Borax relieved the acrylamide-induced hematotoxic, hepatotoxic, immunotoxic and genotoxic damages in rainbow trout by regulating apoptosis and Nrf2 signaling pathway


ATAMANALP M., TÜRKEZ H., Yeltekin A. Ç. , ÖZGERİŞ F. B. , UÇAR A., ÇAĞLAR Ö., ...More

COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY, vol.259, 2022 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 259
  • Publication Date: 2022
  • Doi Number: 10.1016/j.cbpc.2022.109396
  • Journal Name: COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY
  • Journal Indexes: Science Citation Index Expanded, Scopus, Academic Search Premier, Animal Behavior Abstracts, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, MEDLINE, Veterinary Science Database
  • Keywords: Acrylamide, Borax, Genotoxicity, Immunotoxicity, Oxidative DNA damage, Rainbow trout, OXIDATIVE STRESS, BORIC-ACID, TOXICITY, ZEBRAFISH, RATS, INFLAMMATION, EXPOSURE, TISSUES, KIDNEY, BORON

Abstract

Acrylamide(AA) is a compound with wide usage areas including paper, dyes, and plastics industries. Due to its broad spectrum and water solubility suggest that this vinyl compound may cause serious environmental problems. AA was shown to exhibit neurotoxic, immunotoxic, reproductive toxicant as well as carcinogenic potency on animals. Especially in recent years, the therapeutic effects of boron and boron containing compounds like borax(BX), ulexite(ULX) and colemanite(COL) had been reported. However, the ameliorative potential by boron compounds against AA-induced toxicities had not been investigated yet. Therefore, in this investigation rainbow trout were exposed acutely to AA in the presence and absence of BX. The hematological indices and genotoxic end-points were examined in the fish blood tissue. In addition to oxidative stress response, the levels of DNA damage, CASP3, TNF-alpha, Nrf-2 as well as IL-6 amounts were determined in both blood and liver tissues of fish. The obtained results executed that AA induced toxic conditions in both tissues. In fact, an increase in the amount of oxidative stress and ROS, and a decrease in GSH levels were observed. AA exposure led to an increase in CASP3levels and 8-OHdG formation. It was also found that Nrf-2 pathway contributed to the initiation of oxidative stress that associated with AA-induced toxicity. On the contrary, our findings indicated that co-exposure of BX with AA elicited oxidative stress and cell death. In a conclusion BX was suggested as a useful and effective natural agent for the prevention and early treatment of AA toxicity in fish.