Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A variety of milk proteins including lactoferrin, angiogenin-1, alpha-lactalbumin, beta-lactoglobulin, lactoperoxidase, casein and the novel whey proteins lactogenin and glycolactin were tested for inhibitory activity toward human immunodeficiency virus-1 reverse transcriptase (HIV-1 RT), alpha-glucosidase, beta-glucosidase and beta-glucuronidase. Lactoferrin exerted the most potent inhibitory action with an IC50 of about 6 microM. Lactoperoxidase, lactogenin, angiogenin-1 and glycolactin inhibited HIV-1 RT activity with decreasing potencies. Beta-lactoglobulin, alpha-lactalbumin and casein displayed little or no inhibitory effect. Succinylation with succinic anhydride augmented the inhibitory effect of glycolactin, beta-lactoglobulin, alpha-lactalbumin, casein and human lactoferrin. The inhibitory effect of the various milk proteins on the activities of alpha-glucosidase, beta-glucosidase and beta-glucuronidase was meager. Succinylation tended to increase the alpha-glucosidase-inhibitory effect of milk proteins but neither their beta-glucosidase-inhibitory nor beta-glucuronidase-inhibitory effect was affected.
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PMID:First demonstration of an inhibitory activity of milk proteins against human immunodeficiency virus-1 reverse transcriptase and the effect of succinylation. 1110 90

Infants who consume casein hydrolysate formula have been shown to have lower neonatal jaundice levels than infants who consume routine formula or breast milk. Because casein hydrolysate has been shown to contain a beta-glucuronidase inhibitor, one possible mechanism to explain this finding is blockage of the enterohepatic circulation of bilirubin by a component of the formula. The aim of this research was to identify the source of the beta-glucuronidase inhibition in hydrolyzed casein. A beta-glucuronidase inhibition assay and measurements of physical and kinetic parameters were used to analyze the components of hydrolyzed casein and infant formulas. Kinetic studies used purified beta-glucuronidase. The L-aspartic acid in hydrolyzed casein accounts for the majority of the beta-glucuronidase inhibition present. Kinetic studies indicate a competitive inhibition mechanism. L-aspartic acid is a newly identified competitive inhibitor of beta-glucuronidase.
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PMID:A novel inhibitor of beta-glucuronidase: L-aspartic acid. 1156 88

We had previously found that p-nonylphenol (NP) at 1000-2000 ppm in a soy- and alfalfa-free diet induced severe polycystic kidney disease (PKD) in both male and female pups exposed from gestation day 7 through postnatal day (PND) 50 and hypothesized that differences in dietary components contributed to the severity of lesions relative to those reported in other studies using similar doses of NP. The present study investigated the dietary modulation of NP-induced PKD using the same exposure regimen with 2000 ppm NP in four different diets: the natural ingredient soy- and alfalfa-free diet that had been used in the earlier study, Purina 5K96; two defined diets AIN-93G, designated AIN-CAS, and a modified AIN-93G with soy protein isolate replacing casein as the protein source (AIN-SPI); and the commonly used natural ingredient diet Purina 5001 (P5001). Serum isoflavone levels were negligible in animals fed the soy-free AIN-CAS and 5K96 diets and were 2- to 18-fold higher in animals fed P5001 than in those fed AIN-SPI. Consumption of P5001 was significantly greater than consumption of the other diets, and those animals fed P5001 were generally significantly heavier than animals receiving the other diets. NP significantly reduced body weight gain in male pups regardless of the diet fed. There was no evidence of NP-induced kidney toxicity in male pups at PND 2, 14, or 21 or in the dams. In PND 50 male pups, serum blood urea nitrogen was significantly elevated by NP in all diet groups. Urine volume and urinary N-acetyl beta-glucuronidase were significantly increased by NP in the soy-free 5K96 and AIN-CAS diet groups. Relative kidney weights were increased by NP in all diet groups except P5001, with the greatest increase in AIN-CAS and 5K96 diet groups. Microscopic evaluation of kidneys from the PND 50 males showed that NP induced PKD in all diet groups but with marked variation in the severity depending on the diet. PKD was severe in 100% of the NP-treated animals in the AIN-CAS and 5K96 groups, moderate in 88% of the AIN-SPI diet group, and mild in only 40% of the P5001 diet group. Thus, diet can significantly modulate the development of PKD induced by dietary NP in rats. Soy components, as well as other complex dietary factors, may account for the level of protection afforded by the P5001 diet.
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PMID:Dietary modulation of p-nonylphenol-induced polycystic kidneys in male Sprague-Dawley rats. 1655 16


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