Sıçan böbrek dokusunda etanolün akut toksisitesi ve borik asitin koruyucu rolü

Yıl 2022, Cilt: 15 Sayı: 1, 107 - 113, 15.04.2022

Tuğçe Gül Güney Aleyna Çalışkan Fatih Kar Ayşe Çakır Gündoğdu Cansu Özbayer

https://doi.org/10.46309/biodicon.2022.1084827

Cited By: 2

Öz

Bu çalışmada, akut alkol toksisitesine bağlı olarak böbrek dokusu üzerinde oksidatif stresin indüklenmesi ile geçen süreçte borik asidin potansiyel koruyucu etkisinin olup olamayacağı biyokimyasal ve histolojik inceleme yöntemleri ile değerlendirilmiştir. Akut etanol toksisitesi arttıkça lipit peroksidasyonu ve oksidatif stresi arttırmaktadır. Çalışmada 250-300 gr. ağırlığında, yaşça ve ağırlıkça eşleşen 3-4 aylık Wistar albino cinsi dişi sıçanlar kullanılmıştır. Her grupta yedi hayvan olacak şekilde 28 dişi sıçan kullanıldı: kontrol, etanol, borik asit (BA) ve etanol + BA. Histoloji ve biyokimya için böbrek dokusu örnekleri alındı. Böbrek hasarı, hematoksilen ve eozin (H&E) boyaması kullanılarak değerlendirildi. Aynı zamanda, biyokimyasal belirteçler olarak oksidatif stresi değerlendirmek için total antioksidan seviyesi (TAS), total oksidan seviyesi (TOS) ve oksidatif stres indeksi (OSI) ölçüldü. BA grubunda TOS ve OSI seviyeleri etanol grubuna göre anlamlı olarak düşerken (p<0.05), TAS seviyesinde istatistiksel olarak bir değişiklik gözlemlenmedi. Etanol uygulanan grupta, H&E boyamasında epitel hücrelerin lümene dökülmesi sonucu tübül morfolojisinde bozulma meydana geldi. Borik asit uygulanan grupta ise böbrek korteksinin yapısı kontrol grubuna benzer şekilde normal olarak gözlemlendi. Borik asit+etanol grubunda ise renal tübüllerin normal yapıda olduğu etanol uygulanan gruba göre dilatasyonun daha az olduğu gözlemlendi. BA uygulaması, hem biyokimyasal parametreler hem de histolojik sonuçlarla gösterildiği gibi, akut etanol toksisitesi oksidatif stres indüklü böbrek hasarını azalttığı gözlemlenmiştir.

Anahtar Kelimeler

Borik asit, Akut etanol toksisitesi, Böbrek, Oksidatif stres

Destekleyen Kurum

Kütahya Sağlık Bilimleri Üniversitesi

Proje Numarası

FBA-2021-88

Teşekkür

Bu çalışma, Kütahya Sağlık Bilimleri Üniversitesi Bilimsel Araştırma Projeleri Koordinasyon Birimi tarafından “FBA-2021-88” kodlu proje ile desteklenmiştir.

Acute toxicity of ethanol and protective role of boric acıd in rat kidney tissue

Öz

In this study, the potential protective effect of boric acid in the process of inducing oxidative stress on kidney tissue due to acute alcohol toxicity was evaluated by biochemical and histological examination methods. In the study, 250-300 gr. Wistar albino female rats aged 3-4 months, matched in weight, age and weight, were used. 28 female rats were used, seven animals in each group: control, ethanol, boric acid (BA) and ethanol + BA.Renal tissue samples were taken for histology and biochemistry. Kidney damage was assessed using hematoxylin and eosin (H&E) staining. At the same time, total antioxidant level (TAS), total oxidant level (TOS) and oxidative stress index (OSI) were measured to evaluate oxidative stress as biochemical markers. While TOS and OSI levels were significantly lower in the BA group compared to the ethanol group (p<0.05), no statistically significant change was observed in the TAS level. In the ethanol-treated group, deterioration in tubule morphology occurred as a result of epithelial cells spilling into the lumen in H&E staining. In the boric acid administered group, the structure of the renal cortex was observed to be normal, similar to the control group.In the boric acid+ethanol group, dilatation was observed to be less than in the ethanol administered group with normal renal tubules. As acute ethanol toxicity increases, lipid peroxidation and oxidative stress increase. BA administration has been observed to reduce acute ethanol toxicity oxidative stress-induced kidney damage, as demonstrated by both biochemical parameters and histological results.

Anahtar Kelimeler

Boric acid, Acute ethanol consumption, Kidney, Oxidative stress

Proje Numarası

FBA-2021-88

Kaynakça

• [1] Bondy, S. C. (1992). Ethanol toxicity and oxidative stress. Toxicology letters, 63(3), 231-241.
• [2] French, S. W. (1971). Acute and chronic toxicity of alcohol. In The biology of alcoholism (pp. 437-511). Springer, Boston, MA.
• [3] Scott, R. B., Reddy, K. S., Husain, K., Schlorff, E. C., Rybak, L. P., & Somani, S. M. (2000). Dose response of ethanol on antioxidant defense system of liver, lung, and kidney in rat. Pathophysiology, 7(1), 25-32.
• [4] Bashan, N., Kovsan, J., Kachko, I., Ovadia, H., & Rudich, A. (2009). Positive and negative regulation of insulin signaling by reactive oxygen and nitrogen species. Physiological reviews.
• [5] Sivapiriya, V., & Venkatraman, S. (2006). Effects of dimethoate (O, O-dimethyl S-methyl carbamoyl methyl phosphorodithioate) and ethanol in antioxidant status of liver and kidney of experimental mice. Pesticide biochemistry and physiology, 85(2), 115-121.
• [6] Ozbek, E. (2012). Induction of oxidative stress in kidney. International journal of nephrology, 2012.
• [7] Rodrigo, R., & Rivera, G. (2002). Renal damage mediated by oxidative stress: a hypothesis of protective effects of red wine. Free Radical Biology and Medicine, 33(3), 409-422.
• [8] Sogut, I., Oglakci, A., Kartkaya, K., Ol, K. K., Sogut, M. S., Kanbak, G., & Inal, M. E. (2015). Effect of boric acid on oxidative stress in rats with fetal alcohol syndrome. Experimental and therapeutic medicine, 9(3), 1023-1027.
• [9] Ince, S., Kucukkurt, I., Cigerci, I. H., Fidan, A. F., & Eryavuz, A. (2010). The effects of dietary boric acid and borax supplementation on lipid peroxidation, antioxidant activity, and DNA damage in rats. Journal of Trace Elements in Medicine and Biology, 24(3), 161-164.
• [10] Ince, S., Keles, H., Erdogan, M., Hazman, O., & Kucukkurt, I. (2012). Protective effect of boric acid against carbon tetrachloride–induced hepatotoxicity in mice. Drug and chemical toxicology, 35(3), 285-292.
• [11] Nielsen, F. H. (2008). Is boron nutritionally relevant?. Nutrition reviews, 66(4), 183-191.
• [12] Kar, F., Hacıoğlu, C., Özkoç, M., Üstünışık, N., Bütün, A., Uslu, S., & Kanbak, G. (2018). The new perspective neuroprotective effect of boric acid against ethanol-induced oxidative damage on synaptosome. Journal of Applied Biological Sciences, 12(2), 28-33.
• [13] AL-SHABANAH, O. A., AL-HARBI, M. M., AL-BEKAIRI, A. M., RAZA, M., & QURESHI, S. (2002). A STUDY OF BORIC ACID PRETREATMENT ON THE PROTECTION OF GASTRIC MUCOSA AGAINST TOXIC DAMAGE IN WISTAR ALBINO RATS. Arab Journal of Pharmaceutical Sciences, 2(1), 11-26.
• [14] Niemelä, O. (2001). Distribution of ethanol-induced protein adducts in vivo: relationship to tissue injury. Free Radical Biology and Medicine, 31(12), 1533-1538.
• [15] Latchoumycandane, C., Nagy, L. E., & McIntyre, T. M. (2014). Chronic ethanol ingestion induces oxidative kidney injury through taurine-inhibitable inflammation. Free Radical Biology and Medicine, 69, 403-416.
• [16] Sogut, I., & Kanbak, G. (2010). In vitro effects of ethanol with aspirin on rat brain synaptosomes: the potential protective role of betaine. International Journal of Neuroscience, 120(12), 774-783.
• [17] Sies, H. (1986). Biochemistry of oxidative stress. Angewandte Chemie International Edition in English, 25(12), 1058-1071.
• [18] Kucukkurt, I., Ince, S., Demirel, H. H., Turkmen, R., Akbel, E., & Celik, Y. (2015). The Effects of Boron on Arsenic‐Induced Lipid Peroxidation and Antioxidant Status in Male and Female Rats. Journal of Biochemical and Molecular Toxicology, 29(12), 564-571.
• [19] Sogut, I., Paltun, S. O., Tuncdemir, M., Ersoz, M., & Hurdag, C. (2018). The antioxidant and antiapoptotic effect of boric acid on hepatoxicity in chronic alcohol-fed rats. Canadian Journal of Physiology and Pharmacology, 96(4), 404-411.
• [20] Hunt, C. D. (2012). Dietary boron: progress in establishing essential roles in human physiology. Journal of trace elements in medicine and biology, 26(2-3), 157-160.
• [21] Cikler-Dulger, E., & Sogut, I. (2020). Investigation of the protective effects of boric acid on ethanol induced kidney injury. Biotechnic & Histochemistry, 95(3), 186-193.