Gum Arabic: A Reducing Agent of Uric Acid and a Supportive Treatment of Gout

Abstract

Gum arabic (GA) from Acacia senegal var. senegal was orally administered to patients suffering from gout. Out of fifty randomly selected patients, twenty-five patients were given a GA dose of 50 g/day for 120 days, and the remaining twenty-five patients represented the control group. Blood samples were collected from all patients on the first day of administering GA, and once every two weeks. Uric acid, urea, creatinine, haemoglobin (Hb), packed cell volume (PCV) and erythrocyte sedimentation rate (ESR), were determined using standard methods. After a 60 day depletion period, the same parameters were determined using doses of 75 and 25 g/day of GA. The results indicate that GA consumption reduces average serum uric acid levels in both male and female gout patients in a dose dependent manner, higher doses (50 and 75 g/day) causing uric acid levels to fall below normal levels. Urea and creatinine levels, which were initially within the normal range, also decreased significantly in a GA dose dependent manner. Hb and PCV levels, which were initially decreased (compared to the control group), increased significantly in a GA dose dependent manner back towards normal (control group) levels, and at the highest GA dose (75 g/day) increased beyond normal levels. ESR levels, which were initially elevated (compared to the control group), decreased significantly in a GA dose dependent manner back towards normal (control group) levels, and at the higher GA doses (50 and 75 g/day) decreased below normal levels.

Hepato-toxic risk of gum arabic during adenine-induced renal toxicity prevention

“…This may be explained on the basis of GA antioxidant effect that protects against cellular leakage and loss of functional integrity of hepatocytes cell membranes. In addition to Babiker et al (2017) and Eyibo et al (2018), our results regarding GA effect on liver were in the same line with Moustafa et al (2014) who observed that GA did not protect or repair hepatocytes deterioration induced by diethylnitrosamine/CCl 4 and did not induce cellular apoptosis. Besides, even liver histology of healthy mice treated with GA alone in Al-Kenanny et al (2012) study showed many pathological changes in hepatic architecture.…”

“…Antioxidant effect of GA is still a matter of argument and it has not been resolved; some studies confirmed it and others not (Hamid et al, 2018;Nasir, 2013). Moustafa et al (2014) observed MDA elevations in GA group (injected once with a dose of 0.2 mg/100 μl/mice) (p > 0.05) and GA plus laser group as well as hepatic hyperplasia groups treated with GA plus laser (p < 0.05) compared with control. While Al-Kenanny et al (2012) observed a significant decrease in MDA in mice with liver injury induced by gentamycin treated with GA (dose of 10 g/ kg orally for 8 days).…”

“…Physically, treatment of rats with AD significantly caused a gradual dramatic decrease in rats' body weight. This reduction could be attributed to a reduction in food intake due to uremia (Johari et al, 2008), as a compensatory response increased glycogen, lipid, and protein degradation takes place leading to continued weight loss. Actually, concomitant oral administration of GA with AD did not normalize rat body weight but it just lowered its reduction from −25% to −3.5% indicating that GA administration did not significantly alter food intake alternatively it slowed intestinal glucose transport.…”