Fucoidan Modulated Oxidative Stress and Caspase-3 mRNA Expression Induced by Sulfoxaflor in the Brain of Mice

• Published in: Neurotoxicity research Vol. 39; no. 6; pp. 1908 - 1919
• Main Authors: Piner Benli, Petek, Kaya, Merve, Coskun, Cagil
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-12-2021
• Subjects: Animals; Biomedical and Life Sciences; Biomedicine; Brain - drug effects; Brain - enzymology; Brain - metabolism; Caspase 3 - drug effects; Caspase 3 - metabolism; Cell Biology; Dose-Response Relationship, Drug; Glutathione - metabolism; Male; Mice; Neurobiology; Neurochemistry; Neurology; Neuroprotective Agents - pharmacology; Neurosciences; Original Article; Oxidative Stress - drug effects; Pharmacology/Toxicology; Polysaccharides - pharmacology; Pyridines - adverse effects; Sulfur Compounds - adverse effects; Transcriptome - drug effects; Sulfoxaflor; Oxidative stress; Brain; Mice; Fucoidan; Caspase-3 gene expression
• ISSN: 1029-8428; 1476-3524
• DOI: 10.1007/s12640-021-00415-0

The current study aimed to investigate the role of fucoidan in the oxidative and apoptotic effects of sulfoxaflor, a neonicotinoid sulfoximine insecticide, in the brain of Swiss albino mice (
Mus musculus
). Sulfoxaflor and fucoidan were administered to mice at doses of 15 mg/kg/day (1/50 oral LD
50
) and 50 mg/kg/day, respectively, by oral gavage for 24 h or 7 days. The tGSH, TBARS and protein levels, and GPx, GR, and GST enzyme activities were determined by spectrophotometric methods. Caspase-3 gene expression level was determined by RT-PCR. Data analysis showed that brains of sulfoxaflor-treated mice exhibited higher TBARS levels; GPx, GR, and GST enzyme activities; and caspase-3 expression levels, as well as lower levels of tGSH. Co-administration of fucoidan and sulfoxaflor reduced the TBARS levels, increased tGSH levels, and increased GPx, GR, and GST enzyme activities. Fucoidan also decreased the sulfoxaflor-induced up-regulation of caspase-3 mRNA expression. Results of the present study showed that sulfoxaflor caused oxidative stress by inducing lipid peroxidation and altering GSH-dependent antioxidants in the brain of mice. In addition, sulfoxaflor may trigger apoptotic cell death shown by the up-regulation of caspase-3. Fucoidan treatment modulated all the aforementioned alterations in the brain of mice. It was concluded that fucoidan might have antioxidant effects that support the GSH-dependent antioxidant system and can play a modulator role in oxidative stress and caspase-3 expression in the brain of sulfoxaflor treated-mice.