{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,11,13]],"date-time":"2023-11-13T02:40:42Z","timestamp":1699843242188},"reference-count":15,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,7,11]],"date-time":"2006-07-11T00:00:00Z","timestamp":1152576000000},"content-version":"vor","delay-in-days":9841,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[1979,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Erythrocytes from ten patients with severe liver disease displayed low methylene blue\u2010stimulated hexose monophosphate (HMP) shunt activity and glucose recycling despite elevated total glucose consumption when compared to controls. Heinz body formation was increased and reduced glutathione concentration significantly decreased. After hemolysis, no differences in methylene\u2010blue stimulated HMP shunt activity or glucose recycling could be demonstrated between patients and controls. The addition of 2\u2010 and 4\u2010mM NADP to the hemolysates produced significantly greater HMP shunt activity and glucose recycling in the patients' hemolysates. The addition of NADPH to the incubation mixture produced no significant stimulation of either HMP shunt activity or glucose recycling, unless methylene blue was also added. Omission of NAD or phosphate from the incubation mixture produced no change in shunt metabolism. The absence of supplemental ATP resulted in extremely low shunt metabolism and refractoriness to NADP stimulation in both patients and controls. In the absence of additional magnesium, a reduction of shunt metabolism was noted.<\/jats:p><jats:p>These data suggest that the defect in stimulated shunt metabolism in the intact erythrocytes of patients with hepatic disease does not result from an absolute enzyme deficiency, but rather from an unavailability of NADP or other cofactor.<\/jats:p>","DOI":"10.1002\/ajh.2830060403","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T05:22:47Z","timestamp":1172035367000},"page":"313-321","source":"Crossref","is-referenced-by-count":5,"title":["Abnormal erythrocyte metabolism in hepatic disease: Effects of NADP repletion"],"prefix":"10.1002","volume":"6","author":[{"given":"J. Robert","family":"Smith","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Neil E.","family":"Kay","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arlan J.","family":"Gottlieb","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Frank A.","family":"Oski","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,11]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"crossref","first-page":"955","DOI":"10.1182\/blood.V46.6.955.955","article-title":"Abnormal erythrocyte metabolism in hepatic disease","volume":"46","author":"Smith JR","year":"1975","journal-title":"Blood"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2362.1975.tb00432.x"},{"key":"e_1_2_1_4_2","doi-asserted-by":"crossref","first-page":"99","DOI":"10.1182\/blood.V43.1.99.99","article-title":"Regulatory mechanism of glutathione reductase activity in human red cells","volume":"43","author":"Yawata Y","year":"1974","journal-title":"Blood"},{"key":"e_1_2_1_5_2","first-page":"40","article-title":"The hemolytic effect of primaquine. 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