Borax Supplementation Alleviates Hematotoxicity and DNA Damage in Rainbow Trout (Oncorhynchus mykiss) Exposed to Copper.

Heavy metals have harmful effects on health of both ecosystems and organisms to their accumulation ability. Copper (Cu) is an essential element for organism survival, but EPA considers Cu as a priority pollutant. On the other hand, boron has well-defined biological effects in living organisms including cytoprotection and genoprotection, although borax (BX) metabolism is poorly described in fish. Moreover, the effects of boron supplementation against Cu-induced hematotoxicity and DNA damage in aquatic organisms are still undetermined. Therefore, the main aim of this study was to provide an overview of the strategy for therapeutic potential of BX against Cu exposure in rainbow trout, Oncorhynchus mykiss. For this aim, fish were fed with different doses of BX and/or copper (1.25, 2.5, and 5 mg/kg of BX; 500 and 1000 mg/kg of Cu) for 21 days in pretreatment and combined treatment options. At the end of the treatments (pre and combined), the hematological index (total erythrocytes count (RBC), total leucocytes count (WBC), hemoglobin (Hb), hematocrit (Hct), total platelet count (PLT), mean cell hemoglobin concentration (MCHC), mean cell hemoglobin (MCH), mean cell volume (MCV)), oxidative DNA damage (8-hydroxy-2-deoxyguanosine (8-OHdG)), and nuclear abnormalities in blood samples of treated and untreated fish were investigated. The statistically significant (p < 0.05) and dose-dependent increases in hematological indices, 8-OH-dG level, and rates of nuclear abnormalities were observed after exposure to Cu in both treatment group fish as compared to untreated group. On the contrary, treatments with BX doses alone did not alter these hematological and DNA damage endpoints. Moreover, both pretreatment and combined treatments with BX significantly alleviated Cu-induced hematotoxicity and genotoxicity. In a conclusion, the obtained data firstly revealed that borax exhibited hematoprotective and genoprotective effects against copper-induced toxicity in fish.