The Effect of Boric Acid and Borax on Oxidative Stress, Inflammation, ER Stress and Apoptosis in Cisplatin Toxication and Nephrotoxicity Developing as a Result of Toxication

Abstract

The development of treatment protocols that can reduce side effects in chemotherapy applications is extremely important in terms of cancer treatment. In this context, it was aimed to investigate the effects of boric acid and borax on cisplatin toxicity (nephrotoxicity) in rats. In the experimental phase, eight groups were formed from rats. Boric acid and borax were given to the treatment groups with three different doses using gavage. On the fifth day of the study, cisplatin (10 mg/kg) was administered to all rats except the control group. At the end of the study, oxidative stress-related (GSH, MDA, PCO, GPx, 8-OHdG), inflammation-related (TNF-α, IL-1β, IL-18, MCP-1, ICAM, TGF-β), apoptosis-related (p53, caspase 1, 3, 8, 12, bcl-2, bcl-xL, NFkB), and ER stress-related (GRP78, ATF-6, PERK) basic parameters were analyzed in serum, erythrocyte, and kidney tissues. Kidney tissues were also examined by histopathological and immunohistochemical methods. Borax and boric acid at different doses decreased inflammation and oxidative stress caused by cisplatin toxicity and increased ER stress. As a result of the treatments applied to experimental animals, it was determined that boric acid and borax reduced apoptotic damage in kidney tissue, but the decrease was statistically significant only in 200 mg/kg boric acid-administered group. In the study, low anti-apoptotic effects of borate doses with the anti-inflammatory and antioxidant effect may be due to increased ER stress at the relevant doses. Further studies on the effects of boron compounds on ER stress and apoptotic mechanisms may clarify this issue. Thus, possible side effects or if there are new usage areas of borone compounds which have many usage areas in clinics can be detected.

Oxidative and DNA Damage Potential of Colemanite on Zebrafish: Brain, Liver and Blood

“…As in the present study, boron containing (ulexite, colemanite, borax, etc.) agents used in therapy might induce apoptosis that activates caspase 3 and suppressed certain mechanisms (Hazman, Bozkurt, Fidan, Uysal, & Çelik, 2018). Apoptosis suppressing by borax has also been reported in a small number of aquaculture studies investigating the anti-apoptotic effect of borax on toxicity models (Alak et al 2018;2019a;2019b;2019c).…”

(1 → 3)‐β‐ d ‐glucan enhances the toxicity induced by Bortezomib in rat testis

“…Based on previous studies, it seems reasonable to conclude that the process of chemotherapy leads to trigger the activation of transcription factor NF‐κB and inflammatory cytokines (Keleş et al, ). Recently, several studies have reported that the activation of NF‐κB may induce the progression of some pathologic situations (Hazman, Bozkurt, Fidan, Uysal, & Çelik, ; Shrestha, Sorolla, Fromont, Blancafort, & Flematti, ). According to the results of immunohistochemical NF‐κB staining, positive cell densities increased in the (1 → 3)‐β‐D‐glucan and/or Bortezomib‐treated testes of rats compared with the control group.…”

Effect of rutin on oxidative and proinflammatory damage induced by cisplatin in blood serum, ureter, bladder and urethra in rats

“…Furthermore, it was also noted in our study that IL-1b and TNF-a levels have increased in the blood serum of the group given cisplatin and these parameters were found to be at reference levels in ureter, bladder and urethra tissues. Although it is not known whether cisplatin has any effects to the proinflammatory IL-1b and TNF-a levels in ureter, bladder and urethra in literature, it has been found that it increases the level of these cytokines in the uterus, ovary and many organ tissues [34,35]. In addition, it was stated that cisplatin elevated IL-1b and TNF-a levels in renal tissue at oxidative stress-forming dose [36].…”

“…In addition, it was stated that cisplatin elevated IL-1b and TNF-a levels in renal tissue at oxidative stress-forming dose [36]. Hazman et al [35] have expressed that the increased level of IL-1b and TNF-a in blood serum with cisplatin is associated with tissue damage. TNF-a and IL-1b are seen in the early stage of inflammation and initiate the release of ROS [37].…”