Leukocytes content

O Brien K, McDonald TO, Chart A, etal. Neovascular expression of E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in human atherosclerosis and their relation to intimal leukocyte content. Circulation 1996 93 672-682. 

About 70% of blood ascorbate is in plasma and erythrocytes (which do not concentrate the vitamin from plasma). The remainder is in white cells, which have a marked ability to concentrate ascorbate mononuclear leukocytes achieve 80-fold, platelets 40-fold, and granulocytes 25-fold concentration, compared with plasma concentration. In adequately nourished subjects, and those receiving supplements, the ascorbate concentration in erythrocytes, platelets, and granulocytes, but not in mononuclear leukocytes, is correlated with plasma concentration. Mononuclear leukocytes concentrate ascorbate independendy of plasma concentration (Evans et al., 1982). In deficiency, as plasma concentrations of ascorbate fall, mononuclear leukocyte, granulocyte, and platelet concentrations of ascorbate are protected to a considerable extent. As discussed in Section 13.5.2, the leukocyte content of ascorbate is used as an index ofvitamin C nutritional status, but in view of the differing capacity of different cell types to accumulate the vitamin, differential white cell counts are essential to interpret the results. 

The concentration of ascorbate in leukocytes is well correlated with the concentrations in other tissues and falls more slowly than plasma concentration in depletion studies. The reference range of leukocyte ascorbate is 1.1 to 2.8 pmol per 10 cells a significant loss of leukocyte ascorbate coincides with the development of clear clinical signs of scurvy. Predictably, at high levels of ascorbate intake, although the plasma concentration continues to increase with intake, the leukocyte content does not, because the cells, like othertissues, are saturated. 

K D. O Brien, T. O. McDonald, A. Chait, M. D. Allen and C. E. Alpers, Neovascular Expression of E- Selectin, Intercellular Adhesion Molecule-1, and Vascular Cell Adhesion Molecule-1 in Human Atherosclerosis and Their Relation to Intimal Leukocyte Content, Circulation 93 (1996) 672-682. 

A number of early in vitro studies demonstrated a considerable role of free radicals in liver injury (see, for example, Proceedings of International Meeting on Free Radicals in Liver Injury [341]). Later on, it was shown that chronic inflammation in the liver-induced oxidative DNA damage stimulated chronic active hepatitis and increased the risk of hepatocarcinogenesis [342,343]. Farinati et al. [344] showed that 8-OHdG content increased in circulating leukocytes of patients with chronic hepatitis C virus (HCV) infection. DNA oxidative damage is supposedly an early event of HCV-related hepatitis. The formation of isoprostanes in the liver of carbon tetrachloride-treated rats can be suppressed by the administration of vitamin E [345],... 

Overproduction of free radicals by erythrocytes and leukocytes and iron overload result in a sharp increase in free radical damage in T1 patients. Thus, Livrea et al. [385] found a twofold increase in the levels of conjugated dienes, MDA, and protein carbonyls with respect to control in serum from 42 (3-thalassemic patients. Simultaneously, there was a decrease in the content of antioxidant vitamins C (44%) and E (42%). It was suggested that the iron-induced liver damage in thalassemia may play a major role in the depletion of antioxidant vitamins. Plasma thiobarbituric acid-reactive substances (TBARS) and conjugated dienes were elevated in (3-thalassemic children compared to controls together with compensatory increase in SOD activity [386]. The development of lipid peroxidation in thalassemic erythrocytes probably depends on a decrease in reduced glutathione level and decreased catalase activity [387]. 

Results are calculated from the cahbration curve after adjusting for the blank. The protein content of the leukocyte homogenate is measured with the method described by Lowry et al. [43]. Results are usually expressed as nmol/min-mg protein for leukocyte homogenates and as nmol/spot incubation time for dried blood specimens. 

Treatment with glucocorticoids can result in minor increases in the urinary content of leukocytes and erythrocytes without clear renal injury (164). 

Hematologic Studies Hematologic study includes estimations of hemoglobin content, packed-cell volume, total erythrocytes, total leukocytes, platelets, or other measures of clotting potential. These should be performed on blood samples collected from all nonrodents, from 10 rats of both genders, from all groups at 3 months, 6 months, thereafter at approximately 6-month intervals, and at termination. If possible, these collections should be from the same rats of each interval. In additions, a pretest sample should be collected from nonrodents. 

Human leukocyte elastase (HLE EC 3.4.21.37 also known as human neutrophil elastase, HNE) [1] is a strongly basic glycoprotein which is produced by polymorphonuclear leukocytes (neutrophils) and is released from their azurophilic granules [2]. HLE exists as at least four distinct isozymes, which range in molecular weight from 24 [3] to 30 kDa [4] and appear to differ only in carbohydrate content [5]. Furthermore, human sputum elastase (HSE), which is isolated from purulent sputum as at least five distinct isozymes [6], is both immunologically and catalytically indistinguishable from HLE [7] and is believed to be identical to it. 

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