Sulfoxaflor is the first member of the neonicotinoid-sulfoximine insecticides that acts as an agonist of nicotinic acetylcholine receptors (nAChRs). This study investigated the acute effects of sulfoxaflor on acetylcholinesterase (AChE; EC 3.1.1.7) enzyme activity in the brain and muscle tissues of zebrafish (Danio rerio) as a model organism. The zebrafish were exposed to 0.87 mg/L (2.5% of 96 h 50% lethal concentration (LC50), 1.75 mg/L (5% of 96 h LC50) and 3.51 mg/L (10% of 96 h LC50) of sulfoxaflor for 24 h–48 h and 96 h periods. AChE enzyme activities were analysed by a spectrophotometric method in the brain and muscle tissues. The results of this study showed that in vivo acute sulfoxaflor exposure significantly increased AChE enzyme activity in the brain and muscle tissues of zebrafish. The induction percentages of AChE were between 10 and 83%, and 19 and 79% for brain and muscle tissues, respectively. As a result, it was found that sulfoxaflor had an effect on AChE enzyme activity in the two main tissues containing this enzyme, and it can be considered as a potential neuroactive compound for zebrafish.
The use of neonicotinoid insecticides has progressively increased worldwide when compared with other insecticide groups. Due to this increase, non-target animal species such as fish are exposed to neonicotinoids from different sources, so they can be accumulated at trophic levels and cause various toxic effects by reaching humans. There are limited studies related to the toxic effects of neonicotinoid sulfoximine insecticides including sulfoxaflor on non-target species. The purpose of the present study was to evaluate the effects of sulfoxaflor on GSH-related antioxidants and to determine oxidative stress-producing effect of sulfoxaflor in the gill of zebrafish ( Danio rerio). For this purpose, three sublethal concentrations of sulfoxaflor 0.87 mg/L (2.5% of 96 h LC50), 1.75 mg/L (5% of 96 h LC50), 3.51 mg/L (10% of 96 h LC50) of sulfoxaflor were exposed to zebrafish for 24, 48, and 96 h. GSH related antioxidants were evaluated by analyzing tGSH levels and GPx, GR, GST specific enzyme activities in the gill of zebrafish. The oxidative damage of sulfoxaflor on gill cells was determined by measuring TBARS levels. The results of this study demonstrated that sulfoxaflor activated GSH related antioxidants by increasing tGSH levels, GPx, GR enzyme activities and by diminishing GST enzyme activity in the gill of zebrafish. Sulfoxaflor also caused oxidative damage in the gill of zebrafish by increasing lipid peroxidation. In conclusion, this study indicated that sulfoxaflor led to oxidative stress and activation of GSH related antioxidants in the gill of zebrafish.
Fucoidan is a sulfated polysaccharide which can be found among a number of macroalgea species. It has a broad spectrum of biological activities including anti-oxidant, anti-tumor, immunoregulation, anti-viral and anti-coagulant. The current study was performed to investigate possible protective effects of fucoidan for sulfoxaflor-induced hematological/biochemical alterations and oxidative stress in the blood of male Swiss albino mice. For this purpose, sulfoxaflor was administered at a dose of 15 mg/kg/day (1/50 oral LD50), and fucoidan was administered at a dose of 50 mg/kg/day by oral gavage alone and combined for 24 h and 7 days. Hematological parameters (RBC, HGB, HCT, MCV, MCH, MCHC, Plt, WBC, Neu, Lym and Mon), serum biochemical parameters (AST, ALT, GGT, LDH, BUN, Cre and TBil), and serum oxidative stress/antioxidant markers (8-OHdG, MDA, POC and GSH) were analyzed. The results indicated that sulfoxaflor altered hematological and biochemical parameters and caused oxidative stress in mice; fucoidan ameliorated some hematological and biochemical parameters and exhibited a protective role as an antioxidant against sulfoxaflor-induced oxidative stress.
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