title: Boric Acid Reduces the Formation of DNA Double Strand Breaks and Accelerates Wound Healing Process.
abstract: Boron is absorbed by the digestive and respiratory system, and it was considered that it is converted to boric acid (BA), which was distributed to all tissues above 90 %. The biochemical essentiality of boron element is caused by boric acid because it affects the activity of several enzymes involved in the metabolism. DNA damage repair mechanisms and oxidative stress regulation is quite important in the transition stage from normal to cancerous cells; thus, this study was conducted to investigate the protective effect of boric acid on DNA damage and wound healing in human epithelial cell line. For this purpose, the amount of DNA damage occurred with irinotecan (CPT-11), etoposide (ETP), doxorubicin (Doxo), and H2O2was determined by immunofluorescence through phosphorylation of H2AX(Ser139)and pATM(Ser1981)in the absence and presence of BA. Moreover, the effect of BA on wound healing has been investigated in epithelial cells treated with these agents. Our results demonstrated that H2AX(Ser139)foci numbers were significantly decreased in the presence of BA while wound healing was accelerated by BA compared to that in the control and only drug-treated cells. Eventually, the results indicate that BA reduced the formation of DNA double strand breaks caused by agents as well as improving the wound healing process. Therefore, we suggest that boric acid has important therapeutical effectiveness and may be used in the treatment of inflammatory diseases where oxidative stress and wound healing process plays an important role.
authors.affiliation: Department of Medical Biology, Faculty of Medicine, Celal Bayar University, 45030, Manisa, Turkey. burcu_erbaykent@yahoo.com.
authors.forename: Burcu Erbaykent
authors.initials: BE
authors.lastname: Tepedelen
authors.affiliation: Department of Medical Biology, Faculty of Medicine, Celal Bayar University, 45030, Manisa, Turkey.
authors.forename: Elif
authors.initials: E
authors.lastname: Soya
authors.affiliation: Department of Medical Biology, Faculty of Medicine, Celal Bayar University, 45030, Manisa, Turkey.
authors.forename: Mehmet
authors.initials: M
authors.lastname: Korkmaz
mesh_terms: D064007:Ataxia Telangiectasia Mutated Proteins / Q000378:metabolism; D001888:Boric Acids / Q000494:pharmacology*; D002460:Cell Line; D053903:DNA Breaks, Double-Stranded / Q000187:drug effects*; D004847:Epithelial Cells / Q000378:metabolism*; D006657:Histones / Q000378:metabolism; D006801:Humans; D010766:Phosphorylation / Q000187:drug effects; D014945:Wound Healing / Q000187:drug effects*
chemical_list: D001888:Boric Acids; D006657:Histones; C576324:ATM protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; C032688:boric acid
keywords: Boric acid; DNA damage; Doxorubicin; Inflammation; Wound healing; γH2AX(Ser139)