TY - JOUR
T1 - New model for adenine-induced chronic renal failure in mice, and the effect of gum acacia treatment thereon
T2 - Comparison with rats
AU - Ali, Badreldin H.
AU - Al-Salam, Suhail
AU - Al Za'abi, Mohammed
AU - Waly, Mostafa I.
AU - Ramkumar, Aishwarya
AU - Beegam, Sumyia
AU - Al-Lawati, Intisar
AU - Adham, Sirin A.
AU - Nemmar, Abderrahim
N1 - Funding Information:
This work was supported by a grant from the Research Council of Oman (RC/Med/Pharm/10/01) and SQU . Thanks are due to the staff of the SQU Small Animal House for looking after the animals. GA was a kind gift from Sanwa-Cho, Toyonaka, Osaka, Japan.
PY - 2013/11
Y1 - 2013/11
N2 - Introduction: This study aimed at comparing the effects of feeding mice and rats with adenine to induce a state of chronic renal failure (CRF), and to assess the effect of treatment with gum acacia (GA) thereon. Methods: We compared the outcome, in mice, of feeding adenine at three different doses (0.75%, 0.3%, and 0.2%, w/w). Biochemical and histopathological studies were conducted in plasma, urine and renal homogenates from both species. Results: When mice and rats were fed adenine (0.75%, w/w), all treated rats survived the treatment, but all treated mice died within 1-2. days. The dosage in mice was reduced to 0.3%, w/w, for 4. weeks, but again all treated mice died within 3-4. days. A further reduction in the dosage in mice to 0.2%, w/w, for 4. weeks resulted in no mortality, and produced alterations similar to those observed in rats fed adenine at a dose of 0.75%,w/w, for 4. weeks. Plasma creatinine, urea and urinary protein were significantly increased (P< 0.001) in adenine-treated mice and rats, and this action was incompletely, but significantly (P< 0.05), reversed by GA. Adenine significantly (P< 0.001) reduced superoxide dismutase (SOD) activity and reduced glutathione (GSH) concentration in renal homogenates from both species, and these reductions were significantly (P< 0.05) ameliorated by GA. Discussion: Our data suggest that mice are more sensitive to adenine than rats, and that a dose of adenine of 0.2%, w/w, for 4. weeks in mice is suggested as a model for CRF. In both models, GA (15%, w/v, in the drinking water for 4. weeks) given concomitantly with adenine ameliorated the severity of CRF to a similar extent.
AB - Introduction: This study aimed at comparing the effects of feeding mice and rats with adenine to induce a state of chronic renal failure (CRF), and to assess the effect of treatment with gum acacia (GA) thereon. Methods: We compared the outcome, in mice, of feeding adenine at three different doses (0.75%, 0.3%, and 0.2%, w/w). Biochemical and histopathological studies were conducted in plasma, urine and renal homogenates from both species. Results: When mice and rats were fed adenine (0.75%, w/w), all treated rats survived the treatment, but all treated mice died within 1-2. days. The dosage in mice was reduced to 0.3%, w/w, for 4. weeks, but again all treated mice died within 3-4. days. A further reduction in the dosage in mice to 0.2%, w/w, for 4. weeks resulted in no mortality, and produced alterations similar to those observed in rats fed adenine at a dose of 0.75%,w/w, for 4. weeks. Plasma creatinine, urea and urinary protein were significantly increased (P< 0.001) in adenine-treated mice and rats, and this action was incompletely, but significantly (P< 0.05), reversed by GA. Adenine significantly (P< 0.001) reduced superoxide dismutase (SOD) activity and reduced glutathione (GSH) concentration in renal homogenates from both species, and these reductions were significantly (P< 0.05) ameliorated by GA. Discussion: Our data suggest that mice are more sensitive to adenine than rats, and that a dose of adenine of 0.2%, w/w, for 4. weeks in mice is suggested as a model for CRF. In both models, GA (15%, w/v, in the drinking water for 4. weeks) given concomitantly with adenine ameliorated the severity of CRF to a similar extent.
KW - Adenine
KW - Animal model
KW - Chronic renal failure
KW - Mice
KW - Rats
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U2 - 10.1016/j.vascn.2013.05.001
DO - 10.1016/j.vascn.2013.05.001
M3 - Article
C2 - 23669035
AN - SCOPUS:84886405565
SN - 1056-8719
VL - 68
SP - 384
EP - 393
JO - Journal of Pharmacological and Toxicological Methods
JF - Journal of Pharmacological and Toxicological Methods
IS - 3
ER -