Altered Urinary Excretion of Lysosomal Hydrolases in Pregnancy

Jackson, David W.; Carder, Elizabeth A.; Voss, Carolyn; Fry, Donald E.; Glew, Robert H.

doi:10.1016/s0272-6386(12)80426-4

Cited by 12 publications

(3 citation statements)

References 22 publications

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“…The P values between the 45-minute and 90-The glycohydrolases were assayed by measuring the fluorescence minute groups of the lysosomal and cytosolic b-glucosidase activities of the 4-methylumbelliferone product liberated from the appropriate were obtained using Student's t test. glycoside substrate as described by Jackson et al 20 The b-hexosaminidase incubation mixture contained 6.25 mmol/L 4-methylumbellif-…”

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confidence: 99%

Glycohydrolases As Markers of Hepatic Ischemia–Reperfusion Injury and Recovery

Liu¹,

Schöb²,

Pugmire³

et al. 1996

Hepatology

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ism itself. A number of hypotheses have been articulated to Advances in liver surgery and transplantation have provide mechanistic explanations for reperfusion injury: free lead to a steady increase in the number of these interradical generation and attack of unsaturated lipids, proteins, ventions. Prompt quantitative assessment of hepatic and nucleic acids; increased turnover of membrane phosphofunction and a patient's subsequent morbidity and morlipids; and disturbances of calcium homeostasis at the cellutality following surgery remain difficult despite the curlar level. The liver is one of the organs that is most sensitive to hepatic ischemia, the systemic release of eight different ischemia. [5][6][7] Advances in liver surgery and liver transplantaglycohydrolases and lipid peroxides into serum were de-tion in particular have stimulated the search for quantitative termined and compared with pre-and postischemic se-biochemical markers that would provide surgeons and clinirum levels of LDH, GGT, and AST. The rapid release of cians with a means of assessing objectively and expeditiously glycohydrolases into serum was directly proportional to the functional integrity of the liver after various surgeries the length of the ischemic period from 30 to 90 minutes have been performed, in particular those which require iso-(e.g., b-glucosidase, mean 1.9-fold increase at 30 minutes; lating the organ from its normal blood supply for significant 8.3-fold at 45 minutes; and 22.8-fold at 90 minutes; P õ periods of time. The enzymes that have been used historically .002) and the activities peaked within the first 3 hours' and which are still relied upon today to monitor liver function postischemia. In contrast, AST, LDH, and GGT were re-postsurgically, include lactate dehydrogenase (LDH), g-gluleased slowly and peaked 20 to 30 hours after hepatic tamyl transpeptidase (GGT), and aspartate transaminase blood flow was restored. In swine with fatal outcomes (AST). Increased plasma activities of a number of glycohydro-(90 minutes of ischemia), all enzyme levels increased lases have been found to result from a variety of liver injuries, continuously during the final hours of life. However, in including: carbon tetrachloride-induced liver cirrhosis, 8 parswine that survived hepatic ischemia/reperfusion injury tial hepatectomy, 9,10 hepatic dearterialization, 11 hepatic cryo-(45 minutes of ischemia) the glycohydrolases, but not surgery, 12 and cold and warm hepatic ischemia. [13][14][15] Free radi-AST, LDH, and GGT, declined after 2 to 3 hours' postisch-cals produced by liver injury are thought to be the mediators emia and the serum lipid peroxide levels followed the responsible for hepatic damage and have been described in same pattern. Serum b-galactosidase and b-glucosidase many animal models. 6,7,16-18 In 1991, Chang et al. 19 reported levels are sensitive markers that rise as quickly as tradi-that following liver transplantation in the pig the activity tional enzyme markers (AST, LDH, GGT) following he-levels of several glycohy...

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confidence: 99%

Glycohydrolases As Markers of Hepatic Ischemia–Reperfusion Injury and Recovery

Liu¹,

Schöb²,

Pugmire³

et al. 1996

Hepatology

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“…Furthermore, the likelihood is low that a glomerular defect or increased glomerular filtration is the cause of the lysosomal enzymuria in the severe PEM cases. In addition, having documented a 10-fold increase in the ·-mannosidase levels in the urine of the severe PEM subjects (table 4) and knowing that the molecular weight of ·-mannosidase is 225,000 [7], it is doubtful this urinary enzyme arose from increased filtration of blood proteins through the glomerulus into the urine.…”

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confidence: 99%

“…The activities of ·-galactosidase, ß-galactosidase, ß-hexosaminidase, ß-glucuronidase and ·-mannosidase were determined using the appropriate 4-methylumbelliferone glycoside substrates (Sigma Chemical Co., St. Louis, Mo., USA) and assay procedures described elsewhere [7]. The quantity of 4-methylumbelliferone liberated was measured flourometrically (Turner flourometer, Model III; Sequoia-Turner Corp., Mountain View, Calif., USA) as described elsewhere [11] with an excitation wavelength set at 360 nm and emission measured at 520-580 nm.…”

Section: Methodsmentioning

confidence: 99%

Lysosomal Enzymuria in Protein Energy Malnutrition

Yazzie

Dasgupta²,

Okolo

et al. 1998

Am J Nephrol

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Protein energy malnutrition (PEM) is common in underprivileged populations in many parts of the world and results from diets deficient in protein (kwashiorkor) or protein and calories (marasmus). The literature documents renal tubular abnormalities in children with PEM. In PEM the reabsorption of amino acids and phosphate is defective. In many kidney disorders in which renal tubular function is impaired (e.g., diabetes, preeclampsia, nephrotic syndrome, sickle cell anemia), lysosomal enzymuria ensues. We compared the urinary excretion of the following five lysosomal enzymes in 31 Nigerian children with marasmus, kwashiorkor, or marasmic-kwashiorkor: β-hexosaminidase, α-galactosidase, β-galactosidase, β-glucuronidase, and α-mannosidase. All of the protein energy malnourished children and the 18 age- and gender-matched controls were from the city of Jos, located in central Nigeria. In the severely malnourished children, the urine levels of all five lysosomal enzymes (expressed as units of enzyme activity per mg creatinine) were markedly increased. The greatest increases were seen with β-hexosaminidase (16-fold) and β-glucuronidase (14-fold). Routine clinical analyses also revealed that, relative to the control population, the sera of the 14 most severely malnourished patients contained 2- to 5-fold more vitamin B₁₂ and markedly reduced levels (15%, p < 0.00001) of calcium. These data are significant in that they document lysosomal enzymuria in Nigerian children with severe PEM and point to the potential diagnostic utility of the urinary β-galactosidase determination for assessing renal function in children with this disorder.

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