Effect of commercial or depurinized milk on rat liver growth-regulatory kinases, nuclear factor-kappa B, and endonuclease in experimental hyperuricemia: comparison with allopurinol therapy.

Hyperuricemia is a biochemical hallmark of gout, renal urate lithiasis, and inherited purine disorders, and may be a result of enormous ATP breakdown or purine release as a result of cardiovascular disease, hypertension, kidney disease, eclampsia, obesity, metabolic syndrome, psoriasis, tumor lysis syndrome, or intense physical training. The beneficial role of dairy products on hyperuricemia management and prevention is well documented in the literature. The primary aim of our experimental study was to examine the effect of milk dietary regimen (commercial 1.5% fat UHT milk or patented depurinized milk) compared with allopurinol therapy on experimental hyperuricemia induced by oxonic acid in rats. Principal component analysis was applied on a data set consisting of 11 variables for 8 different experimental groups. Among the 11 parameters measured (plasma uric acid and the liver parameters NFκB-p65, Akt kinase/phospho-Akt kinase, ERK kinase/phospho-ERK kinase, IRAK kinase/phospho IRAK kinase, p38/phospho-p38, and DNase), Akt/phospho Akt and ERK/phospho-ERK signaling were extracted as the most discriminating. We also compared the content of various potentially toxic compounds (sulfur compounds, ketones, aldehydes, alcohols, esters, carboxylic acids, and phthalates) in untreated commercial milk and depurinized milk. Of all the compounds investigated in this study that were observed in commercial milk (24 volatile organic compounds and 4 phthalates), 6 volatile organic compounds were not detected in depurinized milk. For almost all of the other compounds, significant decreases in concentration were observed in depurinized milk compared with commercial milk. In conclusion, a depurinized milk diet may be recommended in nutritional treatment of primary and secondary hyperuricemia to avoid uric acid and other volatile, potentially toxic compounds that may slow down liver regeneration and may induce chronic liver diseases.