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Gum acacia mitigates genetic damage in adenine‐induced chronic renal failure in rats
Author(s) -
Ali B.H.,
Al Balushi K.,
AlHusseini I.,
Mandel P.,
Nemmar A.,
Schupp N.,
Ribeiro D.A.
Publication year - 2015
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.12501
Subject(s) - dna damage , gum acacia , nucleic acid , chemistry , comet assay , urinary system , medicine , kidney , oxidative damage , chronic renal failure , endocrinology , biochemistry , dna , food science , antioxidant
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‐ OH dg) 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 .