Measurements of plasma zinc

Davies, I. J. T.; Musa, M; Dormandy, T. L.

doi:10.1136/jcp.21.3.359

Cited by 237 publications

(62 citation statements)

References 15 publications

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“…The tumour itself is probably not the source of the serum zinc as the levels are low. Similar values have been reported in hepatic metastases (Olson et al, 1958) which are not associated with raised serum levels (Vikbladh, 1951;Wolff, 1956;Davies, Musa and Dormandy, 1968).…”

Section: Discussionsupporting

confidence: 86%

Hepatic zinc concentrations in primary cancer of the liver

Kew¹,

Mallett²

1974

Br J Cancer

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Section: Discussionsupporting

confidence: 86%

Hepatic zinc concentrations in primary cancer of the liver

Kew¹,

Mallett²

1974

Br J Cancer

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“…Zn 2ϩ titration against the HRPII effect showed that Zn 2ϩ interacts with HRPII with a K d of approximately 7M ( Figure 4B), which is around the physiologic concentration of Zn 2ϩ . 36 Data for the titration of HRPII at fixed AT-heparin for the inhibition of FXa and thrombin are presented in Figure 5. In the presence of Ca 2ϩ and Zn 2ϩ , the apparent IC 50 value for the HRPII neutralization of FXa inhibition by AT-heparin is approximately 30nM ( Figure 5A).…”

mentioning

confidence: 99%

Inhibition of antithrombin by Plasmodium falciparum histidine-rich protein II

Ndonwi¹,

Burlingame²,

Miller³

et al. 2011

Blood

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Histidine-rich protein II (HRPII) is an abundant protein released into the bloodstream by Plasmodium falciparum, the parasite that causes the most severe form of human malaria. Here, we report that HRPII binds tightly and selectively to coagulation-active glycosaminoglycans (dermatan sulfate, heparan sulfate, and heparin) and inhibits antithrombin (AT). In purified systems, recombinant HRPII neutralized the heparin-catalyzed inhibition of factor Xa and thrombin by AT in a Zn 2؉ -dependent manner. The observed 50% inhibitory concentration (IC 50 ) for the HRPII neutralization of AT activity is approximately 30nM for factor Xa inhibition and 90nM for thrombin inhibition. Zn 2؉ was required for these reactions with a distribution coefficient (K d ) of approximately 7M. Substituting Zn 2؉ with Cu 2؉ , but not with Ca 2؉ , Mg 2؉ , or Fe 2؉ , maintained the HRPII effect. HRPII attenuated the prolongation in plasma clotting time induced by heparin, suggesting that HRPII inhibits AT activity by preventing its stimulation by heparin. In the microvasculature, where erythrocytes infected with P falciparum are sequestered, high levels of released HRPII may bind cellular glycosaminoglycans, prevent their interaction with AT, and thereby contribute to the procoagulant state associated with P falciparum infection. (Blood. 2011;117(23): 6347-6354) IntroductionMalaria is an ancient parasitic disease that continues to take an enormous toll on persons and communities, as well as on global economies. In humans, the disease is caused by 5 protozoan parasites of the genus Plasmodium, including P ovale, P malariae, P vivax, P knowlesi, and P falciparum. Current infection rates are estimated at 250 million annually, with approximately 1 million of those cases resulting in fatalities. 1,2 P falciparum infection is the most dreaded, accounting for almost all malaria deaths. Morbidity and mortality from P falciparum malaria result from serious complications that arise during the course of the infection, including severe anemia, neurologic impairment, acute renal failure, and coagulopathy. Coagulation disturbances may contribute to the inflammation and organ failure associated with severe disease. 3,4 Patients with P falciparum infections have prolonged prothrombin time and activated partial thromboplastin time (aPTT), 5,6 reduced levels of clotting factors, including antithrombin (AT), 7,8 and elevated levels of fibrin degradation products. 9,10 Although uncommon, frank disseminated intravascular coagulation is observed in severe cases. 5,9,11 Activation of the intrinsic coagulation cascade and induction of tissue factor expression have been proposed, [12][13][14] but the precise mechanisms leading to hemostatic alterations in P falciparum infection remain poorly understood. Whether secreted parasite products are involved has not been established. Products released by intraerythrocytic parasites include a pair of proteins with unusually high histidine content: histidine-rich protein II (HRPII) and HRPIII. 15 Of these 2 homologous proteins...

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“…Others (Davies et al, 1968;Davies 1972) Zinc plays an important role in nucleic acid and protein synthesis (Vallee, 1977) and tumour growth is retarded in zincdeficient rats (De Wys et al, 1970 (Schwartz et al, 1974 (Smith et al, 1973) and an effect of malnutrition on RBP synthesis cannot altogether be excluded. Against this explanation, however, is the finding of normal plasma protein levels in the lung-cancer patients.…”

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confidence: 99%

Vitamin A, zinc and lung cancer

Atukorala¹,

Basu²,

Dickerson³

et al. 1979

Br J Cancer

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Summary.-Serum vitamin A concentrations were measured in 26 newly diagnosed lung -cancer patients and found to be significantlv lower than those of patients of similar age with either non-malignant lung or non-lung diseases. The levels of vitamin A in the lung-cancer patients, but not in the controls, were significantly correlated with serum concentrations of retinol-binding protein (RBP) and zinc. It is suggested that low levels of zinc might reduce the synthesis of RBP and thus reduce the mobilization of vitamin A from the liver.

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Measurements of plasma zinc

Cited by 237 publications

References 15 publications

Hepatic zinc concentrations in primary cancer of the liver

Hepatic zinc concentrations in primary cancer of the liver

Inhibition of antithrombin by Plasmodium falciparum histidine-rich protein II

Vitamin A, zinc and lung cancer

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