ملخص
Background: Subjects with chronic renal failure (CRF) exhibit oxidative genome damage, which may predispose to carcinogenesis, and Gum acacia (GumA) ameliorates this condition in humans and animals. We evaluated here renal DNA damage and urinary excretion of four nucleic acid oxidation adducts namely 8-oxoguanine (8-oxoGua), 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), 8-oxoguanosine (8-oxoGuo) and 8-hydroxy-2-deoxyguanisone (8-OHdg) in rats with adenine (ADE)-induced CRF with and without GumA treatment.
Materials and methods: Twenty-four rats were divided into four equal groups and treated for 4 weeks. The first group was given normal food and water (control). The second group was given normal food and GumA (15% w/v) in drinking water. The third group was fed powder diet containing adenine (ADE) (0·75% w/w in feed). The fourth group was fed like in the third group, plus GumA in drinking water (15%, w/v).
Results: ADE feeding induced CRF (as measured by several physiological, biochemical and histological indices) and also caused a significant genetic damage and significant decreases in urinary 8-oxo Gua and 8-oxoGuo, but not in the other nucleic acids. However, concomitant GumA treatment reduced the level of genetic damage in kidney cells as detected by Comet assay and significantly reversed the effect of adenine on urinary 8-oxoGuo.
Conclusions: Treatment with GumA is able to mitigate genetic damage in renal tissues of rats with ADE-induced CRF.
Materials and methods: Twenty-four rats were divided into four equal groups and treated for 4 weeks. The first group was given normal food and water (control). The second group was given normal food and GumA (15% w/v) in drinking water. The third group was fed powder diet containing adenine (ADE) (0·75% w/w in feed). The fourth group was fed like in the third group, plus GumA in drinking water (15%, w/v).
Results: ADE feeding induced CRF (as measured by several physiological, biochemical and histological indices) and also caused a significant genetic damage and significant decreases in urinary 8-oxo Gua and 8-oxoGuo, but not in the other nucleic acids. However, concomitant GumA treatment reduced the level of genetic damage in kidney cells as detected by Comet assay and significantly reversed the effect of adenine on urinary 8-oxoGuo.
Conclusions: Treatment with GumA is able to mitigate genetic damage in renal tissues of rats with ADE-induced CRF.
| اللغة الأصلية | English |
|---|---|
| الصفحات (من إلى) | 1221-1227 |
| عدد الصفحات | 7 |
| دورية | European Journal of Clinical Investigation |
| مستوى الصوت | 45 |
| رقم الإصدار | 12 |
| المعرِّفات الرقمية للأشياء | |
| حالة النشر | Published - ديسمبر 1 2015 |
ASJC Scopus subject areas
- ???subjectarea.asjc.2700.2700???
- ???subjectarea.asjc.1300.1308???
- ???subjectarea.asjc.1300.1303???