Neuroprotective properties of borax against aluminum hydroxide-induced neurotoxicity: Possible role of Nrf-2/BDNF/AChE pathways in fish brain

• Published in: Brain research Vol. 1803; p. 148241
• Main Authors: Alak, Gonca, Turkez, Hasan, Ucar, Arzu, Yeltekin, Aslı Cilingir, Ozgeris, Fatma Betul, Parlak, Veysel, Atamanalp, Muhammed
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 15.03.2023
• Subjects: Acetylcholinesterase - metabolism; Aluminum hydroxide; Aluminum Hydroxide - metabolism; Aluminum Hydroxide - pharmacology; Animals; Antioxidants - metabolism; Antioxidants - pharmacology; Borax; Brain; Brain - metabolism; Brain-Derived Neurotrophic Factor - metabolism; Fish; Glutathione - metabolism; Neuroproptective action; Neuroprotective Agents - metabolism; Neuroprotective Agents - pharmacology; Neurotoxicity; Oxidative Stress; Superoxide Dismutase - metabolism; Brain; Fish; Neurotoxicity; Borax; Neuroproptective action; Aluminum hydroxide
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2023.148241

[Display omitted] •BX can be use for preventing neurological and neurodegenerative as a natural supplement.•AH induced oxidative stress, disrupted the Nrf-2 pathway, and gave rise to neurotoxicity.•BX clearly activating the Nrf-2/ROS signaling pathway. The current study was designed to assess the possible neuroprotective effect of borax (BX) against the toxicity of aluminum hydroxide [AH, Al (OH)3] on brain of rainbow trout (Oncorhynchus mykiss) with multibiomarker approaches. For this purpose, the presence of the neuroprotective action by BX against the AH exposure was assessed by the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), myeloperoxidase (MPO), acetylcholinesterase (AChE). In addition, we evaluated glutathione (GSH), malondialdehyde (MDA), DNA damage (8-OHdG), apoptosis (caspase 3), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), nuclear factor erythroid-2 (Nrf-2), and brain-derived neurotrophic factor (BDNF) levels in 96 h semi-static treatment. In the 48th and 96th hour samplings, apoptosis induced by AH in the Nrf-2/BDNF/AChE pathways in rainbow trout brain tissue was revealed by DNA damage, enzyme inhibitions and lipid peroxidations. On the contrary applications of BX supported antioxidant capacity without leading apoptosis, lipid peroxidation, inflammatory response and DNA damage. BX also increased the BDNF levels and AChE activity. Moreover, BX exerted a neuroprotective effect against AH-induced neurotoxicity via down-regulating cytokine-related pathways, minimising DNA damage, apoptosis as well as up-regulating GSH, AChE, BDNF and antioxidant enzyme levels. It can be concluded that the combination of borax with AH modulated the toxic effects of AH.